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In an observational longitudinal study of a sub-sample of the Aberdeen 1936 birth cohort, from age 62 to 77 years, we investigated childhood intelligence, social class, education, life-course social mobility, memory test performance and memory decline in late life. We examined 388 local residents who had attended school in Aberdeen in 1947 and measured Auditory-Verbal Learning Test (AVLT) at recruitment age about 64 years and up to five times until age about 77 years. Better performance at age about 64 on AVLT was predicted by early socioeconomic status (SES), social mobility and childhood intelligence. The trajectory of AVLT decline was steeper in those who had received less education. This relationship was independent of childhood ability, sex, SES in childhood and social mobility. The protection of memory by education suggests that education supports resilience to age-related cognitive impairment. Upward social mobility does not enhance this effect, suggesting that resilience to age-related decline may be established in early life.

Objectives: the '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., Methods: we 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., Results: occupational 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)., Conclusions: childhood 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., (© The Author 2016. Published by Oxford University Press on behalf of the British Geriatrics Society. All rights reserved. For Permissions, please email: journals.permissions@oup.com.)

Previous functional gene group analyses implicated common single nucleotide polymorphisms (SNPs) in heterotrimeric G protein coding genes as being associated with differences in human intelligence. Here, we sought to replicate this finding using five independent cohorts of older adults including current IQ and childhood IQ, and using both gene- and SNP-based analytic strategies. No significant associations were found between variation in heterotrimeric G protein genes and intelligence in any cohort at either of the two time points. These results indicate that, whereas G protein systems are important in cognition, common genetic variation in these genes is unlikely to be a substantial influence on human intelligence differences.

Differences in general cognitive ability (intelligence) account for approximately half of the variation in any large battery of cognitive tests and are predictive of important life events including health. Genome-wide analyses of common single-nucleotide polymorphisms indicate that they jointly tag between a quarter and a half of the variance in intelligence. However, no single polymorphism has been reliably associated with variation in intelligence. It remains possible that these many small effects might be aggregated in networks of functionally linked genes. Here, we tested a network of 1461 genes in the postsynaptic density and associated complexes for an enriched association with intelligence. These were ascertained in 3511 individuals (the Cognitive Ageing Genetics in England and Scotland (CAGES) consortium) phenotyped for general cognitive ability, fluid cognitive ability, crystallised cognitive ability, memory and speed of processing. By analysing the results of a genome wide association study (GWAS) using Gene Set Enrichment Analysis, a significant enrichment was found for fluid cognitive ability for the proteins found in the complexes of N-methyl-D-aspartate receptor complex; P=0.002. Replication was sought in two additional cohorts (N=670 and 2062). A meta-analytic P-value of 0.003 was found when these were combined with the CAGES consortium. The results suggest that genetic variation in the macromolecular machines formed by membrane-associated guanylate kinase (MAGUK) scaffold proteins and their interaction partners contributes to variation in intelligence.

Background: The influence of white matter lesions on depressive symptoms in healthy ageing populations remains unclear. In this study, we examined the relationship between depressive symptoms and magnetic resonance imaging (MRI) detected cerebrovascular disease in a normal population living independently in the community, and measured the influence of location of brain abnormalities, fluid intelligence, living alone, and sex., Methods: Prospective cohort: 497 community dwelling individuals all born in 1936, who took part in the Scottish Mental Survey of 1947, were followed up in 2000 and at biannual intervals in a longitudinal study of health and cognitive aging. Two hundred forty-four volunteered for brain MRI in 2004-2006. Suitable data were available in 219/244, of whom 115 were men. Brain hyperintensities in lobar white matter, basal ganglia , periventricular, and infratentorial regions were measured using Scheltens' scale. Depressed mood was assessed using the Hospital Anxiety and Depression Scale (HADS) on three biannual intervals. Relationships between Scheltens' scores, HADS-D scores, fluid intelligence, living alone, and sex were assessed using general linear modeling., Results: The main predictor of depressive symptom scores was poorer fluid intelligence (partial η(2) =0.023-0.028, P < .05). Ischemic change in the brainstem (partial η(2) = 0.026, P ≤.05) and basal ganglia (partial η(2) =0.018, P ≤ .05) also predicted HADS-D scores. There was no relationship with sex or living alone., Conclusions: Hyperintensities in the brainstem and basal ganglia are associated with depressive symptoms. Higher fluid intelligence is associated with lower depressive symptoms in this normal, ageing population., (© 2012 Wiley Periodicals, Inc.)

The objectives of this study are to model the relative effects of positive (childhood intelligence) and negative (magnetic resonance imaging (MRI)-derived white matter hyperintensities (WMH)) predictors of late-life intelligence in two well-characterised normal cohorts aged 68 and 78 and to measure the influence of hypertension on WMH and lifelong cognitive change. The Scottish Mental Surveys of 1932 and 1947 tested the intelligence of almost all school children at age 11. One hundred and one participants born in 1921 and 233 participants born in 1936 had brain MRI, with measurement of WMH using Scheltens' scale, and tests of late-life fluid intelligence. Structural equation models of the effect of childhood intelligence and brain WMH on the general intelligence factor 'g' in late life in the two samples were constructed using AMOS 18. Similar models were constructed to test the effect of hypertension on WMH and lifelong cognitive change. Fluid intelligence scores were lower and WMH scores were higher in the older samples. Hypertensive participants in both samples had more WMH than normotensive participants. The positive influence of childhood intelligence on 'g' was greater in the younger sample. The negative effect of WMH on 'g' was linear and greater in the older sample due to greater WMH burden. The negative effect of hypertension on lifelong cognitive ageing was all mediated via MRI-derived brain WMH. The positive relationship between childhood and late-life intelligence decreases with age. The negative relationship between WMH and late-life intelligence is linear and increases with age.

Understanding the determinants of healthy mental ageing is a priority for society today. So far, we know that intelligence differences show high stability from childhood to old age and there are estimates of the genetic contribution to intelligence at different ages. However, attempts to discover whether genetic causes contribute to differences in cognitive ageing have been relatively uninformative. Here we provide an estimate of the genetic and environmental contributions to stability and change in intelligence across most of the human lifetime. We used genome-wide single nucleotide polymorphism (SNP) data from 1,940 unrelated individuals whose intelligence was measured in childhood (age 11 years) and again in old age (age 65, 70 or 79 years). We use a statistical method that allows genetic (co)variance to be estimated from SNP data on unrelated individuals. We estimate that causal genetic variants in linkage disequilibrium with common SNPs account for 0.24 of the variation in cognitive ability change from childhood to old age. Using bivariate analysis, we estimate a genetic correlation between intelligence at age 11 years and in old age of 0.62. These estimates, derived from rarely available data on lifetime cognitive measures, warrant the search for genetic causes of cognitive stability and change.

General intelligence is an important human quantitative trait that accounts for much of the variation in diverse cognitive abilities. Individual differences in intelligence are strongly associated with many important life outcomes, including educational and occupational attainments, income, health and lifespan. Data from twin and family studies are consistent with a high heritability of intelligence, but this inference has been controversial. We conducted a genome-wide analysis of 3511 unrelated adults with data on 549,692 single nucleotide polymorphisms (SNPs) and detailed phenotypes on cognitive traits. We estimate that 40% of the variation in crystallized-type intelligence and 51% of the variation in fluid-type intelligence between individuals is accounted for by linkage disequilibrium between genotyped common SNP markers and unknown causal variants. These estimates provide lower bounds for the narrow-sense heritability of the traits. We partitioned genetic variation on individual chromosomes and found that, on average, longer chromosomes explain more variation. Finally, using just SNP data we predicted ∼1% of the variance of crystallized and fluid cognitive phenotypes in an independent sample (P=0.009 and 0.028, respectively). Our results unequivocally confirm that a substantial proportion of individual differences in human intelligence is due to genetic variation, and are consistent with many genes of small effects underlying the additive genetic influences on intelligence.

Epigenetic mechanisms have been implicated in syndromes associated with mental impairment but little is known about the role of epigenetics in determining the normal variation in human intelligence. We measured polymorphisms in four DNA methyltransferases (DNMT1, DNMT3A, DNMT3B and DNMT3L) involved in epigenetic marking and related these to childhood and adult general intelligence in a population (n = 1542) consisting of two Scottish cohorts born in 1936 and residing in Lothian (n = 1075) or Aberdeen (n = 467). All subjects had taken the same test of intelligence at age 11yrs. The Lothian cohort took the test again at age 70yrs. The minor T allele of DNMT3L SNP 11330C>T (rs7354779) allele was associated with a higher standardised childhood intelligence score; greatest effect in the dominant analysis but also significant in the additive model (coefficient = 1.40(additive); 95%CI 0.22,2.59; p = 0.020 and 1.99(dominant); 95%CI 0.55,3.43; p = 0.007). The DNMT3L C allele was associated with an increased risk of being below average intelligence (OR 1.25(additive); 95%CI 1.05,1.51; p = 0.011 and OR 1.37(dominant); 95%CI 1.11,1.68; p = 0.003), and being in the lowest 40(th) (p(additive) = 0.009; p(dominant) = 0.002) and lowest 30(th) (p(additive) = 0.004; p(dominant) = 0.002) centiles for intelligence. After Bonferroni correction for the number variants tested the link between DNMT3L 11330C>T and childhood intelligence remained significant by linear regression and centile analysis; only the additive regression model was borderline significant. Adult intelligence was similarly linked to the DNMT3L variant but this analysis was limited by the numbers studied and nature of the test and the association was not significant after Bonferroni correction. We believe that the role of epigenetics in the normal variation in human intelligence merits further study and that this novel finding should be tested in other cohorts.

Intelligence is a life-long trait that exerts powerful influences on educational success, occupational status, use of health services, life style and recreational choices. Until recently, the influence of cognitive performance on time to death was thought largely to be based on failing cognition in the time immediately before death or because lower mental ability was associated with low socioeconomic status and socioeconomic disadvantage. Children who were systematically IQ tested early in the twentieth century have now completed most of their life expectancy and permit evaluation of a possible link between childhood IQ and survival. This link is discussed as it affects people with intellectual disability and as a possible contributor to the acquisition of a healthy life style or use of health services. Studies on the topic are affected by many methodological pitfalls. Recently, as cohorts IQ tested as adolescents have completed middle age, new relevant data have become available. These suggest that earlier attempts to tease out the confounding effects of socioeconomic status on the relationship between childhood IQ and mortality did not take account of the full effects of childhood adversity on IQ and disease risk. When statistical models that include childhood adversity are tested, these attenuate and sometimes remove the contribution of IQ to morbidity and premature death., (Copyright 2009 Elsevier Ireland Ltd. All rights reserved.)

Recent studies have made great strides towards identifying putative genetic events underlying the evolution of the human brain and its emergent cognitive capacities. One of the most intriguing findings is the recurrent identification of adaptive evolution in genes associated with primary microcephaly, a developmental disorder characterized by severe reduction in brain size and intelligence, reminiscent of the early hominid condition. This has led to the hypothesis that the adaptive evolution of these genes has contributed to the emergence of modern human cognition. As with other candidate loci, however, this hypothesis remains speculative due to the current lack of methodologies for characterizing the evolutionary function of these genes in humans. Two primary microcephaly genes, ASPM and Microcephalin, have been implicated not only in the adaptive evolution of the lineage leading to humans, but in ongoing selective sweeps in modern humans as well. The presence of both the putatively adaptive and neutral alleles at these loci provides a unique opportunity for using normal trait variation within humans to test the hypothesis that the recent selective sweeps are driven by an advantage in cognitive abilities. Here, we report a large-scale association study between the adaptive alleles of these genes and normal variation in several measures of IQ. Five independent samples were used, totaling 2393 subjects, including both family-based and population-based datasets. Our overall findings do not support a detectable association between the recent adaptive evolution of either ASPM or Microcephalin and changes in IQ. As we enter the post-genomic era, with the number of candidate loci underlying human evolution growing rapidly, our findings highlight the importance of direct experimental validation in elucidating their evolutionary role in shaping the human phenotype.

Objective: To investigate whether, in old age, brain volume differences are associated with age-related change in general mental ability and/or specific cognitive abilities., Methods: The authors investigate the association between brain volumes and current cognitive function in a well-characterized sample of healthy old people (aged 79-80) whose intelligence was recorded at age 11. This allowed estimation of intellectual change over the life span., Results: After accounting for childhood intelligence, associations were found between specific cognitive measures and brain volumes. An association was also found between volumes and the general intelligence factor g. After removing the influence of g from each of the specific cognitive measures, no remaining significant associations were found between brain volumes and the specific part of each test., Conclusions: Generalized cognitive aging is associated with brain volume differences, but there is no evidence in this sample that specific components of cognitive aging are associated with differences in brain volume.

A polymorphism (Val66Met) in the gene encoding brain-derived neurotrophic factor (BDNF) has previously been associated with impaired hippocampal function and scores on the Logical Memory subtest of the Wechsler Memory Scale-Revised (WMS-R). Despite its widespread expression in the brain, there have been few studies examining the role of BDNF on cognitive domains, other than memory. We examined the association between BDNF Val66Met genotype and non-verbal reasoning, as measured by Raven's standard progressive matrices (Raven), in two cohorts of relatively healthy older people, one aged 79 (LBC1921) and the other aged 64 (ABC1936) years. LBC1921 and ABC1936 subjects had reasoning measured at age 11 years, using the Moray House Test (MHT), in the Scottish Mental Surveys of 1932 and 1947, respectively. BDNF genotype was significantly associated with later life Raven scores, controlling for sex, age 11 MHT score and cohort (P = 0.001). MHT, Verbal Fluency and Logical Memory scores were available, in later life, for LBC1921 only. BDNF genotype was significantly associated with age 79 MHT score, controlling for sex and age 11 MHT score (P = 0.016). In both significant associations, Met homozygotes scored significantly higher than heterozygotes and Val homozygotes. This study indicates that BDNF genotype contributes to age-related changes in reasoning skills, which are closely related to general intelligence.

Objective: To test the hypothesis that white matter integrity, as measured by diffusion tensor and magnetization transfer MRI is significantly associated with cognitive ability measured in youth and old age., Methods: Forty, nondemented, surviving participants of the Scottish Mental Survey of 1932 underwent brain MRI and a battery of psychometric tests covering major cognitive domains and tests of information processing efficiency. IQ scores were available from age 11. Mean diffusivity, fractional anisotropy (FA), and magnetization transfer ratio (MTR) were measured in frontal and parieto-occipital white matter and centrum semiovale., Results: Centrum semiovale FA correlated (r = 0.36 to 0.56; p < 0.02) with contemporaneous (age 83) scores on psychometric tests of nonverbal reasoning, working memory, executive function, and information processing efficiency. Centrum semiovale FA also correlated with IQ at age 11 (r = 0.37; p = 0.02). Controlling for IQ at age 11 and information processing at age 83 attenuated the association between centrum semiovale FA and general cognitive ability by approximately 85%. MTR, largely, did not show significant correlations with cognitive test scores., Conclusions: These data support the information processing efficiency hypothesis of cognitive aging and suggest one foundation for individual differences in processing efficiency. They also suggest that studies of imaging and cognition in the elderly should take into account prior mental ability rather than assuming that any associations between imaging parameters and cognitive test scores are the result of age-related changes.

A polymorphism (Val 158 Met) in the gene for catechol-O-methyl transferase (COMT) was previously associated with differences in cognitive ability and personality. Here we examine associations between this polymorphism and cognitive ability, cognitive aging, personality and mood in 460 relatively healthy people born in 1921. All had cognitive ability measured at age 11 in the Scottish Mental Survey of 1932, and again at age 79. COMT genotype was not associated with childhood IQ. At age 79, COMT genotype was significantly related to differences in verbal declarative memory (scores on the Logical Memory test; p=0.028) and to scores on the personality trait of intellect/imagination (p=0.023), adjusted for sex and childhood IQ. In both cases the Val/Met heterozygotes had higher scores than both homozygous groups. There were trends toward the heterozygotes having higher scores on the personality traits of agreeableness and conscientiousness. The effect of COMT genotype on Logical Memory scores was independent of the effect of APOE genotype, and similar in effect size. Therefore, COMT genotype may contribute to differences in normal cognitive aging and to differences in some of the major personality traits in old age.

Objective: To investigate the associations of childhood IQ and adult social factors, and smoking behaviour, lung function (forced expiratory volume in one second; FEV(1)), and smoking-related outcomes in adulthood., Design: Retrospective cohort study., Method: Participants were from the Midspan prospective studies conducted on Scottish adults in the 1970s. The sample consisted of 938 Midspan participants born in 1921 who were successfully matched with their cognitive ability test results on the Scottish Mental Survey 1932., Results: Structural equation modelling showed that age 11 IQ was not directly associated with smoking consumption, but that IQ and adult social class had indirect effects on smoking consumption via deprivation category. The influence of IQ on FEV(1) was partly indirect via social class. Gender influenced smoking consumption and also IQ and social class. There was a 21% higher risk of having a smoking-related hospital admission, cancer, or death during 25 years of follow-up for each standard deviation disadvantage in IQ. Adjustment for adult social class, deprivation category, and smoking reduced the association to 10%., Conclusion: Childhood IQ was associated with social factors which influenced lung function in adulthood, but was not associated directly with smoking consumption. In future studies, it is important to consider other pathways which may account for variance in the link between childhood IQ and health in later life.

The objective of the study was to investigate the relationship between childhood IQ of parents and characteristics of their adult offspring. It was a prospective family cohort study linked to a mental ability survey of the parents and set in Renfrew and Paisley in Scotland. Participants were 1921-born men and women who took part in the Scottish Mental Survey in 1932 and the Renfrew/Paisley study in the 1970s, and whose offspring took part in the Midspan Family study in 1996. There were 286 offspring from 179 families. Parental IQ was related to some, but not all characteristics of offspring. Greater parental IQ was associated with taller offspring. Parental IQ was inversely related to number of cigarettes smoked by offspring. Higher parental IQ was associated with better education, offspring social class and offspring deprivation category. There were no significant relationships between parental IQ and offspring systolic blood pressure, diastolic blood pressure, cholesterol, glucose, lung function, weight, body mass index, waist hip ratio, housing, alcohol consumption, marital status, car use and exercise. Structural equation modelling showed parental IQ associated with offspring education directly and mediated via parental social class. Offspring education was associated with offspring smoking and social class. The smoking finding may have implications for targeting of health education.

Twin studies provide estimates of genetic and environmental contributions to cognitive ability differences, but could be based on biased samples. Here we report whole-population estimates using twins from unique mental surveys in Scotland. The Scottish Mental Surveys of 1st June 1932 (SMS1932) and 4th June 1947 (SMS1947), respectively, administered the same validated verbal reasoning test to almost everyone born in 1921 or 1936 and attending school in Scotland. There were 572 twin pairs from the SMS1932, and 517 pairs from the SMS1947. Information on zygosity was unavailable. A novel application of a mixture distribution was used to estimate genetic and environmental components of verbal reasoning variation by maximum likelihood. We found consistent heritability (approximately 0.70) and shared environment (approximately 0.21) estimates. The estimates did not change substantially when additional quantitative traits (height and weight) were added in a multivariate analysis. More generally for studies in genetics, the methodological innovation developed here implies that large (national) data collections can provide sufficient information on twin pairs to estimate genetic parameters, even without zygosity.

Objectives: The objective was to investigate how childhood IQ related to all-cause mortality before and after age 65., Design: The Midspan prospective cohort studies, followed-up for mortality for 25 years, were linked to individuals' childhood IQ from the Scottish Mental Survey 1932., Methods: The Midspan studies collected data on risk factors for cardiorespiratory disease from a questionnaire and at a screening examination, and were conducted on adults in Scotland in the 1970s. An age 11 IQ from the Scottish Mental Survey 1932, a cognitive ability test conducted on 1921-born children attending schools in Scotland, was found for 938 Midspan participants. The relationship between childhood IQ and mortality risk, adjusting for adulthood socio-economic confounders, was analysed. The effect of adjustment for childhood IQ on the relationship between established risk factors (blood pressure, smoking, height and respiratory function) and mortality was also investigated., Results: For deaths occurring up to age 65, there was a 36% increased risk per standard deviation decrease (15 points) in childhood IQ which was reduced to 29% after adjusting for social class and deprivation category. There was no statistically significant relationship between childhood IQ and deaths occurring after the age of 65. Adjustment for childhood IQ attenuated the risk factor-mortality relationship in deaths occurring up to age 65, but had no effect in deaths occurring after age 65., Conclusions: Childhood IQ was significantly related to deaths occurring up to age 65, but not to deaths occurring after age 65.

This study examined the influence of a variation in the KLOTHO gene on cognitive ability at age 11 and age 79 in 464 people from the Lothian Birth Cohort 1921 (LBC1921), and at age 11 and age 64 in 451 people in the Aberdeen Birth Cohort 1936 (ABC1936). In the LBC1921, people with the KLOTHO V/V genotype had lower verbal reasoning ability at age 11 and age 79, and lower non-verbal reasoning at age 79, than those with the F/F genotype, or heterozygotes. The effect of the KLOTHO polymorphism on cognition at age 79 was non-significant when adjusted for IQ at age 11. In this sample, KLOTHO V allele status accounts for about 2% of the variance in life-long traits related to verbal and non-verbal reasoning, but not to age-related cognitive change. These results were not replicated in the ABC1936 sample. In a combined analysis of the LBC1921 and the ABC1936 cohorts there was a significant KLOTHOxsex interaction: women with the V/V genotype had lower non-verbal reasoning scores at age 79, after adjustment for cognitive ability at age 11. Variation in the KLOTHO gene is a possible contributor to life-long reasoning differences in humans and/or to the ageing of non-verbal reasoning, especially in women.

We investigated whether smoking is a risk factor for relative cognitive decline from age 11 to 64 years. The potentially confounding effects of childhood IQ, occupational status, level of education, presence of heart disease, hypertension, and lung function were examined. Subjects were nondemented and living independently. They were all born in 1936, had been participants in the same Scottish national IQ survey in 1947, and were reexamined at age about 64 years in 2000-2002. Current smokers and nonsmokers had significantly different mental test scores at age 64. This difference remained after adjustment for childhood IQ. Multiple linear regression identified childhood IQ, level of education, occupational code, lung function, and smoking history as significant independent predictors of mental function at age 64. In this sample, smoking makes a small (<1% variance) independent negative contribution to cognitive aging.

Background: Food supplement use is widely promoted, but little is known about the cognitive effects of food supplements., Objective: We examined the effects of food supplement use on cognitive aging., Design: This was an observational study of subjects born in 1936 whose mental ability was tested in 1947 and who were followed up in 2000-2001, at which time cognition, diet, food supplement use, and risk factors for vascular disease were assessed. In a nested case-control study, fish-oil users were matched with nonusers, and cognitive function was related to erythrocyte n-3 fatty acid composition., Results: Childhood intelligence quotient (IQ) did not differ significantly by category of food supplement use (ie, none, fish oil, vitamins, and other). At the age of 64 y, cognitive function was higher in food supplement users than in nonusers before adjustment for childhood IQ. After adjustment for childhood IQ, digit symbol (mental speed) test scores were higher in food supplement users. Fish-oil supplement users consumed more vitamin C and vegetable and cereal fiber than did non-supplement-users. In a nested case-control study, erythrocyte membrane n-3 content was higher in fish-oil supplement users than in nonusers, but cognitive function did not differ significantly between groups. Total erythrocyte n-3 fatty acids and the ratio of docosahexaenoic acid to arachidonic acid was associated with better cognitive function in late life before and after adjustment for childhood IQ., Conclusions: Food supplement use and erythrocyte n-3 content are associated with better cognitive aging. If associations with n-3 content are causal, optimization of n-3 and n-6 fatty acid intakes could improve retention of cognitive function in old age.

This study investigated the influence of childhood IQ on the relationships between risk factors and cardiovascular disease (CVD), coronary heart disease (CHD) and stroke in adulthood. Participants were from the Midspan prospective cohort studies which were conducted on adults in Scotland in the 1970s. Data on risk factors were collected from a questionnaire and at a screening examination, and participants were followed up for 25 years for hospital admissions and mortality. 938 Midspan participants were successfully matched with their age 11 IQ from the Scottish Mental Survey 1932, in which 1921-born children attending schools in Scotland took a cognitive ability test. Childhood IQ was negatively correlated with diastolic and systolic blood pressure, and positively correlated with height and respiratory function in adulthood. For each of CVD, CHD and stroke, defined as either a hospital admission or death, there was an increased relative rate per standard deviation decrease (15 points) in childhood IQ of 1.11 (95% confidence interval 1.01-1.23), 1.16 (1.03-1.32) and 1.10 (0.88-1.36), respectively. With events divided into those first occurring before and those first occurring after the age of 65, the relationships between childhood IQ and CVD, CHD and stroke were only seen before age 65 and not after age 65. Blood pressure, height, respiratory function and smoking were associated with CVD events. Relationships were stronger in the early compared to the later period for smoking and FEV1, and stronger in the later compared to the earlier period for blood pressure. Adjustment for childhood IQ had small attenuating effects on the risk factor-CVD relationship before age 65 and no effects after age 65. Adjustment for risk factors attenuated the childhood IQ-CVD relationship by a small amount before age 65. Childhood IQ was associated with CVD risk factors and events and can be considered an important new risk factor.

Objectives: To establish the relationship between childhood mental ability and adult hypertension., Design: Retrospective cohort study., Setting: Community., Participants: Non-clinical sample of people born in 1921 who participated in both the Scottish Mental Survey 1932 and the Midspan studies. Nine hundred and thirty-eight people were participants in both studies., Main Outcome Measures: Mid-life systolic and diastolic blood pressure, intelligence quotient (IQ) at age 11 years, sex, social class, height and weight., Results: After adjustment for age, sex, social class, body mass index, height, cholesterol level and smoking, there remained a 3.15 mmHg decrease in systolic blood pressure and a 1.5 mmHg decrease in diastolic blood pressure for each standard deviation increase in childhood IQ., Conclusions: The association between hypertension and lower cognitive function in adulthood is partly accounted for by individual differences in childhood IQ.

Objectives: To determine the association between prescribed medication and life long changes in cognitive ability., Design: Retrospective cohort study., Setting: Community residents of a largely urban region of South East Scotland., Participants: Four hundred and seventy-eight survivors of the 1932 Scottish Mental Health Survey (n=87,498) without dementia., Measurements: The Moray House Test (MHT) of intelligence administered at age 11 and age 80 years. Hospital Anxiety and Depression Scale (HADS) score, history of disease and current prescribed medications age 80 years., Results: After adjusting for sex, neuroactive drugs had a detrimental effect on life long cognitive change age (F=12.2, p=0.001, partial eta-squared=0.026), statins a beneficial effect (F=5.78, p=0.017, partial eta-squared=0.013) and polypharmacy a detrimental effect (F=6.46, p=0.011, partial eta-squared=0.014). In the optimal model estimated marginal means revealed: a relative improvement for statin users, IQ age 11=93.2 (95% CI 87.9-98.4) and age 80=100.6 (95% CI 95.3-105.9); compared with non-users, IQ age 11=100.9 (95% CI 99.4-102.3) and age 80=100.0 (95% CI 98.6-101.5)., Conclusions: Clinically, the degree to which drugs impair cognition in relatively fit, older people may not be apparent. However, in population terms, medication use, particularly polypharmacy, is important. Statins, used as currently indicated for cardiovascular disease, appear promising in ameliorating cognitive decline in older people. However, firm recommendation of their use should await the outcome of ongoing randomised clinical trials., (Copyright 2004 John Wiley & Sons, Ltd.)

The Scottish Mental Surveys of 1932 and 1947 collected valid IQ-type test scores for almost everyone born in 1921 and 1936 and attending school on June 1, 1932 (N=89,498) and June 4, 1947 (N=70,805). These surveys are described. This research, using the surveys' data, examined (a) the stability of intelligence differences across the life span, (b) the determinants of cognitive change from childhood to old age, and (c) the impact of childhood intelligence on survival and health in old age. Surviving participants of the Scottish Mental Surveys were tested, and the surveys' data were linked with public and health records. Novel findings on the stability of IQ scores from age 11 to age 80; sex differences in cognitive aging; the dedifferentiation hypothesis of cognitive aging; and the effect of childhood IQ on all-cause and specific mortality, morbidity, and frailty in old age are presented.

Background: The aim of this study was to examine relationships in old age between Quality of Life (QoL), childhood IQ, current cognitive performance and minor psychological symptoms, and to estimate possible contributions to these relationships made by sex, education, socioeconomic deprivation, current living group, sex, and balance and 6m walk time., Methods: We conducted a follow-up study on 88 community residents without dementia who were survivors of the Aberdeen City 1921 birth cohort. QoL was measured by the Schedule for the Evaluation of Individual QoL-Direct Weighting (SEIQoL-DW), current cognition by MMSE and Raven's Progressive Matrices (RPM), childhood IQ, minor psychological symptoms as assessed by the Hospital Anxiety and Depression Scale (HADS), and optimism by the Life Orientation Test (LOT); we included balance, 6m walk time and demographic data., Results: QoL was better in men than in women. Women reported more anxiety and depression. QoL correlated significantly with current cognition measured by RPM, childhood intelligence, anxiety and depressive symptoms, optimism and balance. The best model to predict QoL relied on childhood intelligence (13.4% of the variance) and was improved by addition of HADS (8.8 %) and LOT (4.8 %). Other variables did not contribute to the prediction of QoL., Conclusion: In the absence of dementia, childhood IQ, HADS and LOT explain 26.9% of the variance in QoL as reported by community-resident old people. The direction of association between current anxiety and depressive symptoms and lower QoL is uncertain. Lower childhood IQ may contribute to coping less well with later life. Lower QoL is not an invariable concomitant of mild cognitive decline.

Aims: Dietary supplement (DS) use is actively promoted among old people but there is little evidence in favour of DS use or information about the demographic, health and cognitive characteristics of DS users., Method: We examined 176 healthy, old people without dementia all born in 1921 and living independently in the community. IQ scores aged about 11 years were available for all subjects. DS users were more often female, had a lower BMI and were taking fewer prescribed medications than non-users., Results: Usual dietary intake, as measured by food frequency questionnaire, did not differ between DS users and DS non-users. DS users were seen to have higher Vitamin C (p<0.05), alpha-carotene (p<0.05) and lower gamma-tocopherol (p<0.001) and homocysteine (p<0.01). DS users did not differ from DS non-users in years of education, indices of occupational code, current socio-economic category or parameters of cardiovascular or respiratory functions. DS users had higher (p<0.05) childhood IQ scores but did not differ in current Mini-Mental State Examination (MMSE) score or performance on Raven's Progressive Matrices (RPM) either before or after adjustment for childhood IQ., Conclusions: DS users may enjoy somewhat better general health than non-users but the source of this difference is unknown. Possible health benefits of DS use merit further study., (Copyright 2003 John Wiley & Sons, Ltd.)

Objective: To investigate how childhood mental ability (IQ) is related to mortality and morbidity risk, when socioeconomic factors are also considered., Methods: Participants were from the Midspan studies conducted on adults in the 1970s; 938 Midspan participants were successfully matched with the Scottish Mental Survey 1932 in which children born in 1921 and attending Scottish schools on June 1, 1932, took a cognitive ability test. Mortality, hospital admissions, and cancer incidence in the 25 years after the Midspan screening were investigated in relation to childhood IQ, social class, and deprivation., Results: The risk of dying in 25 years was 17% higher for each standard deviation disadvantage in childhood IQ. Adjustment for social class and deprivation category accounted for some, but not all, of this higher risk, reducing it to 12%. Analysis by IQ quartile showed a substantial increased risk of death for the lowest-scoring quarter only. Structural equation modeling indicated that the effect of childhood IQ on mortality was partly indirectly influenced by social factors. Cause-specific mortality or hospital admission showed that lower IQ was associated with higher risks for all cardiovascular disease and coronary heart disease. Cause-specific mortality or cancer incidence risk was higher with decreasing IQ for lung cancer., Conclusions: Lower childhood IQ was related to higher mortality risk and some specific causes of death or morbidity. Childhood IQ may be considered as a marker for risk of death or illness in later life in similar and complementary ways to social class or deprivation category.

Objectives: To test the association between childhood IQ and mortality over the normal human lifespan., Design: Longitudinal cohort study., Setting: Aberdeen., Subjects: All 2792 children in Aberdeen born in 1921 and attending school on 1 June 1932 who sat a mental ability test as part of the Scottish mental survey 1932., Main Outcome Measure: Survival at 1 January 1997., Results: 79.9% (2230) of the sample was traced. Childhood mental ability was positively related to survival to age 76 years in women (P<0.0001) and men (P<0.0001). A 15 point disadvantage in mental ability at age 11 conferred a relative risk of 0.79 of being alive 65 years later (95% confidence interval 0.75 to 0.84); a 30 point disadvantage reduced this to 0.63 (0.56 to 0.71). However, men who died during active service in the second world war had a relatively high IQ. Overcrowding in the school catchment area was weakly related to death. Controlling for this factor did not alter the association between mental ability and mortality., Conclusion: Childhood mental ability is a significant factor among the variables that predict age at death.

Background: The National Adult Reading Test (NART) is widely used in research and clinical practice as an estimate of pre-morbid or prior ability. However, most of the evidence on the NART's validity as a measure of prior intellectual ability is based on concurrent administration of the NART and an IQ measure., Method: We followed up 179 individuals who had taken an IQ test (the Moray House Test) at age 11 and administered the NART and the Mini-Mental State Examination (MMSE) at age 77. A subset (N = 97) were also re-administered the original IQ test., Results: The correlation between NART performance at age 77 and IQ age 11 was high and statistically significant (r = 0.73; P < 0001). This correlation was comparable to the correlation between NART and current IQ, and childhood IQ and current IQ, despite the shared influences on the latter variable pairings. The NART had a significant correlation with the MMSE but this correlation fell to near zero (r = 0.02) after partialling out the influence of childhood IQ., Discussion: The pattern of results provides strong support for the claim that the NART primarily indexes prior (rather than current) intellectual ability.