Journal articles
Atkins J (In Press). Hereditary hemochromatosis variant associations with incident non-liver malignancies: 11-year follow-up in UK Biobank. Cancer Epidemiology, Biomarkers and Prevention
Atkins J, Masoli J, Correa-Delgado J, Pilling L, Kuo C-L, Melzer D, Kuchel G (In Press). PREEXISTING COMORBIDITIES PREDICTING COVID-19 AND MORTALITY IN THE UK BIOBANK COMMUNITY COHORT. Journal of Gerontology Series A: Biological Sciences and Medical Sciences
Banfield LR, Knapp KM, Pilling LC, Melzer D, Atkins JL (2023). Hemochromatosis Genetic Variants and Musculoskeletal Outcomes: 11.5‐Year Follow‐Up in the <scp>UK</scp> Biobank Cohort Study.
JBMR Plus,
7(10).
Abstract:
Hemochromatosis Genetic Variants and Musculoskeletal Outcomes: 11.5‐Year Follow‐Up in the UK Biobank Cohort Study
ABSTRACTThe iron overload disorder hemochromatosis is primarily caused by the homozygous HFE p.C282Y variant, but the scale of excess related musculoskeletal morbidity is uncertain. We estimated hemochromatosis‐genotype associations with clinically diagnosed musculoskeletal outcomes and joint replacement surgeries in the UK Biobank community cohort. A total of 451,143 European ancestry participants (40 to 70 years at baseline) were followed in hospital records (mean 11.5‐years). Cox proportional hazards models estimated HFE p.C282Y and p.H63D associations with incident outcomes. Male p.C282Y homozygotes (n = 1294) had increased incidence of osteoarthritis (n = 52, hazard ratio [HR]: 2.12 [95% confidence interval, CI: 1.61 to 2.80]; p = 8.8 × 10−8), hip replacement (n = 88, HR: 1.84 [95% CI: 1.49 to 2.27]; p = 1.6 × 10−8), knee replacement (n = 61, HR: 1.54 [95% CI: 1.20 to 1.98]; p = 8.4 × 10−4), and ankle and shoulder replacement, compared to males with no HFE mutations. Cumulative incidence analysis, using Kaplan–Meier lifetable probabilities demonstrated 10.4% of male homozygotes were projected to develop osteoarthritis and 15.5% to have hip replacements by age 75, versus 5.0% and 8.7% respectively without mutations. Male p.C282Y homozygotes also had increased incidence of femoral fractures (n = 15, HR: 1.72 [95% CI: 1.03 to 2.87]; p = 0.04) and osteoporosis (n = 21, HR: 1.71 [95% CI: 1.11 to 2.64]; p = 0.02), although the latter association was limited to those with liver fibrosis/cirrhosis diagnoses. Female p.C282Y homozygotes had increased incidence of osteoarthritis only (n = 57, HR: 1.46, [95% CI: 1.12 to 1.89]; p = 0.01). Male p.C282Y/p.H63D compound heterozygotes experienced a modest increased risk of hip replacements (n = 234, HR: 1.17 [95% CI: 1.02 to 1.33], p = 0.02), but this did not pass multiple testing corrections. In this large community cohort, the p.C282Y homozygote genotype was associated with substantial excess musculoskeletal morbidity in males. Wider HFE genotype testing may be justified, including in orthopedic clinics serving higher HFE variant prevalence populations. © 2023 the Authors. JBMR Plus published by Wiley Periodicals LLC. on behalf of American Society for Bone and Mineral Research.
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Atkins JL, Lucas MR, Pilling LC, Melzer D (2023). Letter to the editor regarding: “A haemochromatosis-causing HFE mutation is associated with SARS-CoV-2 susceptibility in the Czech population” clinica chimica acta 538 (2023) 211–215. Clinica Chimica Acta, 542, 117271-117271.
Wannamethee SG, Atkins JL (2023). Sarcopenic Obesity and Cardiometabolic Health and Mortality in Older Adults: a Growing Health Concern in an Ageing Population.
Curr Diab Rep,
23(11), 307-314.
Abstract:
Sarcopenic Obesity and Cardiometabolic Health and Mortality in Older Adults: a Growing Health Concern in an Ageing Population.
PURPOSE OF REVIEW: Sarcopenic obesity (SO) is a growing public health problem in older adults. Whether SO confers higher risk of cardiometabolic disease and mortality than obesity or sarcopenia alone is still a matter of debate. We focus on recent findings on SO and cardiometabolic health and mortality in older adults. RECENT FINDINGS: SO is associated with increased mortality compared to non-sarcopenic obesity, but similar mortality risk compared to sarcopenia without obesity. SO is associated with a higher risk of cardiovascular disease (CVD), diabetes, and physical disability than obesity or sarcopenia alone. SO, in the presence of diabetes, is associated with the highest risk of CVD and chronic kidney disease. A definition and diagnostic criteria for SO has recently been proposed (ESPEN and EASO). SO is associated with more adverse outcomes overall than sarcopenia or obesity alone. Future research is required to assess the impact of the new SO definition on health outcomes.
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Kuo C-L, Pilling LC, Atkins JL, Fortinsky RH, Kuchel GA, Melzer D (2022). APOE e4 Genotypes Increase Risk of Delirium During COVID-19-Related Hospitalizations: Evidence from a Large UK Cohort.
J Gerontol a Biol Sci Med Sci,
77(4), 879-880.
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Pilling LC, Atkins JL, Melzer D (2022). Genetic modifiers of penetrance to liver endpoints in HFE hemochromatosis: Associations in a large community cohort.
Hepatology,
76(6), 1735-1745.
Abstract:
Genetic modifiers of penetrance to liver endpoints in HFE hemochromatosis: Associations in a large community cohort.
BACKGROUND: the iron overload condition hereditary hemochromatosis (HH) can cause liver cirrhosis and cancer, diabetes, and arthritis. Males homozygous for the p.C282Y missense mutation in the Homeostatin Iron Regulator (HFE) gene have greatest risk; yet, only a minority develop these conditions. We aimed to determine whether common genetic variants influencing iron levels or liver disease risk in the general population also modify clinical penetrance in HFE p.C282Y and p.H63D carriers. METHODS: We studied 1294 male and 1596 female UK Biobank HFE p.C282Y homozygous participants of European ancestry with medical records up to 14 years after baseline assessment. Polygenic scores quantified genetic effects of blood iron biomarkers and relevant diseases (identified in the general population). Analyses were also performed in other HFE p.C282Y/p.H63D genotype groups. RESULTS: in male p.C282Y homozygotes, a higher iron polygenic score increased the risk of liver fibrosis or cirrhosis diagnoses (odds ratio for the top 20% of iron polygenic score vs. the bottom 20% = 4.90: 95% confidence intervals, 1.63-14.73; p = 0.005), liver cancer, and osteoarthritis but not diabetes. A liver cirrhosis polygenic score was associated with liver cancer diagnoses. In female p.C282Y homozygotes, the osteoarthritis polygenic score was associated with increased osteoarthritis diagnoses and type-2 diabetes polygenic score with diabetes. However, the iron polygenic score was not robustly associated with diagnoses in p.C282Y female homozygotes or in other p.C282Y/p.H63D genotypes. CONCLUSIONS: HFE p.C282Y homozygote penetrance to clinical disease in a large community cohort was partly explained by common genetic variants that influence iron and risks of related diagnoses in the general population, including polygenic scores in HH screening and diagnosis, may help in estimating prognosis and treatment planning.
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Atkins JL, Jylhävä J, Pedersen NL, Magnusson PK, Lu Y, Wang Y, Hägg S, Melzer D, Williams DM, Pilling LC, et al (2021). A genome-wide association study of the frailty index highlights brain pathways in ageing.
Aging Cell,
20(9).
Abstract:
A genome-wide association study of the frailty index highlights brain pathways in ageing.
Frailty is a common geriatric syndrome and strongly associated with disability, mortality and hospitalization. Frailty is commonly measured using the frailty index (FI), based on the accumulation of a number of health deficits during the life course. The mechanisms underlying FI are multifactorial and not well understood, but a genetic basis has been suggested with heritability estimates between 30 and 45%. Understanding the genetic determinants and biological mechanisms underpinning FI may help to delay or even prevent frailty. We performed a genome-wide association study (GWAS) meta-analysis of a frailty index in European descent UK Biobank participants (n = 164,610, 60-70 years) and Swedish TwinGene participants (n = 10,616, 41-87 years). FI calculation was based on 49 or 44 self-reported items on symptoms, disabilities and diagnosed diseases for UK Biobank and TwinGene, respectively. 14 loci were associated with the FI (p
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Pilling LC, Turkmen D, Fullalove H, Atkins JL, Delgado J, Kuo C-L, Kuchel GA, Ferrucci L, Bowden J, Masoli JAH, et al (2021). Analysis of <i>CYP2C19</i> genetic variants with ischaemic events in UK patients prescribed clopidogrel in primary care: a retrospective cohort study.
BMJ OPEN,
11(12).
Author URL.
Kuo C-L, Pilling L, Atkins J, Masoli J, Delgado J, Kuchel G, Melzer D, Levine M (2021). Antipsychotic Prescribing in VA-Contracted Community Nursing Homes and Incident Use Among Veterans. Innovation in Aging, 5(Suppl 1), 333-333.
Kuo C-L, Pilling LC, Atkins JL, Masoli JAH, Delgado J, Tignanelli C, Kuchel GA, Melzer D, Beckman KB, Levine ME, et al (2021). Biological Aging Predicts Vulnerability to COVID-19 Severity in UK Biobank Participants.
The Journals of Gerontology: Series A,
76(8), e133-e141.
Abstract:
Biological Aging Predicts Vulnerability to COVID-19 Severity in UK Biobank Participants
Abstract
.
. Background
. Age and disease prevalence are the 2 biggest risk factors for Coronavirus disease 2019 (COVID-19) symptom severity and death. We therefore hypothesized that increased biological age, beyond chronological age, may be driving disease-related trends in COVID-19 severity.
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. Methods
. Using the UK Biobank England data, we tested whether a biological age estimate (PhenoAge) measured more than a decade prior to the COVID-19 pandemic was predictive of 2 COVID-19 severity outcomes (inpatient test positivity and COVID-19-related mortality with inpatient test-confirmed COVID-19). Logistic regression models were used with adjustment for age at the pandemic, sex, ethnicity, baseline assessment centers, and preexisting diseases/conditions.
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. Results
. Six hundred and thirteen participants tested positive at inpatient settings between March 16 and April 27, 2020, 154 of whom succumbed to COVID-19. PhenoAge was associated with increased risks of inpatient test positivity and COVID-19-related mortality (ORMortality = 1.63 per 5 years, 95% CI: 1.43–1.86, p = 4.7 × 10−13) adjusting for demographics including age at the pandemic. Further adjustment for preexisting diseases/conditions at baseline (ORM = 1.50, 95% CI: 1.30–1.73 per 5 years, p = 3.1 × 10−8) and at the early pandemic (ORM = 1.21, 95% CI: 1.04–1.40 per 5 years, p =. 011) decreased the association.
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. Conclusions
. PhenoAge measured in 2006–2010 was associated with COVID-19 severity outcomes more than 10 years later. These associations were partly accounted for by prevalent chronic diseases proximate to COVID-19 infection. Overall, our results suggest that aging biomarkers, like PhenoAge may capture long-term vulnerability to diseases like COVID-19, even before the accumulation of age-related comorbid conditions.
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Kuo C-L, Pilling LC, Liu Z, Atkins JL, Levine ME (2021). Genetic associations for two biological age measures point to distinct aging phenotypes.
Aging Cell,
20(6).
Abstract:
Genetic associations for two biological age measures point to distinct aging phenotypes.
Biological age measures outperform chronological age in predicting various aging outcomes, yet little is known regarding genetic predisposition. We performed genome-wide association scans of two age-adjusted biological age measures (PhenoAgeAcceleration and BioAgeAcceleration), estimated from clinical biochemistry markers (Levine et al. 2018; Levine, 2013) in European-descent participants from UK Biobank. The strongest signals were found in the APOE gene, tagged by the two major protein-coding SNPs, PhenoAgeAccel-rs429358 (APOE e4 determinant) (p = 1.50 × 10-72 ); BioAgeAccel-rs7412 (APOE e2 determinant) (p = 3.16 × 10-60 ). Interestingly, we observed inverse APOE e2 and e4 associations and unique pathway enrichments when comparing the two biological age measures. Genes associated with BioAgeAccel were enriched in lipid related pathways, while genes associated with PhenoAgeAccel showed enrichment for immune system, cell function, and carbohydrate homeostasis pathways, suggesting the two measures capture different aging domains. Our study reaffirms that aging patterns are heterogeneous across individuals, and the manner in which a person ages may be partly attributed to genetic predisposition.
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Jones G, Trajanoska K, Santanasto AJ, Stringa N, Kuo C-L, Atkins JL, Lewis JR, Duong T, Hong S, Biggs ML, et al (2021). Genome-wide meta-analysis of muscle weakness identifies 15 susceptibility loci in older men and women.
Nature Communications,
12(1).
Abstract:
Genome-wide meta-analysis of muscle weakness identifies 15 susceptibility loci in older men and women
AbstractLow muscle strength is an important heritable indicator of poor health linked to morbidity and mortality in older people. In a genome-wide association study meta-analysis of 256,523 Europeans aged 60 years and over from 22 cohorts we identify 15 loci associated with muscle weakness (European Working Group on Sarcopenia in Older People definition: n = 48,596 cases, 18.9% of total), including 12 loci not implicated in previous analyses of continuous measures of grip strength. Loci include genes reportedly involved in autoimmune disease (HLA-DQA1p = 4 × 10−17), arthritis (GDF5p = 4 × 10−13), cell cycle control and cancer protection, regulation of transcription, and others involved in the development and maintenance of the musculoskeletal system. Using Mendelian randomization we report possible overlapping causal pathways, including diabetes susceptibility, haematological parameters, and the immune system. We conclude that muscle weakness in older adults has distinct mechanisms from continuous strength, including several pathways considered to be hallmarks of ageing.
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Atkins JL, Pilling LC, Heales CJ, Savage S, Kuo C-L, Kuchel GA, Steffens DC, Melzer D (2021). Hemochromatosis Mutations, Brain Iron Imaging, and Dementia in the UK Biobank Cohort.
Journal of Alzheimer's Disease,
79(3), 1203-1211.
Abstract:
Hemochromatosis Mutations, Brain Iron Imaging, and Dementia in the UK Biobank Cohort
Background: Brain iron deposition occurs in dementia. In European ancestry populations, the HFE p.C282Y variant can cause iron overload and hemochromatosis, mostly in homozygous males. Objective: to estimate p.C282Y associations with brain MRI features plus incident dementia diagnoses during follow-up in a large community cohort. Methods: UK Biobank participants with follow-up hospitalization records (mean 10.5 years). MRI in 206 p.C282Y homozygotes versus 23,349 without variants, including T2. measures (lower values indicating more iron). Results: European ancestry participants included 2,890 p.C282Y homozygotes. Male p.C282Y homozygotes had lower T2. measures in areas including the putamen, thalamus, and hippocampus, compared to no HFE mutations. Incident dementia was more common in p.C282Y homozygous men (Hazard Ratio HR = 1.83; 95% CI 1.23 to 2.72, p = 0.003), as was delirium. There were no associations in homozygote women or in heterozygotes. Conclusion: Studies are needed of whether early iron reduction prevents or slows related brain pathologies in male HFE p.C282Y homozygotes.
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Lochlainn MN, Cox NJ, Wilson T, Hayhoe RPG, Ramsay SE, Granic A, Isanejad M, Roberts HC, Wilson D, Welch C, et al (2021). Nutrition and frailty: Opportunities for prevention and treatment.
Nutrients,
13(7).
Abstract:
Nutrition and frailty: Opportunities for prevention and treatment
Frailty is a syndrome of growing importance given the global ageing population. While frailty is a multifactorial process, poor nutritional status is considered a key contributor to its path-ophysiology. As nutrition is a modifiable risk factor for frailty, strategies to prevent and treat frailty should consider dietary change. Observational evidence linking nutrition with frailty appears most robust for dietary quality: for example, dietary patterns such as the Mediterranean diet appear to be protective. In addition, research on specific foods, such as a higher consumption of fruit and vegetables and lower consumption of ultra-processed foods are consistent, with healthier profiles linked to lower frailty risk. Few dietary intervention studies have been conducted to date, although a growing number of trials that combine supplementation with exercise training suggest a multi-domain approach may be more effective. This review is based on an interdisciplinary workshop, held in November 2020, and synthesises current understanding of dietary influences on frailty, focusing on opportunities for prevention and treatment. Longer term prospective studies and well-designed trials are needed to determine the causal effects of nutrition on frailty risk and progression and how dietary change can be used to prevent and/or treat frailty in the future.
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Kuo C-L, Pilling LC, Atkins JL, Kuchel GA, Melzer D (2020). <i>ApoE</i> e2 and aging-related outcomes in 379,000 UK Biobank participants.
Abstract:
ApoE e2 and aging-related outcomes in 379,000 UK Biobank participants
AbstractThe Apolipoprotein E (APOE) e4 allele is associated with reduced longevity and increased Coronary Artery Disease (CAD) and Alzheimer’s disease, with e4e4 having markedly larger effect sizes than e3e4. The e2 longevity promoting variant is less studied. We conducted a phenome-wide association study of ApoE e2e3 and e2e2 with aging phenotypes, to assess their potential as targets for anti-aging interventions. Data were from 379,000 UK Biobank participants, aged 40 to 70 years. e2e3 (n=46,535) had mostly lower lipid-related biomarker levels including reduced total and LDL-cholesterol, and lower risks of CAD (Odds Ratio=0.87, 95% CI: 0.83 to 0.90, p=4.92×10−14) and hypertension(OR=0.94, 95% CI: 0.92 to 0.97, p=7.28×10−7) versus e3e3. However, lipid changes in e2e2 (n=2,398) were more extreme, including a marked increase in triglyceride levels (0.41 Standard Deviations, 95% CI: 0.37 to 0.45, p=5.42×10−92), with no associated changes in CAD risks. There were no associations with biomarkers of kidney function. The effects of both e2e2 and e2e3 were minimal on falls, muscle mass, grip strength or frailty. In conclusion, e2e3 has protective effects on some health outcomes, but the effects of e2e2 are not similar, complicating the potential usefulness of e2 as a target for anti-aging intervention.
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Kuo C-L, Pilling LC, Atkins JL, Masoli JAH, Delgado J, Kuchel GA, Melzer D (2020). APOE e4 Genotype Predicts Severe COVID-19 in the UK Biobank Community Cohort.
J Gerontol a Biol Sci Med Sci,
75(11), 2231-2232.
Author URL.
Kuo C-L, Pilling LC, Atkins JL, Masoli JAH, Delgado J, Kuchel GA, Melzer D (2020). ApoE e4e4 Genotype and Mortality with COVID-19 in UK Biobank. The Journals of Gerontology: Series A, 75(9), 1801-1803.
Atkins JL, Pilling LC, Masoli JAH, Kuo C-L, Shearman JD, Adams PC, Melzer D (2020). Association of Hemochromatosis <i>HFE</i> p.C282Y Homozygosity with Hepatic Malignancy. JAMA, 324(20), 2048-2048.
Pilling LC, Jones LC, Masoli JAH, Delgado J, Atkins JL, Bowden J, Fortinsky RH, Kuchel GA, Melzer D (2020). Low Vitamin D Levels and Risk of Incident Delirium in 351,000 Older <scp>UK</scp> Biobank Participants.
Journal of the American Geriatrics Society,
69(2), 365-372.
Abstract:
Low Vitamin D Levels and Risk of Incident Delirium in 351,000 Older UK Biobank Participants
BACKGROUND/OBJECTIVESDelirium is common in older adults, especially following hospitalization. Because low vitamin D levels may be associated with increased delirium risk, we aimed to determine the prognostic value of blood vitamin D levels, extending our previous genetic analyses of this relationship.DESIGNProspective cohort analysis.SETTINGCommunity‐based cohort study of adults from 22 cities across the United Kingdom (the UK Biobank).PARTICIPANTSAdults aged 60 and older by the end of follow‐up in the linked hospital inpatient admissions data, up to 14 years after baseline (n = 351,320).MEASUREMENTSAt baseline, serum vitamin D (25‐OH‐D) levels were measured. We used time‐to‐event models to estimate hazard ratios (HRs) and 95% confidence intervals (CIs) for the association between vitamin D deficiency and incident hospital‐diagnosed delirium, adjusted for age, sex, assessment month, assessment center, and ethnicity. We performed Mendelian randomization genetic analysis in European participants to further investigate vitamin D and delirium risk.RESULTSA total of 3,634 (1.03%) participants had at least one incident hospital‐diagnosed delirium episode. Vitamin D deficiency (<25 nmol/L) predicted a large incidence in delirium (HR = 2.49; 95% CI = 2.24–2.76; P = 3*10−68, compared with >50 nmol/L). Increased risk was not limited to the deficient group: insufficient levels (25–50 nmol/L) were also at increased risk (HR = 1.38; 95% CI = 1.28–1.49; P = 4*10−18). The association was independent of calcium levels, hospital‐diagnosed fractures, dementia, and other relevant cofactors. In genetic analysis, participants carrying more vitamin D–increasing variants had a reduced likelihood of incident delirium diagnosis (HR =. 80 per standard deviation increase in genetically instrumented vitamin D:. 73–.87; P = 2*10−7).CONCLUSIONProgressively lower vitamin D levels predicted increased risks of incident hospital‐diagnosed delirium, and genetic evidence supports a shared causal pathway. Because low vitamin D levels are simple to detect and inexpensive and safe to correct, an intervention trial to confirm these results is urgently needed.
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Atkins JL, Wannamathee SG (2020). Sarcopenic obesity in ageing: cardiovascular outcomes and mortality.
British Journal of Nutrition,
124(10), 1102-1113.
Abstract:
Sarcopenic obesity in ageing: cardiovascular outcomes and mortality
AbstractObesity is a major public health issue with prevalence increasing worldwide. Obesity is a well-established risk factor for CVD and mortality in adult populations. However, the impact of being overweight or obese in the elderly on CVD and mortality is controversial. Some studies even suggest that overweight and obesity, measured by BMI, are apparently associated with a decreased mortality risk (known as the obesity paradox). Ageing is associated with an increase in visceral fat and a progressive loss of muscle mass. Fat mass is positively associated and lean mass is negatively associated with risk of mortality. Therefore, in older adults BMI is not a good indicator of obesity. Sarcopenia has been defined as the degenerative loss of muscle mass, quality and strength with age and is of major concern in ageing populations. Sarcopenia has previously been associated with increased risks of metabolic impairment, cardiovascular risk factors, physical disability and mortality. It is possible for sarcopenia to co-exist with obesity, and sarcopenic obesity is a new class of obesity in older adults who have high adiposity levels together with low muscle mass, quality or strength. Therefore, sarcopenia with obesity may act together to increase their effect on metabolic disorders, CVD and mortality. This review will discuss the available evidence for the health implications of sarcopenic obesity on CVD and mortality in older adults.
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Tian Q, Pilling LC, Atkins JL, Melzer D, Ferrucci L (2020). The relationship of parental longevity with the aging brain—results from UK Biobank.
GeroScience,
42(5), 1377-1385.
Abstract:
The relationship of parental longevity with the aging brain—results from UK Biobank
A few studies report that parental longevity is associated with preserved cognition and physical function and lower risk of Alzheimer’s disease. However, data on structural neuroimaging correlates of parental longevity and its spatial distribution are limited. This study aims to examine relationships of parental longevity with regional brain structure and to explore sex differences. We identified 12,970 UK Biobank participants (mean age = 64.4, 51.5%women) with data on parental longevity, regional gray matter volumes, and white matter microstructure. Participants were categorized based on whether at least one parent lived to age 85 or older or neither parent survived to age 85. Associations of parental longevity, maternal, and paternal longevity with each neuroimaging marker of interest were examined using linear regression, adjusted for demographics, APOE e4 status, lifestyle, and cardiometabolic conditions. Compared to participants whose both parents died before 85 (43%), those with at least one parent surviving to 85 (57%) had greater volumes in hippocampus, parahippocampal gyrus, middle temporal lobe, and primary sensorimotor cortex and had lower mean diffusivity in posterior thalamic radiation and uncinate fasciculus. Associations were prominent with maternal longevity. Adjustment for cardiometabolic conditions did not affect observed associations except mean diffusivity in posterior thalamic radiation. There were no structural differences in other areas. Parental longevity is associated with preserved brain structure localized in primary sensorimotor cortex and temporal areas including hippocampus. These relationships are prominent with maternal longevity. Longitudinal studies are needed to determine whether changes in these brain structures account for the association between parental longevity and dementia.
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Parsons TJ, Papachristou E, Atkins JL, Papacosta O, Ash S, Lennon LT, Whincup PH, Ramsay SE, Wannamethee SG (2019). Healthier diet quality and dietary patterns are associated with lower risk of mobility limitation in older men.
Eur J Nutr,
58(6), 2335-2343.
Abstract:
Healthier diet quality and dietary patterns are associated with lower risk of mobility limitation in older men.
PURPOSE: to investigate associations between diet quality, dietary patterns and mobility limitation 15 years later in a population-based sample of older British men. METHODS: We used longitudinal data from 1234 men from the British Regional Heart Study, mean age 66 years at baseline. Mobility limitation was defined as difficulty going up- or downstairs or walking 400 yards as a result of a long-term health problem. Dietary intake was measured using a food frequency questionnaire data from which the Healthy Diet Indicator (HDI), the Elderly Dietary Index (EDI), and three a posteriori dietary patterns were derived. The a posteriori dietary patterns were identified using principal components analysis: (1) high fat/low fibre, (2) prudent and (3) high sugar. RESULTS: Men with greater adherence to the EDI or HDI were less likely to have mobility limitation at follow-up, top vs bottom category odds ratio for the EDI OR 0.50, 95% CI 0.34, 0.75, and for the HDI OR 0.55, 95% CI 0.35, 0.85, after adjusting for age, social class, region of residence, smoking, alcohol consumption and energy intake. Men with a higher score for the high-fat/low-fibre pattern at baseline were more likely to have mobility limitation at follow-up, top vs bottom quartile odds ratio OR 3.28 95% CI 2.05, 5.24. These associations were little changed by adjusting for BMI and physical activity. CONCLUSION: Our study provides evidence that healthier eating patterns could contribute to prevention or delay of mobility limitation in older British men.
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Tamosauskaite J, Atkins J, Pilling L, Kuo C-L, Kuchel G, Ferrucci L, Melzer D (2019). Hereditary Hemochromatosis Associations with Frailty, Sarcopenia and Chronic Pain: Evidence from 200,975 Older UK Biobank Participants. Journals of Gerontology - Series a Biological Sciences and Medical Sciences
Atkins JL, Delgado J, Melzer D (2019). Life’s Simple 7 likely to be associated with dementia risk reduction in both midlife and older age groups. BMJ, l5491-l5491.
Parsons TJ, Papachristou E, Atkins JL, Papacosta O, Ash S, Lennon LT, Whincup PH, Ramsay SE, Wannamethee SG (2019). Physical frailty in older men: prospective associations with diet quality and patterns.
Age Ageing,
48(3), 355-360.
Abstract:
Physical frailty in older men: prospective associations with diet quality and patterns.
BACKGROUND: increasing numbers of older adults are living with frailty and its adverse consequences. We investigated relationships between diet quality or patterns and incident physical frailty in older British men and whether any associations were influenced by inflammation. METHODS: prospective study of 945 men from the British Regional Heart Study aged 70-92 years with no prevalent frailty. Incident frailty was assessed by questionnaire after 3 years of follow-up. Frailty was defined as having at least three of: low grip strength, low physical activity, slow walking speed, unintentional weight loss and feeling of low energy, all based on self-report. The Healthy Diet Indicator (HDI) based on WHO dietary guidelines and the Elderly Dietary Index (EDI) based on a Mediterranean-style dietary intake were computed from questionnaire data and three dietary patterns were identified using principal components analysis: prudent, high fat/low fibre and high sugar. RESULTS: men in the highest EDI category and those who followed a prudent diet were less likely to become frail [top vs bottom category odds ratio (OR) (95% CI) 0.49 (0.30, 0.82) and 0.53 (0.30, 0.92) respectively] after adjustment for potential confounders including BMI and prevalent cardiovascular disease. No significant association was seen for the HDI. By contrast those who had a high fat low fibre diet pattern were more likely to become frail [OR (95% CI) 2.54 (1.46, 4.40)]. These associations were not mediated by C-reactive protein (marker of inflammation). CONCLUSIONS: the findings suggest adherence to a Mediterranean-style diet is associated with reduced risk of developing frailty in older people.
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Atkins JL, Delgado J, Pilling L, Bowman K, Masoli J, Kuchel G, Ferrucci L, Melzer D (2018). Impact of Low Cardiovascular Risk Profiles on Geriatric Outcomes: Evidence from 421,000 Participants in Two Cohorts. Journals of Gerontology: Medical Sciences
Pilling LC, Atkins JL, Kuchel GA, Ferrucci L, Melzer D (2018). Red cell distribution width and common disease onsets in 240,477 healthy volunteers followed for up to 9 years.
PLoS ONE,
13(9).
Abstract:
Red cell distribution width and common disease onsets in 240,477 healthy volunteers followed for up to 9 years
Higher Red Blood Cell Distribution Width (RDW or anisocytosis) predicts incident coronary artery disease (CAD) plus all-cause and cardiovascular mortality, but its predictive value for other common diseases in healthy volunteers is less clear. We aimed to determine the shorter and longer term associations between RDW and incident common conditions in participants free of baseline disease, followed for 9 years. We undertook a prospective analysis of RDW% using 240,477 healthy UK Biobank study volunteers aged 40–70 years at baseline, with outcomes ascertained during follow-up (9 years). Participants were free of anemia, CAD, type-2 diabetes, stroke, hypertension, COPD, and any cancer (except non-melanoma skin cancer) at baseline. Survival models (with competing Hazards) tested associations with outcomes from hospital admission records and death certificates. High RDW (15% variation, n = 6,050) compared to low (
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Bowman K, Atkins JL, Delgado J, Kos K, Kuchel GA, Ble A, Ferrucci L, Melzer D (2017). Central adiposity and the overweight risk paradox in aging: follow-up of 130,473 UK Biobank participants.
Am J Clin Nutr,
106(1), 130-135.
Abstract:
Central adiposity and the overweight risk paradox in aging: follow-up of 130,473 UK Biobank participants.
Background: for older groups, being overweight [body mass index (BMI; in kg/m2): 25 to
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Hawkesworth S, Silverwood RJ, Armstrong B, Pliakas T, Nanchahal K, Sartini C, Amuzu A, Wannamethee G, Atkins J, Ramsay SE, et al (2017). Investigating the importance of the local food environment for fruit and vegetable intake in older men and women in 20 UK towns: a cross-sectional analysis of two national cohorts using novel methods.
INTERNATIONAL JOURNAL OF BEHAVIORAL NUTRITION AND PHYSICAL ACTIVITY,
14 Author URL.
Pilling LC, Atkins JL, Duff MO, Beaumont RN, Jones SE, Tyrrell J, Kuo C-L, Ruth KS, Tuke MA, Yaghootkar H, et al (2017). Red blood cell distribution width: Genetic evidence for aging pathways in 116,666 volunteers.
PLoS One,
12(9).
Abstract:
Red blood cell distribution width: Genetic evidence for aging pathways in 116,666 volunteers.
INTRODUCTION: Variability in red blood cell volumes (distribution width, RDW) increases with age and is strongly predictive of mortality, incident coronary heart disease and cancer. We investigated inherited genetic variation associated with RDW in 116,666 UK Biobank human volunteers. RESULTS: a large proportion RDW is explained by genetic variants (29%), especially in the older group (60+ year olds, 33.8%,
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Author URL.
Atkins JL, Whincup PH, Morris RW, Lennon LT, Papacosta O, Wannamethee SG (2016). Dietary patterns and the risk of CVD and all-cause mortality in older British men.
Br J Nutr,
116(7), 1246-1255.
Abstract:
Dietary patterns and the risk of CVD and all-cause mortality in older British men.
Dietary patterns are a major risk factor for cardiovascular morbidity and mortality; however, few studies have examined this relationship in older adults. We examined prospective associations between dietary patterns and the risk of CVD and all-cause mortality in 3226 older British men, aged 60-79 years and free from CVD at baseline, from the British Regional Heart Study. Baseline FFQ data were used to generate thirty-four food groups. Principal component analysis identified dietary patterns that were categorised into quartiles, with higher quartiles representing higher adherence to the dietary pattern. Cox proportional hazards examined associations between dietary patterns and risk of all-cause mortality and cardiovascular outcomes. We identified three interpretable dietary patterns: 'high fat/low fibre' (high in red meat, meat products, white bread, fried potato, eggs), 'prudent' (high in poultry, fish, fruits, vegetables, legumes, pasta, rice, wholemeal bread, eggs, olive oil) and 'high sugar' (high in biscuits, puddings, chocolates, sweets, sweet spreads, breakfast cereals). During 11 years of follow-up, 899 deaths, 316 CVD-related deaths, 569 CVD events and 301 CHD events occurred. The 'high-fat/low-fibre' dietary pattern was associated with an increased risk of all-cause mortality only, after adjustment for confounders (highest v. lowest quartile; hazard ratio 1·44; 95 % CI 1·13, 1·84). Adherence to a 'high-sugar' diet was associated with a borderline significant trend for an increased risk of CVD and CHD events. The 'prudent' diet did not show a significant trend with cardiovascular outcomes or mortality. Avoiding 'high-fat/low-fibre' and 'high-sugar' dietary components may reduce the risk of cardiovascular events and all-cause mortality in older adults.
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Author URL.
Atkins JL, Pilling LC, Ble A, Dutta A, Harries LW, Murray A, Brayne C, Robine JM, Kuchel GA, Ferrucci L, et al (2016). Longer-Lived Parents and Cardiovascular Outcomes: 8-Year Follow-Up in 186,000 U.K. Biobank Participants. Journal of the American College of Cardiology, 68(8), 874-875.
Atkins JL, Ramsay SE, Whincup PH, Morris RW, Lennon LT, Wannamethee SG (2015). Diet quality in older age: the influence of childhood and adult socio-economic circumstances.
British Journal of Nutrition,
113(9), 1441-1452.
Abstract:
Diet quality in older age: the influence of childhood and adult socio-economic circumstances
Socio-economic gradients in diet quality are well established. However, the influence of material socio-economic conditions particularly in childhood, and the use of multiple disaggregated socio-economic measures on diet quality have been little studied in the elderly. In the present study, we examined childhood and adult socio-economic measures, and social relationships, as determinants of diet quality cross-sectionally in 4252 older British men (aged 60–79 years). A FFQ provided data on daily fruit and vegetable consumption and the Elderly Dietary Index (EDI), with higher scores indicating better diet quality. Adult and childhood socio-economic measures included occupation/father's occupation, education and household amenities, which combined to create composite scores. Social relationships included social contact, living arrangements and marital status. Both childhood and adult socio-economic factors were independently associated with diet quality. Compared with non-manual social class, men of childhood manual social class were less likely to consume fruit and vegetables daily (OR 0·80, 95 % CI 0·66, 0·97), as were men of adult manual social class (OR 0·65, 95 % CI 0·54, 0·79), and less likely to be in the top EDI quartile (OR 0·73, 95 % CI 0·61, 0·88), similar to men of adult manual social class (OR 0·66, 95 % CI 0·55, 0·79). Diet quality decreased with increasing adverse adult socio-economic scores; however, the association with adverse childhood socio-economic scores diminished with adult social class adjustment. A combined adverse childhood and adulthood socio-economic score was associated with poor diet quality. Diet quality was most favourable in married men and those not living alone, but was not associated with social contact. Diet quality in older men is influenced by childhood and adulthood socio-economic factors, marital status and living arrangements.
Abstract.
Wannamethee SG, Atkins JL (2015). Muscle loss and obesity: the health implications of sarcopenia and sarcopenic obesity.
Proceedings of the Nutrition Society,
74(4), 405-412.
Abstract:
Muscle loss and obesity: the health implications of sarcopenia and sarcopenic obesity
This paper reviews the health implications of obesity, sarcopenia and sarcopenic obesity on CVD and mortality in older adults and discusses the obesity paradox seen in patients with CVD. Obesity is a major public health problem with increasing prevalence worldwide. It is an established risk factor for cardiovascular morbidity and mortality in adult populations. However, there is controversy surrounding the effects of obesity as measured by BMI in older people, and overweight and obesity (BMI ⩾ 25 kg/m2) are apparently associated with increased survival in those with CVD (obesity paradox). Ageing is associated with an increase in visceral fat and a progressive loss of muscle mass which have opposing effects on mortality. Thus BMI is not a good indicator of obesity in older adults. Sarcopenia, the age-associated loss of skeletal muscle mass, is a major concern in ageing populations and has been associated with metabolic impairment, CVD risk factors, physical disability and mortality. Sarcopenia often coexists with obesity. Sarcopenic obesity is a new category of obesity in older adults who have high adiposity coupled with low muscle mass. To fully understand the effect of obesity on mortality in the elderly it is important to take muscle mass into account. The evidence suggests that sarcopenia with obesity may be associated with higher levels of metabolic disorders and an increased risk of mortality than obesity or sarcopenia alone. Efforts to promote healthy ageing should focus on both preventing obesity and maintaining or increasing muscle mass.
Abstract.
Atkins JL, Wannamethee SG (2015). The effect of sarcopenic obesity on cardiovascular disease and all-cause mortality in older people.
Reviews in Clinical Gerontology,
25(2), 86-97.
Abstract:
The effect of sarcopenic obesity on cardiovascular disease and all-cause mortality in older people
SummaryObesity is a major public health problem with increasing prevalence worldwide. It is well recognized as a risk factor for cardiovascular morbidity and mortality in adult populations. Obesity prevalence is also increasing with age, and this may be particularly important in an ageing population. Ageing is associated with an increase in visceral fat and a progressive loss of muscle mass. Sarcopenia has been defined as the age-associated loss of skeletal muscle mass and has been associated with metabolic impairment, cardiovascular disease (CVD) risk factors, physical disability and mortality. Sarcopenia is often associated with obesity. Sarcopenic obesity is a new category of obesity in older adults who have high adiposity coupled with low muscle mass. Thus sarcopenia with obesity may synergistically increase their effect on metabolic disorders, CVD and mortality. This review focuses on the effects of sarcopenic obesity on the risk of cardiovascular disease and mortality in older adults.
Abstract.
Atkins JL, Whincup PH, Morris RW, Lennon LT, Papacosta O, Wannamethee SG (2014). High Diet Quality is Associated with a Lower Risk of Cardiovascular Disease and All-Cause Mortality in Older Men. The Journal of Nutrition, 144(5), 673-680.
Atkins JL, Whincup PH, Morris RW, Wannamethee SG (2014). Response to Safer et al. Journal of the American Geriatrics Society, 62(6), 1208-1209.
Atkins JL, Whincup PH, Morris RW, Lennon LT, Papacosta O, Wannamethee SG (2014). Sarcopenic Obesity and Risk of Cardiovascular Disease and Mortality: a Population‐Based Cohort Study of Older Men.
Journal of the American Geriatrics Society,
62(2), 253-260.
Abstract:
Sarcopenic Obesity and Risk of Cardiovascular Disease and Mortality: a Population‐Based Cohort Study of Older Men
ObjectivesTo examine associations between sarcopenia, obesity, and sarcopenic obesity and risk of cardiovascular disease (CVD) and all‐cause mortality in older men.DesignProspective cohort study.SettingBritish Regional Heart Study.ParticipantsMen aged 60–79 years (n = 4,252).MeasurementsBaseline waist circumference (WC) and midarm muscle circumference (MAMC) measurements were used to classify participants into four groups: sarcopenic, obese, sarcopenic obese, or optimal WC and MAMC. The cohort was followed for a mean of 11.3 years for CVD and all‐cause mortality. Cox regression analyses assessed associations between sarcopenic obesity groups and all‐cause mortality, CVD mortality, CVD events, and coronary heart disease (CHD) events.ResultsThere were 1,314 deaths, 518 CVD deaths, 852 CVD events, and 458 CHD events during follow‐up. All‐cause mortality risk was significantly greater in sarcopenic (HR = 1.41, 95% CI = 1.22–1.63) and obese (HR = 1.21, 95% CI = 1.03–1.42) men than in the optimal reference group, with the highest risk in sarcopenic obese (HR = 1.72, 95% CI = 1.35–2.18), after adjustment for lifestyle characteristics. Risk of CVD mortality was significantly greater in sarcopenic and obese but not sarcopenic obese men. No association was seen between sarcopenic obesity groups and CHD or CVD events.ConclusionSarcopenia and central adiposity were associated with greater cardiovascular mortality and all‐cause mortality. Sarcopenic obese men had the highest risk of all‐cause mortality but not CVD mortality. Efforts to promote healthy aging should focus on preventing obesity and maintaining muscle mass.
Abstract.
Atkins JL, Whincup PH, Morris RW, Wannamethee SG (2013). Low muscle mass in older men: the role of lifestyle, diet and cardiovascular risk factors. The journal of nutrition, health & aging, 18(1), 26-33.
Woodhall SC, Atkins JL, Soldan K, Hughes G, Bone A, Gill ON (2012). Repeat genital<i>Chlamydia trachomatis</i>testing rates in young adults in England, 2010. Sexually Transmitted Infections, 89(1), 51-56.
Nicolaou N, Shane S, Cherkas L, Hunkin J, Spector TD (2008). Is the Tendency to Engage in Entrepreneurship Genetic?.
Management Science,
54(1), 167-179.
Abstract:
Is the Tendency to Engage in Entrepreneurship Genetic?
We used quantitative genetics techniques to compare the entrepreneurial activity of 870 pairs of monozygotic (MZ) and 857 pairs of same-sex dizygotic (DZ) twins from the United Kingdom. We ran model-fitting analyses to estimate the genetic, shared environmental and nonshared environmental effects on the propensity of people to become entrepreneurs. We found relatively high heritabilities for entrepreneurship across different operationalizations of the phenomenon, with little effect of family environment and upbringing. Our findings suggest the importance of considering genetic factors in explanations for why people engage in entrepreneurial activity.
Abstract.
Kimura M, Cherkas LF, Kato BS, Demissie S, Hjelmborg JB, Brimacombe M, Cupples A, Hunkin JL, Gardner JP, Lu X, et al (2008). Offspring's Leukocyte Telomere Length, Paternal Age, and Telomere Elongation in Sperm. PLoS Genetics, 4(2), e37-e37.
Cherkas LF (2008). The Association Between Physical Activity in Leisure Time and Leukocyte Telomere Length. Archives of Internal Medicine, 168(2), 154-154.
Stubbe JH, Boomsma DI, Vink JM, Cornes BK, Martin NG, Skytthe A, Kyvik KO, Rose RJ, Kujala UM, Kaprio J, et al (2006). Genetic Influences on Exercise Participation in 37.051 Twin Pairs from Seven Countries. PLoS ONE, 1(1), e22-e22.
Paul SN, Kato BS, Hunkin JL, Vivekanandan S, Spector TD, Fields KB (2006). The Big Finger: the second to fourth digit ratio is a predictor of sporting ability in women. Commentary. British Journal of Sports Medicine, 40(12), 981-983.
Cherkas LF, Aviv A, Valdes AM, Hunkin JL, Gardner JP, Surdulescu GL, Kimura M, Spector TD (2006). The effects of social status on biological aging as measured by white‐blood‐cell telomere length.
Aging Cell,
5(5), 361-365.
Abstract:
The effects of social status on biological aging as measured by white‐blood‐cell telomere length
SummaryLow socio‐economic status (SES) is associated with a shortened life expectancy, but its effect on aging is unknown. The rate of white‐blood‐cell (WBC) telomere attrition may be a biological indicator of human aging. We tested the hypothesis that SES is associated with telomere attrition independent of known risk factors influencing the aging process. We studied 1552 female twins. A venous blood sample was taken from each twin and isolated WBCs used for extraction of DNA. Terminal restriction fragment length (TRFL) was measured. Questionnaire data were collected on occupation, education, income, smoking, exercise, height and weight. Standard multiple linear regression and multivariate analyses of variance tested for associations between SES and TRFL, adjusting for covariates. A discordant twin analysis was conducted on a subset to verify findings. WBC telomere length was highly variable but significantly shorter in lower SES groups. The mean difference in TRFL between nonmanual and manual SES groups was 163.2 base pairs (bp) of which 22.9 bp (∼14%) was accounted for by body mass index, smoking and exercise. Comparison of TRFL in the 17 most discordant SES twin pairs confirmed this difference. Low SES, in addition to the harmful effects of smoking, obesity and lack of exercise, appears to have an impact on telomere length.
Abstract.
Conferences
Atkins JL, Pilling LC, Heales CJ, Savage S, Kuo C-L, Kuchel GA, Steffens DC, Melzer D (2022). Hereditary haemochromatosis mutations, brain iron imaging and dementia risk in the UK Biobank cohort.
Author URL.
Atkins JL, Pilling LC, Melzer D (2022). OP56 Hereditary haemochromatosis: genetic iron overload – a missed opportunity for diagnosis and treatment. SSM Annual Scientific Meeting.
Masoli J, Atkins J, Delgado J, Pilling L, Melzer D (2021). BEING NON-FRAIL AND FREE FROM CARDIOVASCULAR DISEASE REDUCES COVID-19 RISK IN 269,164 OLDER UK BIOBANK PARTICIPANTS.
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Kuo C-L, Pilling L, Atkins J, Masoli J, Delgado J, Kuchel G, Melzer D, Levine M (2021). BIOLOGICAL AGING PREDICTS VULNERABILITY TO COVID-19 SEVERITY IN UK BIOBANK PARTICIPANTS.
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Kuo C-L, Pilling L, Atkins J, Masoli J, Delgado J, Kuchel G, Melzer D, Levine M (2021). Biological Aging Predicts Vulnerability to COVID-19 Severity in UK Biobank Participants.
Masoli J, Kuo CL, Atkins J, Pilling L, Delgado J, Kuchel G, Melzer D (2021). DEMENTIA, ApoE AND COVID-19 SEVERITY.
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Atkins J, Masoli J, Delgado J, Pilling L, Kuo C-L, Kuchel G, Melzer D (2021). Preexisting Comorbidities Predicting COVID-19 and Mortality in the UK Biobank Community Cohort.
Atkins J, Pilling LC, Williams D, Jylhävä J, Melzer D (2019). CAUSES OF FRAILTY: GENETIC ANALYSIS IN 164,000 UK BIOBANK PARTICIPANTS.
Jylhava J, Pilling L, Williams D, Lu Y, Pedersen NL, Melzer D, Atkins J (2019). Genome-wide association study of a frailty Index in UK Biobank and TwinGene.
Author URL.
Atkins J, Pilling L, Melzer D (2019). OP37: HEREDITARY HAEMOCHROMATOSIS: ASSOCIATIONS
WITH MORBIDITY AND IRON SUPPLEMENT USE IN
451,243 UK BIOBANK PARTICIPANTS. Society for Social Medicine & Population Health and International Epidemiology Association European Congress Joint Annual Scientific Meeting. 4th - 6th Sep 2019.
Atkins JL, Delgado J, Pilling LC, Bowman K, Masoli JAH, Kuchel GA, Ferrucci L, Melzer D (2018). #IDEAL CARDIOVASCULAR RISK PROFILES AND AGEING: EVIDENCE FROM 421,000 OLDER PERSONS IN TWO COHORTS.
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Melzer D, Pilling L, Atkins J, Tamosauskaite J (2018). IRON OVERLOAD AS a TREATABLE CAUSE OF FRAILTY: GENETIC EVIDENCE IN 200,000 SUBJECTS.
Atkins J, Pilling LC, Melzer D, Bowman K (2017). CAN GENETICS CLARIFY THE RISK PARADOXES OF LATER LIFE?.
Parsons TJ, Papachristou E, Ramsay SE, Atkins JL, Papacosta O, Lennon LT, Ash S, Whincup PH, Wannamethee SG (2017). DIET QUALITY, SARCOPENIA AND FRAILTY IN OLDER MEN: CROSS SECTIONAL ANALYSIS FROM THE BRITISH REGIONAL HEART STUDY.
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Pilling LC, Atkins J, Melzer D (2017). GENETIC VARIANTS FOR AGING WELL SUGGEST POTENTIAL FOR INTERVENTION.
Atkins J, Pilling L, Ble A, Dutta A, Harries L, Murray A, Brayne C, Robine J, Kuchel G, Ferrucci L, et al (2016). OP82 Long-lived parents and cardiovascular outcomes: 8 year follow-up in 189,000 UK Biobank participants.
Atkins JL, Whincup PH, Morris RW, Lennon LT, Papacosta P, Wannamethee SG (2015). Abstract P049: Principal Component Analysis of Dietary Patterns and the Risk of Cardiovascular Disease and Mortality in Older British Men.
Atkins JL, Whincup PH, Morris RW, Lennon LT, Papacosta O, Wannamethee SG (2013). Dietary patterns and the risk of cardiovascular disease and mortality: a population-based cohort study of older British men.
Atkins JL, Whincup PH, Morris RW, Wannamethee SG (2013). Dietary patterns in older British men: the influence of early life social circumstances and area of residence.
Atkins JL, Whincup PH, Morris RW, Wannamethee SG (2013). OP86 Dietary Patterns in Older Men: Influence of Early Life Social Circumstances and Area of Residence.
Atkins JL, Whincup PH, Morris RW, Wannamethee SG (2013). T1: P.039 Sarcopenic obesity and the risk of cardiovascular disease and mortality: a population-based cohort study of older men.
Atkins JL, Whincup PH, Morris RW, Wannamethee SG (2013). T2: P.057 Dietary patterns in the elderly: Influence of early life social circumstances and area of residence.
Atkins JL, Whincup PH, Morris RW, Wannamethee SG (2012). PS38 Sarcopenic Obesity and Risk of All-Cause and Cardiovascular Mortality in Older Men.
Cherkas L, Harris J, Hunkin J, Kato B, Zhang G, Valdes A, Aviv A, Spector TD, Atkins JL (2007). Twins, telomeres and aging.
