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  • 1.
    Dahl, Anna
    et al.
    Högskolan i Jönköping, Hälsohögskolan, HHJ, Institutet för gerontologi. Högskolan i Jönköping, Hälsohögskolan, HHJ. Åldrande - livsvillkor och hälsa.
    Hassing, Linda
    Fransson, Eleonor
    Högskolan i Jönköping, Hälsohögskolan, HHJ. Åldrande - livsvillkor och hälsa. Högskolan i Jönköping, Hälsohögskolan, HHJ, Avd. för naturvetenskap och biomedicin.
    Margaret, Gatz
    Reynolds, Chandra
    Pedersen, Nancy
    Body mass index across midlife and cognitive change in late life2013Ingår i: International Journal of Obesity, ISSN 0307-0565, E-ISSN 1476-5497, Vol. 37, nr 2, s. 296-302Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Background: High midlife body mass index (BMI) has been linked to a greater risk of dementia in late life, but few have studied the effect of BMI across midlife on cognitive abilities and cognitive change in a dementia-free sample.

    Methods: We investigated the association between BMI, measured twice across midlife (mean age 40 and 61 years, respectively), and cognitive change in four domains across two decades in the Swedish Adoption/Twin Study of Aging.

    Results: Latent growth curve models fitted to data from 657 non-demented participants showed that persons who were overweight/obese in early midlife had significantly lower cognitive performance across domains in late life and significantly steeper decline in perceptual speed, adjusting for cardio-metabolic factors. Both underweight and overweight/obesity in late midlife were associated with lower cognitive abilities in late life. However, the association between underweight and low cognitive abilities did not remain significant when weight decline between early and late midlife was controlled for.

    Conclusion: There is a negative effect on cognitive abilities later in life related to being overweight/obese across midlife. Moreover, weight decline across midlife rather than low weight in late midlife per se was associated with low cognitive abilities. Weight patterns across midlife may be prodromal markers of late life cognitive health.

  • 2.
    Dahl, Anna
    et al.
    Högskolan i Jönköping, Hälsohögskolan, HHJ. Åldrande - livsvillkor och hälsa. Högskolan i Jönköping, Hälsohögskolan, HHJ, Institutet för gerontologi.
    Reynolds, Chandra
    Department of Psychology, University of California Riverside, Riverside, CA 92521, USA.
    Fall, Tove
    Uppsala University.
    Magnusson, Patrik
    Karolinska Institutet.
    Pedersen, Nancy
    Karolinska Institutet.
    Multifactorial analysis of changes in body mass index across the adult life course: a study with 65 years of follow-up2014Ingår i: International Journal of Obesity, ISSN 0307-0565, E-ISSN 1476-5497, Vol. 38, nr 8, s. 1133-1141Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Background: Although the negative consequences on health of being obese are well known, most adults gain weight across the lifespan. The general increase in body mass index (BMI) is mainly considered to originate from behavioral and environmental changes; however, few studies have evaluated the influence of these factors on change in BMI in the presence of genetic risk. We aimed to study the influence of multifactorial causes of change in BMI, over 65 years.

    Methods and Findings: Totally, 6130 participants from TwinGene, who had up to five assessments, and 536 from the Swedish Adoption/Twin Study of Aging, who had up to 12 assessments, ranging over 65 years were included. The influence of lifestyle factors, birth cohort, cardiometabolic diseases and an individual obesity genetic risk score (OGRS) based on 32 single nucleotide polymorphisms on change in BMI was evaluated with a growth model. For both sexes, BMI increased from early adulthood to age of 65 years, after which the increase leveled off; BMI declined after age of 80 years. A higher OGRS, birth after 1925 and cardiometabolic diseases were associated with higher average BMI and a steeper increase in BMI prior to 65 years of age. Among men, few factors were identified that influence BMI trajectories in late life, whereas for women type 2 diabetes mellitus and dementia were associated with a steeper decrease in BMI after the age of 65 years.

    Conclusions: There are two turning points in BMI in late adulthood, one at the age of 65 years and one at the age 80 years. Factors associated with an increase in BMI in midlife were not associated with an increase in BMI after the age of 65 years. These findings indicate that the causes and consequences of change in BMI differ across the lifespan. Current health recommendations need to be adjusted accordingly.

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  • 3. Hassing, Linda B.
    et al.
    Dahl, Anna
    Högskolan i Jönköping, Hälsohögskolan, HHJ, Institutet för gerontologi. Högskolan i Jönköping, Hälsohögskolan, HHJ. Åldrande - livsvillkor och hälsa.
    Thorvaldsson, Valgeir
    Berg, Stig
    Högskolan i Jönköping, Hälsohögskolan, HHJ, Institutet för gerontologi. Högskolan i Jönköping, Hälsohögskolan, HHJ. Åldrande - livsvillkor och hälsa.
    Gatz, Margaret
    Pedersen, Nancy L.
    Johansson, Boo
    Overweight in midlife and risk of dementia: a 40-year follow-up study2009Ingår i: International Journal of Obesity, ISSN 0307-0565, E-ISSN 1476-5497, Vol. 33, nr 8, s. 893-898Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Objective:

    This study examines whether overweight in midlife increases dementia risk later in life.

    Methods:

    In 1963 body mass index was assessed in 1152 participants of The Swedish Twin Registry, at the age of 45–65 years. These participants were later screened for dementia in a prospective study with up to 40 years follow-up. A total of 312 participants were diagnosed with dementia.

    Results:

    Logistic regression analyses adjusted for demographic factors, smoking and alcohol habits, indicated that men and women categorized as overweight in their midlife had an elevated risk of dementia (OR=1.59; 95% CI: 1.21–2.07, P=0.002), Alzheimer's disease (OR=1.71; 95% CI: 1.24–2.35, P=0.003), and vascular dementia (OR=1.55; 95% CI: 0.98–2.47, P=0.059). Further adjustments for diabetes and vascular diseases did not substantially affect the associations, except for vascular dementia (OR=1.36; 95% CI: 0.82–2.56, P=0.116), reflecting the significance of diabetes and vascular diseases in the etiology of vascular dementia. There was no significant interaction between overweight and APOE ɛ4 status, indicating that having both risk factors does not have a multiplicative effect with regard to dementia risk.

    Conclusions:

    This study gives further support to the notion that overweight in midlife increases later risk of dementia. The risk is increased for both Alzheimer's disease and vascular dementia, and follows the same pattern for men and women.

  • 4.
    Karlsson, Ida K.
    et al.
    Högskolan i Jönköping, Hälsohögskolan, HHJ, Institutet för gerontologi. Högskolan i Jönköping, Hälsohögskolan, HHJ. ARN-J (Aging Research Network - Jönköping). Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Ericsson, M.
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Wang, Y.
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Jylhävä, J.
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Hägg, S.
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Pedersen, N. L.
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Reynolds, C. A.
    Department of Psychology, University of California, Riverside, CA, United States.
    Dahl Aslan, Anna K.
    Högskolan i Jönköping, Hälsohögskolan, HHJ, Institutet för gerontologi. Högskolan i Jönköping, Hälsohögskolan, HHJ. ARN-J (Aging Research Network - Jönköping). Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Replicating associations between DNA methylation and body mass index in a longitudinal sample of older twins2019Ingår i: International Journal of Obesity, ISSN 0307-0565, E-ISSN 1476-5497Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Background:

    There is an important interplay between epigenetic factors and body weight, and previous work has identified ten sites where DNA methylation is robustly associated with body mass index (BMI) cross-sectionally. However, interpretation of the associations is complicated by the substantial changes in BMI often occurring in late-life, and the fact that methylation is often driven by genetic variation. This study therefore investigated the longitudinal association between these ten sites and BMI from midlife to late-life, and whether associations persist after controlling for genetic factors.

    Methods:

    We used data from 535 individuals (mean age 68) in the Swedish Adoption/Twin Study of Aging (SATSA) with longitudinal measures of both DNA methylation from blood samples and BMI, spanning up to 20 years. Methylation levels were measured with the Infinium Human Methylation 450K or Infinium MethylationEpic array, with seven of the ten sites passing quality control. Latent growth curve models were applied to investigate longitudinal associations between methylation and BMI, and between–within models to study associations within twin pairs, thus adjusting for genetic factors.

    Results:

    Baseline DNA methylation levels at five of the seven sites were associated with BMI level at age 65 (cg00574958 [CPT1A]; cg11024682 [SREBF1]), and/or change (cg06192883 [MYO5C]; cg06946797 [RMI2]; cg08857797 [VPS25]). For four of the five sites, the associations remained comparable within twin pairs. However, the effects of cg06192883 were substantially attenuated within pairs. No change in DNA methylation was detected for any of the seven evaluated sites.

    Conclusion:

    Five of the seven sites investigated were associated with late-life level and/or change in BMI. The effects for four of the sites remained similar when examined within twin pairs, indicating that the associations are mainly environmentally driven. However, the substantial attenuation in the association between cg06192883 and late-life BMI within pairs points to the importance of genetic factors in this association.

  • 5.
    Virtanen, M.
    et al.
    School of Educational Sciences and Psychology, University of Eastern Finland, Joensuu, Finland.
    Jokela, M.
    Department of Psychology and Logopedics, University of Helsinki, Helsinki, Finland.
    Lallukka, T.
    Finnish Institute of Occupational Health, Helsinki, Finland.
    Magnusson Hanson, L.
    Stress Research Institute, Stockholm University, Stockholm, Sweden.
    Pentti, J.
    Department of Public Health, Clinicum, University of Helsinki, Helsinki, Finland.
    Nyberg, S. T.
    Department of Public Health, Clinicum, University of Helsinki, Helsinki, Finland.
    Alfredsson, L.
    Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden.
    Batty, G. D.
    Department of Epidemiology & Public Health, University College London, London, United Kingdom.
    Casini, A.
    IPSY, Université catholique de Louvain (UCLouvain), Louvain-la-Neuve & School of Public Health, Université libre de Bruxelles (ULB), Brussels, Belgium.
    Clays, E.
    Department of Public Health, Ghent University, Ghent, Belgium.
    DeBacquer, D.
    Department of Public Health, Ghent University, Ghent, Belgium.
    Ervasti, J.
    Finnish Institute of Occupational Health, Helsinki, Finland.
    Fransson, Eleonor I.
    Högskolan i Jönköping, Hälsohögskolan, HHJ, Avd. för naturvetenskap och biomedicin. Högskolan i Jönköping, Hälsohögskolan, HHJ. ADULT. Högskolan i Jönköping, Hälsohögskolan, HHJ. ARN-J (Aging Research Network - Jönköping). Högskolan i Jönköping, Hälsohögskolan, HHJ, Institutet för gerontologi. Stress Research Institute, Stockholm University, Stockholm, Sweden.
    Halonen, J. I.
    Stress Research Institute, Stockholm University, Stockholm, Sweden.
    Head, J.
    Department of Epidemiology & Public Health, University College London, London, United Kingdom.
    Kittel, F.
    IPSY, Université catholique de Louvain (UCLouvain), Louvain-la-Neuve & School of Public Health, Université libre de Bruxelles (ULB), Brussels, Belgium.
    Knutsson, A.
    Department of Health Sciences, Mid Sweden University, Sundsvall, Sweden.
    Leineweber, C.
    Stress Research Institute, Stockholm University, Stockholm, Sweden.
    Nordin, M.
    Department of Psychology, Umeå University, Umeå, Sweden.
    Oksanen, T.
    Finnish Institute of Occupational Health, Helsinki, Finland.
    Pietiläinen, O.
    Department of Public Health, Clinicum, University of Helsinki, Helsinki, Finland.
    Rahkonen, O.
    Department of Public Health, Clinicum, University of Helsinki, Helsinki, Finland.
    Salo, P.
    Finnish Institute of Occupational Health, Helsinki, Finland.
    Singh-Manoux, A.
    Department of Epidemiology & Public Health, University College London, London, United Kingdom.
    Stenholm, S.
    Department of Public Health, University of Turku and Turku University Hospital, Turku, Finland.
    Suominen, S. B.
    Department of Public Health, University of Turku and Turku University Hospital, Turku, Finland.
    Theorell, T.
    Stress Research Institute, Stockholm University, Stockholm, Sweden.
    Vahtera, J.
    Department of Public Health, University of Turku and Turku University Hospital, Turku, Finland.
    Westerholm, P.
    Occupational and Environmental Medicine, Uppsala University, Uppsala, Sweden.
    Westerlund, H.
    Stress Research Institute, Stockholm University, Stockholm, Sweden.
    Kivimäki, M.
    Department of Public Health, Clinicum, University of Helsinki, Helsinki, Finland.
    Long working hours and change in body weight: analysis of individual-participant data from 19 cohort studies2019Ingår i: International Journal of Obesity, ISSN 0307-0565, E-ISSN 1476-5497Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Objective:

    To examine the relation between long working hours and change in body mass index (BMI).

    Methods:

    We performed random effects meta-analyses using individual-participant data from 19 cohort studies from Europe, US and Australia (n = 122,078), with a mean of 4.4-year follow-up. Working hours were measured at baseline and categorised as part time (<35 h/week), standard weekly hours (35–40 h, reference), 41–48 h, 49–54 h and ≥55 h/week (long working hours). There were four outcomes at follow-up: (1) overweight/obesity (BMI ≥ 25 kg/m2) or (2) overweight (BMI 25–29.9 kg/m2) among participants without overweight/obesity at baseline; (3) obesity (BMI ≥ 30 kg/m2) among participants with overweight at baseline, and (4) weight loss among participants with obesity at baseline.

    Results:

    Of the 61,143 participants without overweight/obesity at baseline, 20.2% had overweight/obesity at follow-up. Compared with standard weekly working hours, the age-, sex- and socioeconomic status-adjusted relative risk (RR) of overweight/obesity was 0.95 (95% CI 0.90–1.00) for part-time work, 1.07 (1.02–1.12) for 41–48 weekly working hours, 1.09 (1.03–1.16) for 49–54 h and 1.17 (1.08–1.27) for long working hours (P for trend <0.0001). The findings were similar after multivariable adjustment and in subgroup analyses. Long working hours were associated with an excess risk of shift from normal weight to overweight rather than from overweight to obesity. Long working hours were not associated with weight loss among participants with obesity.

    Conclusions:

    This analysis of large individual-participant data suggests a small excess risk of overweight among the healthy-weight people who work long hours. 

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