title: Multifactorial analysis of changes in body mass index across the adult life course: a study with 65 years of follow-up.
abstract: 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.
  
  
  RESULTS
  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.
authors.affiliation: 1] Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden [2] School of Health Sciences, Institute of Gerontology, Jönköping University, Jönköping, Sweden.
authors.forename: A K
authors.initials: AK
authors.lastname: Dahl
authors.affiliation: Department of Psychology, University of California Riverside, Riverside, CA 92521, USA.
authors.forename: C A
authors.initials: CA
authors.lastname: Reynolds
authors.affiliation: 1] Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden [2] Department of Medical Sciences, Uppsala University, Uppsala, Sweden.
authors.forename: T
authors.initials: T
authors.lastname: Fall
authors.affiliation: Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
authors.forename: P K E
authors.initials: PK
authors.lastname: Magnusson
authors.affiliation: 1] Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden [2] Department of Psychology, University of Southern California, Los Angeles, CA 90089-1061, USA.
authors.forename: N L
authors.initials: NL
authors.lastname: Pedersen
mesh_terms: D000368:Aged; D000375:Aging; D015992:Body Mass Index; D003924:Diabetes Mellitus, Type 2 / Q000503:physiopathology; D005260:Female; D005500:Follow-Up Studies; D006801:Humans; D008019:Life Style; D008297:Male; D008875:Middle Aged; D009765:Obesity / Q000150:complications / Q000453:epidemiology* / Q000209:etiology* / Q000235:genetics; D020641:Polymorphism, Single Nucleotide; D012307:Risk Factors; D012737:Sex Factors; D011795:Surveys and Questionnaires; D013548:Sweden / Q000453:epidemiology; D013997:Time Factors; D015430:Weight Gain; D044465:White People / Q000235:genetics / Q000706:statistics & numerical data