Evidence for shared genetics between physical activity, sedentary behaviour and adiposity-related traits
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Evidence for shared genetics between physical activity, sedentary behaviour and adiposity-related traits. / Schnurr, Theresia M.; Stallknecht, Bente M.; Sørensen, Thorkild I. A.; Kilpelainen, Tuomas O.; Hansen, Torben.
I: Obesity Reviews, Bind 22, Nr. 4, e13182, 2021.Publikation: Bidrag til tidsskrift › Tidsskriftartikel › Forskning › fagfællebedømt
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TY - JOUR
T1 - Evidence for shared genetics between physical activity, sedentary behaviour and adiposity-related traits
AU - Schnurr, Theresia M.
AU - Stallknecht, Bente M.
AU - Sørensen, Thorkild I. A.
AU - Kilpelainen, Tuomas O.
AU - Hansen, Torben
PY - 2021
Y1 - 2021
N2 - Observational, cross-sectional and longitudinal studies showed that physical activity and sedentary behaviour are associated with adiposity-related traits, apparently in a bidirectional manner. Physical activity is also suggested to suppress the genetic risk of adiposity. Since phenotypic associations with genetic variants are not subject to reverse causation or confounding, they may be used as tools to shed light on cause and effect in this complex interdependency. We review the evidence for shared genetics of physical activity and adiposity-related traits and for gene-by-physical activity interactions on adiposity-related traits in human studies. We outline limitations, challenges and opportunities in studying and understanding of these relationships. In summary, physical activity and sedentary behaviour are genetically correlated with body mass index and fat percentage but may not be correlated with lean body mass. Mendelian randomisation analyses show that physical activity and sedentary behaviour have bidirectional relationships with adiposity. Several studies suggest that physical activity suppresses genetic risk of adiposity. No studies have yet tested whether adiposity enhances genetic predisposition to sedentariness. The complexity of the comprehensive causal model makes the assessment of the single or combined components challenging. Substantial progress in this field may need long-term intervention studies.
AB - Observational, cross-sectional and longitudinal studies showed that physical activity and sedentary behaviour are associated with adiposity-related traits, apparently in a bidirectional manner. Physical activity is also suggested to suppress the genetic risk of adiposity. Since phenotypic associations with genetic variants are not subject to reverse causation or confounding, they may be used as tools to shed light on cause and effect in this complex interdependency. We review the evidence for shared genetics of physical activity and adiposity-related traits and for gene-by-physical activity interactions on adiposity-related traits in human studies. We outline limitations, challenges and opportunities in studying and understanding of these relationships. In summary, physical activity and sedentary behaviour are genetically correlated with body mass index and fat percentage but may not be correlated with lean body mass. Mendelian randomisation analyses show that physical activity and sedentary behaviour have bidirectional relationships with adiposity. Several studies suggest that physical activity suppresses genetic risk of adiposity. No studies have yet tested whether adiposity enhances genetic predisposition to sedentariness. The complexity of the comprehensive causal model makes the assessment of the single or combined components challenging. Substantial progress in this field may need long-term intervention studies.
KW - adiposity
KW - genetic determinants
KW - physical activity
KW - sedentary behaviour
KW - BODY-MASS INDEX
KW - GENOME-WIDE ASSOCIATION
KW - MENDELIAN RANDOMIZATION
KW - ENVIRONMENT INTERACTION
KW - FTO GENE
KW - MISSING HERITABILITY
KW - SUSCEPTIBILITY LOCI
KW - CHILDHOOD OBESITY
KW - REGULAR EXERCISE
KW - POOLED ANALYSIS
U2 - 10.1111/obr.13182
DO - 10.1111/obr.13182
M3 - Journal article
C2 - 33354910
VL - 22
JO - Obesity Reviews
JF - Obesity Reviews
SN - 1467-7881
IS - 4
M1 - e13182
ER -
ID: 255099239