Skip header and navigation

Refine By

64 records – page 1 of 7.

Acquired obesity is associated with changes in the serum lipidomic profile independent of genetic effects--a monozygotic twin study.

https://arctichealth.org/en/permalink/ahliterature165168
Source
PLoS One. 2007;2(2):e218
Publication Type
Article
Date
2007
Author
Kirsi H Pietiläinen
Marko Sysi-Aho
Aila Rissanen
Tuulikki Seppänen-Laakso
Hannele Yki-Järvinen
Jaakko Kaprio
Matej Oresic
Author Affiliation
Obesity Research Unit, Department of Psychiatry, Helsinki University Central Hospital, Helsinki, Finland.
Source
PLoS One. 2007;2(2):e218
Date
2007
Language
English
Publication Type
Article
Keywords
Abdominal Fat - pathology
Adult
Body Composition
Body mass index
Diet Records
Female
Finland
Humans
Insulin Resistance
Lipids - blood
Lysophosphatidylcholines - blood
Magnetic Resonance Imaging
Male
Metabolomics
Obesity - blood - epidemiology - genetics - pathology
Smoking - epidemiology
Sphingomyelins - blood
Subcutaneous Fat - pathology
Twins, Monozygotic - genetics
Young Adult
Abstract
Both genetic and environmental factors are involved in the etiology of obesity and the associated lipid disturbances. We determined whether acquired obesity is associated with changes in global serum lipid profiles independent of genetic factors in young adult monozygotic (MZ) twins. 14 healthy MZ pairs discordant for obesity (10 to 25 kg weight difference) and ten weight concordant control pairs aged 24-27 years were identified from a large population-based study. Insulin sensitivity was assessed by the euglycemic clamp technique, and body composition by DEXA (% body fat) and by MRI (subcutaneous and intra-abdominal fat). Global characterization of lipid molecular species in serum was performed by a lipidomics strategy using liquid chromatography coupled to mass spectrometry. Obesity, independent of genetic influences, was primarily related to increases in lysophosphatidylcholines, lipids found in proinflammatory and proatherogenic conditions and to decreases in ether phospholipids, which are known to have antioxidant properties. These lipid changes were associated with insulin resistance, a pathogonomic characteristic of acquired obesity in these young adult twins. Our results show that obesity, already in its early stages and independent of genetic influences, is associated with deleterious alterations in the lipid metabolism known to facilitate atherogenesis, inflammation and insulin resistance.
Notes
Cites: Cell. 1992 Mar 6;68(5):879-871312391
Cites: J Immunol. 2005 Mar 1;174(5):2981-915728511
Cites: Biochem J. 1992 Oct 1;287 ( Pt 1):237-401417777
Cites: J Stud Alcohol. 1994 Mar;55(2):149-588189735
Cites: Diabetes. 1994 Jul;43(7):915-98013757
Cites: Lipids. 1995 Jan;30(1):1-147760683
Cites: Circ Res. 1996 May;78(5):780-98620597
Cites: Am J Physiol. 1996 Dec;271(6 Pt 1):E941-518997211
Cites: Nat Genet. 1997 Dec;17(4):387-929398838
Cites: Biochem J. 1999 Mar 15;338 ( Pt 3):769-7610051451
Cites: Glia. 2000 Mar;30(1):92-10410696148
Cites: Nature. 2000 Sep 14;407(6801):233-4111001066
Cites: Nat Biotechnol. 2001 Jan;19(1):45-5011135551
Cites: FASEB J. 2001 Feb;15(2):312-2111156947
Cites: Atherosclerosis. 2001 Mar;155(1):45-5211223425
Cites: World Health Organ Tech Rep Ser. 2000;894:i-xii, 1-25311234459
Cites: Cell. 2001 Feb 23;104(4):503-1611239408
Cites: Neuroscientist. 2001 Jun;7(3):232-4511499402
Cites: Hypertension. 2002 Feb;39(2 Pt 2):508-1211882599
Cites: Am J Physiol Heart Circ Physiol. 2002 Aug;283(2):H671-912124215
Cites: Twin Res. 2002 Oct;5(5):366-7112537860
Cites: J Mol Cell Cardiol. 2003 Nov;35(11):1375-8414596794
Cites: Am J Physiol Endocrinol Metab. 2003 Dec;285(6):E1151-6014607781
Cites: Biochim Biophys Acta. 2003 Nov 15;1634(3):6114643793
Cites: Biochem Soc Trans. 2004 Feb;32(Pt 1):147-5014748736
Cites: FASEB J. 2004 Jun;18(9):1040-215084525
Cites: Diabetologia. 2004 Jun;47(6):1118-2515168018
Cites: Arterioscler Thromb Vasc Biol. 2004 Sep;24(9):1640-515178563
Cites: Am J Physiol Endocrinol Metab. 2005 Apr;288(4):E768-7415585588
Cites: J Lipid Res. 2005 May;46(5):839-6115722563
Cites: Curr Mol Med. 2005 May;5(3):297-30815892649
Cites: Am J Physiol Lung Cell Mol Physiol. 2005 Aug;289(2):L176-8515764646
Cites: Proc Natl Acad Sci U S A. 2005 Jul 26;102(30):10604-916009939
Cites: Nat Rev Drug Discov. 2005 Jul;4(7):594-61016052242
Cites: Bioinformatics. 2006 Mar 1;22(5):634-616403790
Cites: Nature. 2006 Apr 13;440(7086):944-816612386
Cites: Mol Diagn Ther. 2006;10(2):101-816669608
Cites: Am J Physiol Lung Cell Mol Physiol. 2006 Jul;291(1):L91-10116461426
Cites: Expert Rev Mol Diagn. 2006 Jul;6(4):575-8516824031
Cites: J Clin Endocrinol Metab. 2006 Jul;91(7):2776-8116608891
Cites: Obesity (Silver Spring). 2006 May;14(5):826-3716855192
Cites: BMC Genomics. 2006;7:14216762068
Cites: Diabetes. 2006 Sep;55(9):2579-8716936207
Cites: PLoS One. 2006;1:e9717183729
Cites: Am J Physiol Heart Circ Physiol. 2007 Feb;292(2):H904-1117012356
Cites: J Clin Endocrinol Metab. 2004 Sep;89(9):4414-2115356040
Cites: Lancet. 2004 Sep 11-17;364(9438):937-5215364185
Cites: J Clin Endocrinol Metab. 1971 Nov;33(5):732-85166455
Cites: Clin Chem. 1972 Jun;18(6):499-5024337382
Cites: Biochim Biophys Acta. 1973 Oct 17;326(1):34-424127872
Cites: Am J Physiol. 1979 Sep;237(3):E214-23382871
Cites: Diabetes. 1985 Oct;34(10):1055-84043554
Cites: J Clin Invest. 1987 Jun;79(6):1713-93294899
Cites: Atherosclerosis. 1999 Mar;143(1):201-410208496
Cites: J Biol Chem. 1999 Sep 3;274(36):25189-9210464236
Cites: Pharmacol Res. 1999 Sep;40(3):211-2510479465
Cites: Twin Res. 2004 Oct;7(5):421-915527657
Cites: Blood. 2005 Feb 1;105(3):1127-3415383458
Cites: Appl Bioinformatics. 2004;3(4):205-1715702951
Cites: Mol Cell Biochem. 1992 Aug 18;113(2):151-691518506
PubMed ID
17299598 View in PubMed
Less detail

Age, Sex, and Genetic and Environmental Effects on Unintentional Injuries in Young and Adult Twins.

https://arctichealth.org/en/permalink/ahliterature298559
Source
Twin Res Hum Genet. 2018 12; 21(6):502-506
Publication Type
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Twin Study
Date
12-2018
Author
Simo Salminen
Eero Vuoksimaa
Richard J Rose
Jaakko Kaprio
Author Affiliation
Department of Social Psychology,University of Helsinki,Helsinki,Finland.
Source
Twin Res Hum Genet. 2018 12; 21(6):502-506
Date
12-2018
Language
English
Publication Type
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Twin Study
Keywords
Adolescent
Adult
Age Factors
Diseases in Twins - epidemiology - genetics
Environment
Female
Finland - epidemiology
Humans
Longitudinal Studies
Male
Middle Aged
Registries
Risk factors
Sex Factors
Twins, Dizygotic - genetics
Twins, Monozygotic - genetics
Wounds and Injuries - epidemiology - genetics
Young Adult
Abstract
The aim of this study was to examine the effects of genetic and environment influences and sex on injury involvement using two sets of Finnish twin data. The younger participants were 955 twins born between 1983 and 1987, aged 20 to 24 years. The older participants were 12,428 twins born between 1930 and 1957, aged 33 to 60 years. Within-twin correlations in monozygotic and dizygotic twins suggested that genetic effects play no role in injury involvement among young twins, but do have some effect at older ages. The results indicated that environmental factors have greater importance in injury involvement than genetic factors in the younger twin data set (FT12), whereas in a middle-aged (33-60 years) twin data set, genetic effects explained about quarter of the variance in injury involvement. Sex was a strong contributing factor, with males being generally more prone to injuries than females.
PubMed ID
30428952 View in PubMed
Less detail

All-cause and disease-specific mortality among male, former elite athletes: an average 50-year follow-up.

https://arctichealth.org/en/permalink/ahliterature271045
Source
Br J Sports Med. 2015 Jul;49(13):893-7
Publication Type
Article
Date
Jul-2015
Author
Jyrki A Kettunen
Urho M Kujala
Jaakko Kaprio
Heli Bäckmand
Markku Peltonen
Johan G Eriksson
Seppo Sarna
Source
Br J Sports Med. 2015 Jul;49(13):893-7
Date
Jul-2015
Language
English
Publication Type
Article
Keywords
Adult
Aged
Aged, 80 and over
Case-Control Studies
Cause of Death
Dementia - mortality
Finland - epidemiology
Follow-Up Studies
Humans
Life expectancy
Male
Middle Aged
Myocardial Infarction - mortality
Neoplasms - mortality
Sports - statistics & numerical data
Stroke - mortality
Survival Analysis
Young Adult
Abstract
To investigate life expectancy and mortality among former elite athletes and controls.
HR analysis of cause-specific deaths sourced from the national death registry for former Finnish male endurance, team and power sports athletes (N=2363) and controls (N=1657). The median follow-up time was 50 years.
Median life expectancy was higher in the endurance (79.1 years, 95% CI 76.6 to 80.6) and team (78.8, 78.1 to 79.8) sports athletes than in controls (72.9, 71.8 to 74.3). Compared to controls, risk for total mortality adjusted for socioeconomic status and birth cohort was lower in the endurance ((HR 0.70, 95% CI 0.61 to 0.79)) and team (0.80, 0.72 to 0.89) sports athletes, and slightly lower in the power sports athletes (0.93, 0.85 to 1.03). HR for ischaemic heart disease mortality was lower in the endurance (0.68, 0.54 to 0.86) and team sports (0.73, 0.60 to 0.89) athletes. HR for stroke mortality was 0.52 (0.33 to 0.83) in the endurance and 0.59 (0.40 to 0.88) in the team sports athletes. Compared to controls, the risk for smoking-related cancer mortality was lower in the endurance (HR 0.20, 0.08 to 0.47) and power sports (0.40, 0.25 to 0.66) athletes. For dementia mortality, the power sports athletes, particularly boxers, had increased risk (HR 4.20, 2.30 to 7.81).
Elite athletes have 5-6 years additional life expectancy when compared to men who were healthy as young adults. Lower mortality for cardiovascular disease was in part due to lower rates of smoking, as tobacco-related cancer mortality was especially low.
PubMed ID
25183628 View in PubMed
Less detail

Appetitive traits as behavioural pathways in genetic susceptibility to obesity: a population-based cross-sectional study.

https://arctichealth.org/en/permalink/ahliterature275595
Source
Sci Rep. 2015;5:14726
Publication Type
Article
Date
2015
Author
Hanna Konttinen
Clare Llewellyn
Jane Wardle
Karri Silventoinen
Anni Joensuu
Satu Männistö
Veikko Salomaa
Pekka Jousilahti
Jaakko Kaprio
Markus Perola
Ari Haukkala
Source
Sci Rep. 2015;5:14726
Date
2015
Language
English
Publication Type
Article
Keywords
Adult
Aged
Anthropometry
Appetite
Body mass index
Cross-Sectional Studies
Feeding Behavior
Female
Finland - epidemiology
Genetic Predisposition to Disease
Humans
Male
Middle Aged
Models, Statistical
Multifactorial Inheritance
Obesity - epidemiology - genetics
Population Surveillance
Quantitative Trait, Heritable
Sex Factors
Young Adult
Abstract
The mechanisms through which genes influence body weight are not well understood, but appetite has been implicated as one mediating pathway. Here we use data from two independent population-based Finnish cohorts (4632 adults aged 25-74 years from the DILGOM study and 1231 twin individuals aged 21-26 years from the FinnTwin12 study) to investigate whether two appetitive traits mediate the associations between known obesity-related genetic variants and adiposity. The results from structural equation modelling indicate that the effects of a polygenic risk score (90 obesity-related loci) on measured body mass index and waist circumference are partly mediated through higher levels of uncontrolled eating (ßindirect = 0.030-0.032, P
Notes
Cites: Am J Clin Nutr. 2009 Dec;90(6):1483-819828706
Cites: J Nutr. 2010 Apr;140(4):831-420181787
Cites: Int J Epidemiol. 2010 Apr;39(2):504-1819959603
Cites: PLoS Med. 2010;7(8). pii: e1000332. doi: 10.1371/journal.pmed.100033220824172
Cites: PLoS Genet. 2010 Sep;6(9):e100111320844574
Cites: Int J Obes (Lond). 2010 Oct;34(10):1538-4520386550
Cites: Am J Clin Nutr. 2010 Nov;92(5):1031-920861176
Cites: Psychol Health. 2011 Jan;26(1):23-3920204980
Cites: Am J Hum Biol. 2011 Nov-Dec;23(6):764-7321957002
Cites: PLoS Med. 2011 Nov;8(11):e100111622069379
Cites: J Occup Environ Med. 2011 Nov;53(11):1287-9322027541
Cites: Am J Clin Nutr. 2011 Dec;94(6):1562-722071702
Cites: Appetite. 2012 Feb;58(1):277-8422037008
Cites: Nicotine Tob Res. 2012 Jun;14(6):720-3322241830
Cites: Nat Neurosci. 2012 Oct;15(10):1343-923007189
Cites: Hypertension. 2013 May;61(5):987-9423509078
Cites: PLoS Genet. 2013;9(7):e100360723935507
Cites: Br J Nutr. 2013 Sep 28;110(6):1151-623433430
Cites: Int J Obes (Lond). 2013 Nov;37(11):1506-923528754
Cites: J Genet Couns. 2014 Apr;23(2):179-8623832708
Cites: JAMA Pediatr. 2014 Apr;168(4):338-4424535189
Cites: Obesity (Silver Spring). 2014 May;22(5):E135-4123929626
Cites: Mol Psychiatry. 2014 Nov;19(11):1154-525266125
Cites: Diabetes. 2014 Dec;63(12):4343-5924969107
Cites: Hum Mol Genet. 2014 Dec 20;23(25):6961-7225104851
Cites: Appetite. 2015 Feb;85:138-4525464025
Cites: Obesity (Silver Spring). 2015 Feb;23(2):305-1225522302
Cites: Nature. 2015 Feb 12;518(7538):197-20625673413
Cites: N Engl J Med. 2008 Dec 11;359(24):2558-6619073975
Cites: Int J Obes Relat Metab Disord. 2000 Dec;24(12):1715-2511126230
Cites: Twin Res. 2002 Oct;5(5):366-7112537860
Cites: J Abnorm Psychol. 2003 Nov;112(4):545-5714674868
Cites: J Nutr. 2004 Sep;134(9):2372-8015333731
Cites: Am J Clin Nutr. 2008 Jul;88(1):22-918614720
Cites: Am J Clin Nutr. 2008 Aug;88(2):263-7118689360
Cites: J Clin Endocrinol Metab. 2008 Sep;93(9):3640-318583465
Cites: Hum Mol Genet. 2008 Nov 15;17(22):3502-818697794
Cites: Int J Obes (Lond). 2009 Jan;33(1):42-518838977
Cites: Int J Obes (Lond). 2009 Mar;33(3):373-819153581
Cites: Int J Obes (Lond). 2009 Jun;33(6):611-2019399021
Cites: Am J Clin Nutr. 2009 Jul;90(1):33-4019439461
Cites: Obesity (Silver Spring). 2009 Oct;17(10):1964-7019360005
Cites: Am J Clin Nutr. 2009 Nov;90(5):1426-3219793853
PubMed ID
26423639 View in PubMed
Less detail

Association between education and future leisure-time physical inactivity: a study of Finnish twins over a 35-year follow-up.

https://arctichealth.org/en/permalink/ahliterature284182
Source
BMC Public Health. 2016 Aug 04;16:720
Publication Type
Article
Date
Aug-04-2016
Author
Maarit Piirtola
Jaakko Kaprio
Urho M Kujala
Kauko Heikkilä
Markku Koskenvuo
Pia Svedberg
Karri Silventoinen
Annina Ropponen
Source
BMC Public Health. 2016 Aug 04;16:720
Date
Aug-04-2016
Language
English
Publication Type
Article
Keywords
Adolescent
Adult
Aged
Cross-Sectional Studies
Educational Status
Environment
Exercise
Family
Female
Finland
Follow-Up Studies
Health Behavior
Humans
Leisure Activities
Male
Middle Aged
Sedentary lifestyle
Social Environment
Surveys and Questionnaires
Twins
Young Adult
Abstract
Education is associated with health related lifestyle choices including leisure-time physical inactivity. However, the longitudinal associations between education and inactivity merit further studies. We investigated the association between education and leisure-time physical inactivity over a 35-year follow-up with four time points controlling for multiple covariates including familial confounding.
This study of the population-based Finnish Twin Cohort consisted of 5254 twin individuals born in 1945-1957 (59 % women), of which 1604 were complete same-sexed twin pairs. Data on leisure-time physical activity and multiple covariates was available from four surveys conducted in 1975, 1981, 1990 and 2011 (response rates 72 to 89 %). The association between years of education and leisure-time physical inactivity (
Notes
Cites: Twin Res. 2002 Oct;5(5):358-6512537859
Cites: Twin Res Hum Genet. 2013 Feb;16(1):157-6223298696
Cites: Am J Epidemiol. 2002 Dec 1;156(11):985-9312446254
Cites: J Health Econ. 2010 Jan;29(1):1-2819963292
Cites: Int J Epidemiol. 2009 Oct;38(5):1310-2219528192
Cites: Scand J Public Health. 2014 Nov;42(7):611-2025201896
Cites: PLoS Med. 2005 Jul;2(7):e16216033303
Cites: Lancet. 2012 Jul 21;380(9838):219-2922818936
Cites: Sports Med. 2012 May 1;42(5):433-4722512413
Cites: Scand J Med Sci Sports. 2012 Jun;22(3):439-4721039899
Cites: Perspect Psychol Sci. 2010 Sep;5(5):546-5621593989
Cites: Am J Prev Med. 2014 Aug;47(2):123-3024877993
Cites: Int J Epidemiol. 2011 Oct;40(5):1382-40022039197
Cites: Compr Physiol. 2012 Apr;2(2):1143-21123798298
Cites: J Health Psychol. 2008 Nov;13(8):1092-10418987082
Cites: Lancet. 2012 Dec 15;380(9859):2224-6023245609
Cites: Behav Genet. 2012 Jul;42(4):559-7822426782
Cites: Twin Res Hum Genet. 2014 Aug;17(4):262-7125034445
Cites: Soc Sci Med. 1998 Dec;47(11):1665-769877337
Cites: Am Psychol. 1994 Jan;49(1):15-248122813
Cites: Scand J Med Sci Sports. 2016 Jan;26(1):93-10025559167
Cites: Eur J Public Health. 2014 Apr;24(2):199-20423748597
Cites: Public Health. 2007 Dec;121(12):909-2217920646
Cites: Nat Rev Genet. 2002 Nov;3(11):872-8212415317
Cites: BMC Public Health. 2014 Dec 29;14:132725547275
Cites: Behav Genet. 2000 Nov;30(6):477-8511523706
Cites: Soc Sci Med. 2015 Feb;127:181-925110343
Cites: BMC Public Health. 2012 Dec 15;12:107923241280
Cites: Econ Hum Biol. 2014 Jul;14:1-2124958450
Cites: J Epidemiol Community Health. 2008 Mar;62(3):239-4418272739
Cites: Med Sci Sports Exerc. 2011 Aug;43(8):1575-8121681120
Cites: J Epidemiol Community Health. 2001 Aug;55(8):562-811449013
Cites: Appl Physiol Nutr Metab. 2012 Jun;37(3):540-222540258
Cites: Int J Epidemiol. 2016 Mar 15;:null26979986
Cites: Soc Sci Med. 2015 Feb;127:171-8025113566
Cites: Int J Obes (Lond). 2008 Feb;32(2):353-6117653065
Cites: Prev Med. 1997 Jul-Aug;26(4):570-99245681
Cites: Science. 2013 Jun 21;340(6139):1467-7123722424
Cites: Prev Med. 2011 Jul-Aug;53(1-2):24-821371494
Cites: Soc Sci Med. 2015 Feb;127:63-7325113567
Cites: JAMA. 1998 Feb 11;279(6):440-49466636
Cites: Int J Obes Relat Metab Disord. 1998 Oct;22(10):949-579806309
Cites: Br J Sports Med. 2014 Jun;48(12):947-5124859181
Cites: Int J Behav Nutr Phys Act. 2012 Sep 19;9:11622992350
Cites: Int J Epidemiol. 2005 Oct;34(5):1089-9916087687
Cites: Am J Epidemiol. 2005 Feb 15;161(4):389-9815692083
Cites: Med Sci Sports Exerc. 2006 Oct;38(10):1716-2317019292
Cites: Econ Educ Rev. 2013 Aug 1;35:null24415826
Cites: Br J Sports Med. 2014 Feb;48(3):171-323134760
Cites: Biomed Res Int. 2014;2014:20914024822182
Cites: Med Sci Sports Exerc. 2011 Jan;43(1):74-920473224
Cites: Lancet. 2012 Jul 21;380(9838):258-7122818938
Cites: Am J Public Health. 2013 Jun;103(6):997-100123597373
Cites: Scand J Public Health. 2010 Mar;38(2):121-820064919
Cites: J Clin Epidemiol. 1988;41(2):139-503335880
Cites: Mol Psychiatry. 2015 Feb;20(1):98-10825224258
Cites: Med Sci Sports Exerc. 2011 Jul;43(7):1229-3421131860
PubMed ID
27492437 View in PubMed
Less detail

Association between long-term smoking and leisure-time physical inactivity: a cohort study among Finnish twins with a 35-year follow-up.

https://arctichealth.org/en/permalink/ahliterature294221
Source
Int J Public Health. 2017 Sep; 62(7):819-829
Publication Type
Journal Article
Twin Study
Date
Sep-2017
Author
Maarit Piirtola
Jaakko Kaprio
Karri Silventoinen
Pia Svedberg
Tellervo Korhonen
Annina Ropponen
Author Affiliation
Department of Public Health, University of Helsinki, P.O. Box 20/FIMM (Tukholmankatu 8, 2B), 00014, Helsinki, Finland. maarit.piirtola@helsinki.fi.
Source
Int J Public Health. 2017 Sep; 62(7):819-829
Date
Sep-2017
Language
English
Publication Type
Journal Article
Twin Study
Keywords
Adolescent
Adult
Aged
Female
Finland - epidemiology
Follow-Up Studies
Humans
Leisure Activities
Male
Middle Aged
Sedentary lifestyle
Smoking - epidemiology - psychology
Surveys and Questionnaires
Twins - psychology - statistics & numerical data
Young Adult
Abstract
To investigate longitudinal associations of smoking and a change in smoking status with leisure-time physical inactivity. In addition, to control whether familial confounding (genetics and shared environment) influences the associations.
Data were based on the population-based Finnish Adult Twin Cohort of 5254 twin individuals born in 1945-1957 (41% men) and who participated in all four surveys over a 35-year follow-up (1975-2011). Logistic and conditional logistic regression models with multiple covariates were used for analyses.
Compared to never-smokers, long-term daily smokers (1975-1990) had the highest likelihood for both long-term inactivity and to change into inactive by 2011. Recurrent smoking was associated with long-term inactivity. Instead, in comparison to persistent daily smokers, quitting smoking decreased the likelihood of becoming physically inactive at leisure time. The associations remained in the analyses which accounted for multiple covariates and/or familial confounding.
Daily smoking increases the likelihood of remaining or becoming physically inactive over the decades. Our results emphasize not only the importance of preventing smoking initiation, but also to support early smoking cessation in promotion of lifelong physical activity.
Notes
Cites: Nicotine Tob Res. 2007 Oct;9(10):1027-32 PMID 17943618
Cites: Twin Res Hum Genet. 2013 Feb;16(1):157-62 PMID 23298696
Cites: Int J Public Health. 2014 Apr;59(2):243-50 PMID 24357049
Cites: Soc Psychiatry Psychiatr Epidemiol. 2004 Dec;39(12):994-9 PMID 15583908
Cites: Lancet. 2012 Jul 21;380(9838):219-29 PMID 22818936
Cites: Perspect Psychol Sci. 2010 Sep;5(5):546-56 PMID 21593989
Cites: Nicotine Tob Res. 2011 Apr;13(4):261-72 PMID 21330272
Cites: Hum Hered. 1978;28(4):241-54 PMID 566252
Cites: Lancet. 2012 Dec 15;380(9859):2224-60 PMID 23245609
Cites: Int J Behav Nutr Phys Act. 2012 Oct 02;9:121 PMID 23031224
Cites: Health Psychol. 1993 Sep;12(5):410-5 PMID 8223366
Cites: Addiction. 2014 Jul;109(7):1172-83 PMID 24690003
Cites: J Adolesc Health. 2004 Sep;35(3):238-44 PMID 15313507
Cites: Am J Health Behav. 2008 Jan-Feb;32(1):93-110 PMID 18021037
Cites: BMJ. 2014 Feb 13;348:g1151 PMID 24524926
Cites: Behav Genet. 2012 Jul;42(4):559-78 PMID 22426782
Cites: Twin Res Hum Genet. 2014 Aug;17(4):262-71 PMID 25034445
Cites: Prev Med. 2013 Nov;57(5):652-7 PMID 23994713
Cites: Scand J Med Sci Sports. 2016 Jan;26(1):93-100 PMID 25559167
Cites: Nat Rev Genet. 2002 Nov;3(11):872-82 PMID 12415317
Cites: Int J Epidemiol. 2017 Feb 1;46(1):116-127 PMID 26979986
Cites: JAMA. 2014 Jan 8;311(2):183-92 PMID 24399557
Cites: Scand J Med Sci Sports. 2002 Jun;12(3):179-85 PMID 12135451
Cites: Chest. 1991 Feb;99(2):315-22 PMID 1989788
Cites: Appl Physiol Nutr Metab. 2012 Jun;37(3):540-2 PMID 22540258
Cites: Addiction. 2003 Jan;98(1):23-31 PMID 12492752
Cites: Int J Epidemiol. 2014 Jun;43(3):775-82 PMID 24711605
Cites: Int J Obes (Lond). 2008 Feb;32(2):353-61 PMID 17653065
Cites: BMJ Open. 2014 Oct 07;4(10):e006141 PMID 25293386
Cites: Prev Med. 2011 Jul-Aug;53(1-2):24-8 PMID 21371494
Cites: Arch Gen Psychiatry. 2008 Aug;65(8):897-905 PMID 18678794
Cites: Addiction. 2007 Jul;102(7):1151-7 PMID 17567404
Cites: Prev Med. 2016 Mar;84:1-5 PMID 26740345
Cites: Biomed Res Int. 2014;2014:209140 PMID 24822182
Cites: Lancet. 2012 Jul 21;380(9838):258-71 PMID 22818938
Cites: N Engl J Med. 1996 Sep 26;335(13):931-7 PMID 8782500
Cites: J Clin Epidemiol. 1988;41(2):139-50 PMID 3335880
Cites: Can J Public Health. 2014 Mar 18;105(1):e69-78 PMID 24735700
Cites: Arch Intern Med. 2001 Feb 26;161(4):546-50 PMID 11252113
PubMed ID
28488098 View in PubMed
Less detail

Association between serum fatty acids and lipoprotein subclass profile in healthy young adults: exploring common genetic and environmental factors.

https://arctichealth.org/en/permalink/ahliterature259002
Source
Atherosclerosis. 2014 Apr;233(2):394-402
Publication Type
Article
Date
Apr-2014
Author
Aline Jelenkovic
Leonie H Bogl
Richard J Rose
Antti J Kangas
Pasi Soininen
Mika Ala-Korpela
Jaakko Kaprio
Karri Silventoinen
Source
Atherosclerosis. 2014 Apr;233(2):394-402
Date
Apr-2014
Language
English
Publication Type
Article
Keywords
Adolescent
Body mass index
Cholesterol - blood
Cross-Sectional Studies
Dietary Fats
Fatty Acids - blood
Finland - epidemiology
Follow-Up Studies
Gene-Environment Interaction
Genetic Pleiotropy
Humans
Lipoproteins - blood - classification
Nuclear Magnetic Resonance, Biomolecular
Particle Size
Phenotype
Questionnaires
Reference Values
Self Report
Triglycerides - blood
Twins, Dizygotic
Twins, Monozygotic
Young Adult
Abstract
Little is known about the associations of serum fatty acids with lipoprotein profile and the underlying genetic and environmental etiology of these relationships. We aimed to analyze the phenotypic association of serum n-6 and n-3 polyunsaturated (PUFAs), monounsaturated (MUFAs) and saturated (SFAs) fatty acids (relative proportion to total fatty acids) with lipids and lipoproteins, and to quantify common genetic and environmental factors determining their covariation.
Two cohorts of healthy Finnish twins were assessed in young adulthood. Data were available for 1269 individual twins including 561 complete pairs. Serum metabolites were measured by nuclear magnetic resonance spectroscopy. Bivariate quantitative genetic models were used to decompose the phenotypic covariance between the pairs of traits into genetic and environmental components.
Among the strongest correlations observed, serum total n-6 PUFAs and linoleic acid were inversely (max. r=-0.65) and MUFAs positively (max. r=0.63) correlated with triglycerides and very low-density lipoprotein (VLDL) particle concentration, particularly with large VLDL (for n-6 PUFAs) and medium VLDL (for MUFAs). Genetic factors significantly contributed to their covariance with bivariate heritability estimates ranging from 44% to 56% for n-6 PUFAs and 58% to 66% for MUFAs. Genetic correlations with lipid traits were moderate to high (max. rA=-0.59 and 0.70 for n-6 PUFAs and MUFAs, respectively). Statistically significant, but substantially weaker phenotypic correlations of total n-3 PUFAs, docosahexaenoic acid (DHA) and SFAs with lipoprotein profile were not decomposed into their genetic and environmental components.
Shared genetic factors are important in explaining why higher concentrations of serum n-6 PUFAs and lower concentrations of serum MUFAs strongly associate with lower triglyceride and VLDL particle concentrations.
PubMed ID
24530769 View in PubMed
Less detail

Association of Protein Phosphatase PPM1G With Alcohol Use Disorder and Brain Activity During Behavioral Control in a Genome-Wide Methylation Analysis.

https://arctichealth.org/en/permalink/ahliterature265754
Source
Am J Psychiatry. 2015 Jun;172(6):543-52
Publication Type
Article
Date
Jun-2015
Author
Barbara Ruggeri
Charlotte Nymberg
Eero Vuoksimaa
Anbarasu Lourdusamy
Cybele P Wong
Fabiana M Carvalho
Tianye Jia
Anna Cattrell
Christine Macare
Tobias Banaschewski
Gareth J Barker
Arun L W Bokde
Uli Bromberg
Christian Büchel
Patricia J Conrod
Mira Fauth-Bühler
Herta Flor
Vincent Frouin
Jürgen Gallinat
Hugh Garavan
Penny Gowland
Andreas Heinz
Bernd Ittermann
Jean-Luc Martinot
Frauke Nees
Zdenka Pausova
Tomáลก Paus
Marcella Rietschel
Trevor Robbins
Michael N Smolka
Rainer Spanagel
Georgy Bakalkin
Jonathan Mill
Wolfgang H Sommer
Richard J Rose
Jia Yan
Fazil Aliev
Danielle Dick
Jaakko Kaprio
Sylvane Desrivières
Gunter Schumann
Source
Am J Psychiatry. 2015 Jun;172(6):543-52
Date
Jun-2015
Language
English
Publication Type
Article
Keywords
Adolescent
Alcohol-Related Disorders - diagnosis - genetics - physiopathology - psychology
Alcoholism - diagnosis - genetics - physiopathology - psychology
DNA Methylation - genetics
Diseases in Twins - diagnosis - genetics - psychology
Epigenesis, Genetic - genetics
Female
Finland
Gene Expression Regulation - genetics
Genetic Markers - genetics
Genome-Wide Association Study
Genotype
Humans
Impulsive Behavior - drug effects - physiology
Internal-External Control
Male
Mental Disorders - diagnosis - genetics - physiopathology - psychology
Oxygen - blood
Phosphoprotein Phosphatases - genetics
Subthalamic Nucleus - drug effects - physiopathology
Twins, Monozygotic
Young Adult
Abstract
The genetic component of alcohol use disorder is substantial, but monozygotic twin discordance indicates a role for nonheritable differences that could be mediated by epigenetics. Despite growing evidence associating epigenetics and psychiatric disorders, it is unclear how epigenetics, particularly DNA methylation, relate to brain function and behavior, including drinking behavior.
The authors carried out a genome-wide analysis of DNA methylation of 18 monozygotic twin pairs discordant for alcohol use disorder and validated differentially methylated regions. After validation, the authors characterized these differentially methylated regions using personality trait assessment and functional MRI in a sample of 499 adolescents.
Hypermethylation in the 3'-protein-phosphatase-1G (PPM1G) gene locus was associated with alcohol use disorder. The authors found association of PPM1G hypermethylation with early escalation of alcohol use and increased impulsiveness. They also observed association of PPM1G hypermethylation with increased blood-oxygen-level-dependent response in the right subthalamic nucleus during an impulsiveness task.
Overall, the authors provide first evidence for an epigenetic marker associated with alcohol consumption and its underlying neurobehavioral phenotype.
Notes
Comment In: Am J Psychiatry. 2015 Jun;172(6):499-50125982661
PubMed ID
25982659 View in PubMed
Less detail

Association of smoking in adolescence with abdominal obesity in adulthood: a follow-up study of 5 birth cohorts of Finnish twins.

https://arctichealth.org/en/permalink/ahliterature153863
Source
Am J Public Health. 2009 Feb;99(2):348-54
Publication Type
Article
Date
Feb-2009
Author
Suoma E Saarni
Kirsi Pietiläinen
Suvi Kantonen
Aila Rissanen
Jaakko Kaprio
Author Affiliation
Department of Public Health, University of Helsinki, Helsinki, Finland. suoma.saarni@helsinki.fi
Source
Am J Public Health. 2009 Feb;99(2):348-54
Date
Feb-2009
Language
English
Publication Type
Article
Keywords
Abdominal Fat
Adolescent
Adult
Cohort Studies
Female
Finland - epidemiology
Humans
Male
Obesity
Odds Ratio
Overweight - epidemiology
Questionnaires
Smoking - epidemiology
Twin Studies as Topic
Young Adult
Abstract
We studied the association of adolescent smoking with overweight and abdominal obesity in adulthood.
We used the FinnTwin16, a prospective, population-based questionnaire study of 5 consecutive and complete birth cohorts of Finnish twins born between 1975 and 1979 (N = 4296) and studied at four points between the ages of 16 and 27 years to analyze the effect of adolescent smoking on abdominal obesity and overweight in early adulthood.
Smoking at least 10 cigarettes daily when aged 16 to 18 years increased the risk of adult abdominal obesity (odds ratio [OR]=1.77; 95% confidence interval [CI] = 1.39, 2.26). After we adjusted for confounders, the OR was 1.44 (95% CI = 1.11, 1.88), and after further adjustment for current body mass index (BMI), the OR was 1.34 (95% CI = 0.95, 1.88). Adolescent smoking significantly increased the risk of becoming overweight among women even after adjustment for possible confounders, including baseline BMI (OR = 1.74; 95% CI = 1.06, 2.88).
Smoking is a risk factor for abdominal obesity among both genders and for overweight in women. The prevention of smoking during adolescence may play an important role in promoting healthy weight and in decreasing the morbidity related to abdominal obesity.
Notes
Cites: Am J Public Health. 1989 Feb;79(2):152-72913832
Cites: Am J Epidemiol. 1982 Nov;116(5):765-757148802
Cites: Ann Intern Med. 1989 Nov 15;111(10):783-72817625
Cites: JAMA. 1993 Mar 17;269(11):1391-58441214
Cites: BMJ. 1995 Nov 25;311(7017):1401-58520275
Cites: Int J Obes Relat Metab Disord. 1997 Mar;21(3):189-969080257
Cites: J Epidemiol Community Health. 1997 Jun;51(3):252-609229053
Cites: Am J Clin Nutr. 1998 May;67(5):846-529583840
Cites: Int J Obes Relat Metab Disord. 1998 Sep;22(9):915-229756252
Cites: Health Psychol. 1998 Sep;17(5):454-89776004
Cites: J Consult Clin Psychol. 1998 Dec;66(6):987-939874912
Cites: Int J Obes Relat Metab Disord. 1999 Feb;23(2):107-1510078843
Cites: Acta Paediatr. 1999 Apr;88(4):431-710342544
Cites: Int J Obes (Lond). 2005 Feb;29(2):236-4315505632
Cites: Int J Obes (Lond). 2005 Jun;29(6):697-70215782226
Cites: Int J Obes (Lond). 2005 Jul;29(7):778-8415917857
Cites: Eur J Public Health. 2005 Jun;15(3):262-915755781
Cites: Circulation. 2005 Aug 9;112(6):862-916061737
Cites: Obes Res. 2005 Aug;13(8):1466-7516129730
Cites: J Clin Epidemiol. 2005 Nov;58(11):1165-7116223660
Cites: Int J Psychophysiol. 2006 Mar;59(3):236-4316325948
Cites: Nutr Rev. 2006 Feb;64(2 Pt 1):53-6616536182
Cites: Psychosom Med. 2006 May-Jun;68(3):414-2016738073
Cites: Am J Clin Nutr. 2006 Aug;84(2):274-8816895873
Cites: Clin Res Cardiol. 2007 Jun;96(6):365-7417453138
Cites: Am J Public Health. 2007 Aug;97(8):1427-3317600242
Cites: Am J Epidemiol. 2008 Jan 15;167(2):188-9218079134
Cites: Behav Neurosci. 2008 Feb;122(1):161-7318298259
Cites: BMJ. 1989 May 13;298(6683):1287-902500198
Cites: BMJ. 2000 May 6;320(7244):1240-310797032
Cites: Nutrition. 2000 Oct;16(10):924-3611054598
Cites: Am J Med. 2000 Nov;109(7):538-4211063954
Cites: J Epidemiol Community Health. 2002 Mar;56(3):167-7011854334
Cites: Obes Rev. 2001 May;2(2):73-8612119665
Cites: Scand J Med Sci Sports. 2002 Jun;12(3):179-8512135451
Cites: Nat Rev Genet. 2002 Nov;3(11):872-8212415317
Cites: Int J Obes Relat Metab Disord. 2002 Dec;26(12):1570-812461673
Cites: Ann Intern Med. 2003 Jan 7;138(1):24-3212513041
Cites: Twin Res. 2002 Oct;5(5):366-7112537860
Cites: Addict Behav. 2003 Apr;28(3):501-1212628622
Cites: J Adolesc Health. 2003 Apr;32(4):306-1312667735
Cites: Eur J Clin Nutr. 2003 Jul;57(7):842-5312821884
Cites: Twin Res. 2003 Oct;6(5):409-2114624725
Cites: Arch Pediatr Adolesc Med. 2003 Dec;157(12):1212-814662578
Cites: Eur J Clin Nutr. 2004 Jan;58(1):180-9014679384
Cites: JAMA. 2004 Mar 10;291(10):1238-4515010446
Cites: Int J Obes Relat Metab Disord. 2004 Jun;28(6):796-80215024402
Cites: Nicotine Tob Res. 2004 Jun;6(3):397-42515203775
Cites: Int J Obes Relat Metab Disord. 2004 Aug;28(8):1091-615197410
Cites: Am J Clin Nutr. 2004 Sep;80(3):569-7515321794
Cites: Hum Hered. 1978;28(4):241-54566252
Comment In: Am J Public Health. 2009 Aug;99(8):135019542028
PubMed ID
19059868 View in PubMed
Less detail

Associations between IQ and cigarette smoking among Swedish male twins.

https://arctichealth.org/en/permalink/ahliterature98720
Source
Soc Sci Med. 2010 Feb;70(4):575-81
Publication Type
Article
Date
Feb-2010
Author
Karin Modig Wennerstad
Karri Silventoinen
Per Tynelius
Lars Bergman
Jaakko Kaprio
Finn Rasmussen
Author Affiliation
Department of Public Health Sciences, Karolinska Institute, Stockholm, Sweden. karin.modig@ki.se
Source
Soc Sci Med. 2010 Feb;70(4):575-81
Date
Feb-2010
Language
English
Publication Type
Article
Keywords
Adolescent
Adult
Humans
Intelligence
Logistic Models
Male
Middle Aged
Registries
Risk factors
Smoking - epidemiology - genetics
Social Environment
Socioeconomic Factors
Sweden - epidemiology
Twins - genetics - psychology
Young Adult
Abstract
It has been suggested that certain health behaviours, such as smoking, may operate as mediators of the well-established inverse association between IQ and mortality risk. Previous research may be afflicted by unadjusted confounding by socioeconomic or psychosocial factors. Twin designs offer a unique possibility to take genetic and shared environmental factors into account. The aim of the present national twin study was to determine the interrelations between IQ at age 18, childhood and attained social factors and smoking status in young adulthood and mid-life. We studied the association between IQ at age 18 and smoking in later life in a population of 11 589 male Swedish twins. IQ was measured at military conscription, and data on smoking and zygosity was obtained from the Swedish Twin Register. Information on social factors was extracted from censuses. Data on smoking was self-reported by the twins at the age of 22-47 years. Logistic regression models estimated with generalised estimating equations were used to explore possible associations between IQ and smoking among the twins as individuals as well as between-and within twin-pairs. A strong inverse association between IQ and smoking status emerged in unmatched analyses over the entire range of IQ distribution. In within-pair and between-pair analyses it transpired that shared environmental factors explained most of the inverse IQ-smoking relationship. In addition, these analyses indicated that non-shared and genetic factors contributed only slightly (and non-significantly) to the IQ-smoking association. Analysis of twin pairs discordant for IQ and smoking status displayed no evidence that non-shared factors contribute substantially to the association. The question of which shared environmental factors might explain the IQ-smoking association is an intriguing one for future research.
PubMed ID
19931961 View in PubMed
Less detail

64 records – page 1 of 7.