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Activity levels and body mass index of children in the United States, Sweden, and Australia.

https://arctichealth.org/en/permalink/ahliterature30804
Source
Med Sci Sports Exerc. 2003 Aug;35(8):1367-73
Publication Type
Article
Date
Aug-2003
Author
Susan D Vincent
Robert P Pangrazi
Anders Raustorp
L Michaud Tomson
Thomas F Cuddihy
Author Affiliation
Brigham Young University, Provo, UT 84602, USA. sue_vincent@byu.edu
Source
Med Sci Sports Exerc. 2003 Aug;35(8):1367-73
Date
Aug-2003
Language
English
Publication Type
Article
Keywords
Age Distribution
Australia - epidemiology
Body mass index
Child
Comparative Study
Exercise - physiology
Female
Humans
Male
Motor Activity - physiology
Multivariate Analysis
Obesity - epidemiology
Sex Distribution
Sweden - epidemiology
United States - epidemiology
Abstract
PURPOSE: Assess the physical activity and body mass index (BMI) levels of children in the United States, Sweden, and Australia. METHODS: A total of 1954 children, 6-12 yr old (711 American, 563 Australian, and 680 Swedish) wore sealed pedometers for four consecutive days. Height and weight measures were obtained. RESULTS: Descriptive data for step counts and BMI by sex, age, and country were calculated to determine activity levels and BMI. Three-way multivariate ANOVA for step counts and BMI between countries at each age and sex found that, in general, the Swedish children were significantly more active than the Australian and American children, and the American children were significantly heavier than the Australian and Swedish children. For boys, the mean step counts ranged from 15673 to 18346 for Sweden, 13864 to 15023 for Australia, and 12554 to 13872 for America. For girls, the mean step counts ranged from 12041 to 14825 for Sweden, 11221 to 12322 for Australia, and 10661 to 11383 for America. The activity curve is somewhat level during the preadolescent years. The rate of increase in BMI with age is much greater in the American children than in the Swedish or Australian children. The percent of American, Swedish, and Australian boys classified as overweight/obese was 33.5, 16.6, and 15.8, respectively. The percent of American, Swedish, and Australian girls classified as overweight/obese was 35.6, 16.8, and 14.4, respectively. Correlation analysis found few significant negative relationships between step counts and BMI. CONCLUSIONS: American children tend to be the least active and heaviest with the greatest rate of increase in BMI. The Swedish children are the most active group followed by Australia. Swedish and Australian children maintain lower BMI throughout their prepubescent years than do the American children who have a greater percentage who are classified as overweight.
PubMed ID
12900692 View in PubMed
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Age-related variations in flavonoid intake and sources in the Australian population.

https://arctichealth.org/en/permalink/ahliterature79676
Source
Public Health Nutr. 2006 Dec;9(8):1045-54
Publication Type
Article
Date
Dec-2006
Author
Johannot Lidwine
Somerset Shawn M
Author Affiliation
School of Public Health and Heart Foundation Research Centre, Griffith University, University Drive, Meadowbrook, Queensland, Australia.
Source
Public Health Nutr. 2006 Dec;9(8):1045-54
Date
Dec-2006
Language
English
Publication Type
Article
Keywords
Adolescent
Adult
Age Factors
Aged
Aged, 80 and over
Australia - epidemiology
Child
Child, Preschool
Eating
Flavonoids
Food Analysis - statistics & numerical data
Food Preferences
Humans
Middle Aged
Nutrition Surveys
Abstract
OBJECTIVE: To estimate flavonoid intake in the Australian population. DESIGN: Flavonoid consumption was estimated from 24-hour recall data and apparent consumption data using US Department of Agriculture flavonoid composition data. SUBJECTS: The National Nutrition Survey 1995 assessed dietary intake (24-hour recall) in a representative sample (n=13,858) of the Australian population aged 2 years and over. RESULTS: Analysis of the 24-hour recall data indicated an average adult intake (>18 years) of 454 mg day(-1) (92% being flavan-3-ols). Apple was the highest quercetin source until age 16-18 years, after which onion became an increasingly important prominent source. Variations in hesperetin consumption reflected orange intake. Apple, apricot and grapes were the major sources of epicatechin and catechin for children, but subsided as wine consumption increased in adulthood. Wine was the main source of malvidin. Naringenin intake remained static as a percentage of total flavonoid intake until age 19-24 years, corresponding to orange intake, and then increased with age from 19-24 years, corresponding to grapefruit intake. Apparent dietary flavonoid consumption was 351 mg person(-1) day(-1), of which 75% were flavan-3-ols. Black tea was the major flavonoid source (predominantly flavan-3-ols) representing 70% of total intake. Hesperetin and naringenin were the next most highly consumed flavonoids, reflecting orange intake. Both 24-hour recall and apparent consumption data indicated that apigenin intake was markedly higher in Australia than reported in either the USA or Denmark, presumably due to differences in consumption data for leaf and stalk vegetables and parsley. CONCLUSIONS: Tea was the major dietary flavonoid source in Australia. Flavonoid consumption profiles and flavonoid sources varied according to age. More consistent methodologies, survey tools validated for specific flavonoid intakes and enhanced local flavonoid content data for foods would facilitate better international comparisons of flavonoid intake.
PubMed ID
17125569 View in PubMed
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Analyzing the etiology of benign rolandic epilepsy: a multicenter twin collaboration.

https://arctichealth.org/en/permalink/ahliterature76297
Source
Epilepsia. 2006 Mar;47(3):550-5
Publication Type
Article
Date
Mar-2006
Author
Lata Vadlamudi
Marianne J Kjeldsen
Linda A Corey
Marit H Solaas
Mogen L Friis
John M Pellock
Karl O Nakken
Roger L Milne
Ingrid E Scheffer
A Simon Harvey
John L Hopper
Samuel F Berkovic
Author Affiliation
Epilepsy Research Centre, Department of Medicine (Neurology), University of Melbourne, Austin Health, Heidelberg, Victoria, Australia.
Source
Epilepsia. 2006 Mar;47(3):550-5
Date
Mar-2006
Language
English
Publication Type
Article
Keywords
Adult
Age of Onset
Australia - epidemiology
Comparative Study
Denmark - epidemiology
Diseases in Twins - diagnosis - epidemiology - genetics
Electroencephalography - statistics & numerical data
Epilepsy, Rolandic - diagnosis - epidemiology - genetics
Family
Female
Genetic Heterogeneity
Genotype
Humans
Male
Models, Genetic
Norway - epidemiology
Pedigree
Prevalence
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Twins, Dizygotic - genetics
Twins, Monozygotic - genetics
United States - epidemiology
Variation (Genetics)
Abstract
PURPOSE: Benign rolandic epilepsy (BRE) is considered a genetically determined idiopathic partial epilepsy. We analyzed a large sample of twins from four international twin registers to probe the genetics of BRE. We also aim to synthesize the apparently conflicting family and twin data into a model of BRE etiology. METHODS: Large population-based twin registries of epilepsies from Odense (Denmark), Richmond, Virginia (United States), and Oslo (Norway) were reviewed for BRE cases and added to our Australian twin data. Diagnosis of classic BRE was based on electroclinical criteria with normal neurologic development. Cases with a compatible electroclinical picture but abnormal neurologic development were termed non-classic BRE. RESULTS: Eighteen twin pairs were identified (10 monozygous; eight dizygous) of whom at least one twin was diagnosed with classic BRE among a total sample of 1,952 twin pairs validated for seizures, and all were discordant for BRE. The estimated monozygous pairwise concordance for BRE in this sample was 0.0 [95% confidence interval (CI), 0.0-0.3). Four twin pairs (one monozygous, three dizygous) had non-classic BRE, and all co-twins had seizures. CONCLUSIONS: The twin data showing an absence of any concordant twin pairs with classic BRE suggest that noninherited factors are of major importance in BRE. Modelling the data shows that the familial occurrence of centrotemporal spikes makes only a minor contribution to the familial aggregation of BRE. Genetic factors are probably more important in non-classic BRE. The etiology and mode(s) of inheritance of BRE are much more complicated than initially conceptualized.
PubMed ID
16529620 View in PubMed
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An evaluation and comparison of three commonly used statistical models for automatic detection of outbreaks in epidemiological data of communicable diseases.

https://arctichealth.org/en/permalink/ahliterature82991
Source
Epidemiol Infect. 2006 Aug;134(4):863-71
Publication Type
Article
Date
Aug-2006
Author
Rolfhamre P.
Ekdahl K.
Author Affiliation
Department of Epidemiology, Swedish Institute for Infectious Disease Control (SMI), Solna, Sweden. per.rolfhamre@smi.ki.se
Source
Epidemiol Infect. 2006 Aug;134(4):863-71
Date
Aug-2006
Language
English
Publication Type
Article
Keywords
Australia - epidemiology
Campylobacter Infections - epidemiology
Disease Outbreaks - statistics & numerical data
England - epidemiology
Hepatitis A - epidemiology
Humans
Infant, Newborn
Models, Statistical
New Zealand - epidemiology
Poisson Distribution
Retrospective Studies
Sensitivity and specificity
Sweden - epidemiology
Tularemia - epidemiology
Wales - epidemiology
Abstract
We evaluated three established statistical models for automated 'early warnings' of disease outbreaks; counted data Poisson CuSums (used in New Zealand), the England and Wales model (used in England and Wales) and SPOTv2 (used in Australia). In the evaluation we used national Swedish notification data from 1992 to 2003 on campylobacteriosis, hepatitis A and tularemia. The average sensitivity and positive predictive value for CuSums were 71 and 53%, for the England and Wales model 87 and 82% and for SPOTv2 95 and 49% respectively. The England and Wales model and the SPOTv2 model were superior to CuSums in our setting. Although, it was more difficult to rank the former two, we recommend the SPOTv2 model over the England and Wales model, mainly because of a better sensitivity. However, the impact of previous outbreaks on baseline levels was less in the England and Wales model. The CuSums model did not adjust for previous outbreaks.
PubMed ID
16371181 View in PubMed
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An international comparison of the estimated effect of the aging of the population on the major cause of disablement, musculoskeletal disorders.

https://arctichealth.org/en/permalink/ahliterature14323
Source
J Rheumatol. 1995 Oct;22(10):1934-40
Publication Type
Article
Date
Oct-1995
Author
E M Badley
M. Crotty
Author Affiliation
Arthritis Community Research and Evaluation Unit, Wellesley Hospital Research Institute, Toronto, Canada.
Source
J Rheumatol. 1995 Oct;22(10):1934-40
Date
Oct-1995
Language
English
Publication Type
Article
Keywords
Adolescent
Adult
Aged
Aging - physiology
Arthritis - epidemiology - physiopathology
Australia - epidemiology
Back Pain - epidemiology - physiopathology
Child
Child, Preschool
Comparative Study
Disabled Persons
Europe - epidemiology
Forecasting
Humans
Infant
Infant, Newborn
Middle Aged
Musculoskeletal Diseases - epidemiology - physiopathology
Prevalence
Research Support, Non-U.S. Gov't
United States - epidemiology
Abstract
OBJECTIVE: To illustrate quantitatively the effect of the aging of the population on the prevalence of chronic disorders by comparing the projected frequency of musculoskeletal (MSK) disorders in 3 comparatively "young" countries, Australia, Canada, and the United States, and 3 comparatively "old" countries, France, the United Kingdom, and Sweden. METHODS: Age specific rates for MSK disability in Canada were applied to World Bank population estimates and projects to estimate prevalence rates and numbers of persons with MSK disability in the years 1985, 2000, 2010, and 2020. RESULTS: The age structure of the populations affected baseline rates for MSK disability. Increases in both prevalence and numbers affected are expected for all countries between 1985 and 2020, up to a 34% increase in prevalence in Canada, and an 88% increase in numbers in Australia. CONCLUSION: The aging of the population is likely to result in a disproportionate increase in the number of people with chronic disabling disorders, which will be taking place against a background of a decreasing or static number of young adults, with implications for meeting needs for health care and community support.
PubMed ID
8991994 View in PubMed
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An inverse association between ovarian cysts and breast cancer in the breast cancer family registry.

https://arctichealth.org/en/permalink/ahliterature173729
Source
Int J Cancer. 2006 Jan 1;118(1):197-202
Publication Type
Article
Date
Jan-1-2006
Author
Julia A Knight
Esther M John
Roger L Milne
Gillian S Dite
Ron Balbuena
Ellen J Q Shi
Graham G Giles
Argyrios Ziogas
Irene L Andrulis
Alice S Whittemore
John L Hopper
Author Affiliation
Samuel Lunenfeld Research Institute, Mount Sinai Hospital, Toronto, Canada.
Source
Int J Cancer. 2006 Jan 1;118(1):197-202
Date
Jan-1-2006
Language
English
Publication Type
Article
Keywords
Adolescent
Adult
Aged
Australia - epidemiology
Breast Neoplasms - epidemiology - prevention & control
California - epidemiology
Case-Control Studies
Female
Humans
Incidence
Middle Aged
Odds Ratio
Ontario - epidemiology
Ovarian Cysts - epidemiology
Registries - statistics & numerical data
Risk assessment
Abstract
Ovarian cysts of several types are common in women of reproductive age. Their etiology is not well understood but is likely related to perturbations in the hypothalamic-pituitary-gonadal axis. The relationship of ovarian cysts to breast cancer risk is not known, although a negative association with polycystic ovarian syndrome has been reported. Incident, invasive female breast cancer cases, population-based controls and unaffected sisters of cases were studied from 3 countries participating in the Breast Cancer Family Registry: Melbourne and Sydney, Australia; the San Francisco Bay Area, USA; and Ontario, Canada. Using the same questionnaire, information was collected on self-reported history of ovarian cysts and other risk factors. Analyses were based on 3,049 cases, 2,344 population controls and 1,934 sister controls from all sites combined. Odds ratios (ORs) and 95% confidence intervals (CIs) were estimated using both unconditional and conditional logistic regression using an offset term to account for sampling fractions at 2 of the sites. A significantly reduced risk of breast cancer was observed for women reporting a history of ovarian cysts (OR = 0.70, 95% CI 0.59-0.82, among all cases and all controls). This risk estimate was similar regardless of control group used, within all 3 sites and in both premenopausal and postmenopausal women (ORs ranging from 0.68-0.75, all 95% CI excluded 1.00). A self-reported history of ovarian cysts was strongly and consistently associated with a reduced risk of breast cancer. Further study of ovarian cysts may increase our understanding of hormonal and other mechanisms of breast cancer etiology.
PubMed ID
16032703 View in PubMed
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An investigation of routes to cancer diagnosis in 10 international jurisdictions, as part of the International Cancer Benchmarking Partnership: survey development and implementation.

https://arctichealth.org/en/permalink/ahliterature288091
Source
BMJ Open. 2016 07 25;6(7):e009641
Publication Type
Article
Date
07-25-2016
Author
David Weller
Peter Vedsted
Chantelle Anandan
Alina Zalounina
Evangelia Ourania Fourkala
Rakshit Desai
William Liston
Henry Jensen
Andriana Barisic
Anna Gavin
Eva Grunfeld
Mats Lambe
Rebecca-Jane Law
Martin Malmberg
Richard D Neal
Jatinderpal Kalsi
Donna Turner
Victoria White
Martine Bomb
Usha Menon
Source
BMJ Open. 2016 07 25;6(7):e009641
Date
07-25-2016
Language
English
Publication Type
Article
Keywords
Analysis of Variance
Antineoplastic Combined Chemotherapy Protocols
Australia - epidemiology
Benchmarking
Breast Neoplasms - diagnosis - epidemiology
Canada - epidemiology
Colorectal Neoplasms - diagnosis - epidemiology
Cross-Sectional Studies
Denmark - epidemiology
Early Detection of Cancer - standards
Female
Humans
Lung Neoplasms - diagnosis - epidemiology
Norway - epidemiology
Ovarian Neoplasms - diagnosis - epidemiology
Pilot Projects
Practice Patterns, Physicians' - organization & administration - statistics & numerical data
Primary Health Care - standards
Registries
Reproducibility of Results
Survival Rate
Sweden - epidemiology
United Kingdom - epidemiology
Abstract
This paper describes the methods used in the International Cancer Benchmarking Partnership Module 4 Survey (ICBPM4) which examines time intervals and routes to cancer diagnosis in 10 jurisdictions. We present the study design with defining and measuring time intervals, identifying patients with cancer, questionnaire development, data management and analyses.
Recruitment of participants to the ICBPM4 survey is based on cancer registries in each jurisdiction. Questionnaires draw on previous instruments and have been through a process of cognitive testing and piloting in three jurisdictions followed by standardised translation and adaptation. Data analysis focuses on comparing differences in time intervals and routes to diagnosis in the jurisdictions.
Our target is 200 patients with symptomatic breast, lung, colorectal and ovarian cancer in each jurisdiction. Patients are approached directly or via their primary care physician (PCP). Patients' PCPs and cancer treatment specialists (CTSs) are surveyed, and 'data rules' are applied to combine and reconcile conflicting information. Where CTS information is unavailable, audit information is sought from treatment records and databases.
Reliability testing of the patient questionnaire showed that agreement was complete (?=1) in four items and substantial (?=0.8, 95% CI 0.333 to 1) in one item. The identification of eligible patients is sufficient to meet the targets for breast, lung and colorectal cancer. Initial patient and PCP survey response rates from the UK and Sweden are comparable with similar published surveys. Data collection was completed in early 2016 for all cancer types.
An international questionnaire-based survey of patients with cancer, PCPs and CTSs has been developed and launched in 10 jurisdictions. ICBPM4 will help to further understand international differences in cancer survival by comparing time intervals and routes to cancer diagnosis.
Notes
Cites: Lancet. 2015 Mar 14;385(9972):977-101025467588
Cites: Health Policy. 2013 Sep;112(1-2):148-5523693117
Cites: Biometrics. 1989 Mar;45(1):255-682720055
Cites: Br J Gen Pract. 2011 Aug;61(589):e508-1221801563
Cites: BMC Fam Pract. 2008 Jan 30;9:918234092
Cites: Br J Cancer. 2012 Oct 9;107(8):1220-622996611
Cites: BMC Med Res Methodol. 2003 Oct 20;3:2114567763
Cites: Nat Rev Cancer. 2006 Aug;6(8):603-1216862191
Cites: JAMA Surg. 2013 Jun;148(6):516-2323615681
Cites: BMC Health Serv Res. 2011 Oct 25;11:28422027084
Cites: Clin Epidemiol. 2014 Jul 17;6:237-4625083137
Cites: Br J Cancer. 2011 Mar 15;104(6):934-4021364593
Cites: Lancet Oncol. 2014 Jan;15(1):23-3424314615
Cites: Br J Cancer. 2013 Feb 5;108(2):292-30023370208
Cites: Acta Oncol. 2013 Jun;52(5):919-3223581611
Cites: Gynecol Oncol. 2012 Oct;127(1):75-8222750127
Cites: BMC Cancer. 2013 Apr 23;13:20323617741
Cites: Lung Cancer. 2012 Oct;78(1):51-622841591
Cites: Br J Cancer. 2008 Jan 15;98(1):60-7018059401
Cites: BMJ Open. 2015 May 27;5(5):e00721226017370
Cites: Fam Pract. 2012 Feb;29(1):69-7821828375
Cites: Eur J Cancer. 2009 Mar;45(5):747-5519117750
Cites: Br J Cancer. 2015 Mar 31;112 Suppl 1:S92-10725734382
Cites: Br J Cancer. 2013 Mar 19;108(5):1195-20823449362
Cites: J Clin Epidemiol. 2012 Jun;65(6):669-7822459430
Cites: Cancer Epidemiol. 2014 Feb;38(1):100-524238619
Cites: Br J Gen Pract. 2011 May;61(586):e215-2221619745
Cites: Lancet. 2011 Jan 8;377(9760):127-3821183212
Cites: Br J Cancer. 2012 Mar 27;106(7):1262-722415239
Cites: Fam Pract. 2007 Feb;24(1):3-617142248
Cites: Thorax. 2013 Jun;68(6):551-6423399908
Cites: Eur J Cancer. 2013 Jun;49(9):2187-9823453935
Cites: Br J Cancer. 2013 Feb 19;108(3):686-9023392082
Cites: Radiother Oncol. 2007 Jul;84(1):5-1017493700
Cites: Br J Gen Pract. 2013 Jan;63(606):e30-623336455
Cites: Am J Public Health. 1989 Aug;79(8):1053-52751028
Cites: PLoS One. 2015 Aug 07;10(8):e013502726252203
Cites: Br J Gen Pract. 2001 Dec;51(473):967-7111766868
PubMed ID
27456325 View in PubMed
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Source
Eur J Epidemiol. 2019 Feb; 34(2):105-114
Publication Type
Journal Article
Date
Feb-2019
Author
Amirhossein Modabbernia
Sven Sandin
Raz Gross
Helen Leonard
Mika Gissler
Erik T Parner
Richard Francis
Kim Carter
Michaeline Bresnahan
Diana Schendel
Mady Hornig
Abraham Reichenberg
Author Affiliation
Department of Psychiatry and Seaver Autism Center, Icahn School of Medicine at Mount Sinai, 1 Gustave L Levy PLC, New York, NY, 10029, USA.
Source
Eur J Epidemiol. 2019 Feb; 34(2):105-114
Date
Feb-2019
Language
English
Publication Type
Journal Article
Keywords
Apgar score
Autism Spectrum Disorder - epidemiology
Birth weight
Cohort Studies
Denmark - epidemiology
Female
Gestational Age
Humans
Infant, Newborn
Male
Norway - epidemiology
Odds Ratio
Prospective Studies
Sweden - epidemiology
Western Australia - epidemiology
Abstract
Low Apgar score has been associated with higher risk for several neurological and psychiatric disorders, including cerebral palsy and intellectual disability. Studies of the association between Apgar score and autism spectrum disorder (ASD) have been inconsistent. We aimed to investigate (1) the association between low Apgar score at 5 min and risk for ASD, and (2) the modifying effects of gestational age and sex on this association in the largest multinational database of ASD. We included prospective data from 5.5 million individuals and over 33,000 cases of ASD from Norway, Sweden, Denmark and Western Australia who were born between 1984 and 2007. We calculated crude and adjusted risk ratios (RR) with 95% confidence intervals (95% CIs) for the associations between low Apgar score and ASD. All analyses for ASD were repeated for autistic disorder (AD). We used interaction terms and stratified analysis to investigate the effects of sex, gestational age, and birth weight on the association. In fully adjusted models, low Apgar scores (1-3) (RR, 1.42; 95% CI, 1.16-1.74), and intermediate Apgar scores (4-6) (RR, 1.50; 95% CI, 1.36-1.65) were associated with a higher RR of ASD than optimal Apgar score (7-10). The point estimates for low (RR, 1.88; 95% CI, 1.41-2.51) and intermediate Apgar score (RR, 1.54; 95% CI, 1.32-1.81) were larger for AD than for ASD. This study suggests that low Apgar score is associated with higher risk of ASD, and in particular AD. We did not observe any major modifying effects of gestational age and sex, although there seems to be substantial confounding by gestational age and birth weight on the observed association.
PubMed ID
30291529 View in PubMed
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Association between class III obesity (BMI of 40-59 kg/m2) and mortality: a pooled analysis of 20 prospective studies.

https://arctichealth.org/en/permalink/ahliterature267096
Source
PLoS Med. 2014 Jul;11(7):e1001673
Publication Type
Article
Date
Jul-2014
Author
Cari M Kitahara
Alan J Flint
Amy Berrington de Gonzalez
Leslie Bernstein
Michelle Brotzman
Robert J MacInnis
Steven C Moore
Kim Robien
Philip S Rosenberg
Pramil N Singh
Elisabete Weiderpass
Hans Olov Adami
Hoda Anton-Culver
Rachel Ballard-Barbash
Julie E Buring
D Michal Freedman
Gary E Fraser
Laura E Beane Freeman
Susan M Gapstur
John Michael Gaziano
Graham G Giles
Niclas Håkansson
Jane A Hoppin
Frank B Hu
Karen Koenig
Martha S Linet
Yikyung Park
Alpa V Patel
Mark P Purdue
Catherine Schairer
Howard D Sesso
Kala Visvanathan
Emily White
Alicja Wolk
Anne Zeleniuch-Jacquotte
Patricia Hartge
Source
PLoS Med. 2014 Jul;11(7):e1001673
Date
Jul-2014
Language
English
Publication Type
Article
Keywords
Australia - epidemiology
Body mass index
Humans
Life expectancy
Obesity - mortality
Prospective Studies
Risk factors
Sweden - epidemiology
United States - epidemiology
Abstract
The prevalence of class III obesity (body mass index [BMI]=40 kg/m2) has increased dramatically in several countries and currently affects 6% of adults in the US, with uncertain impact on the risks of illness and death. Using data from a large pooled study, we evaluated the risk of death, overall and due to a wide range of causes, and years of life expectancy lost associated with class III obesity.
In a pooled analysis of 20 prospective studies from the United States, Sweden, and Australia, we estimated sex- and age-adjusted total and cause-specific mortality rates (deaths per 100,000 persons per year) and multivariable-adjusted hazard ratios for adults, aged 19-83 y at baseline, classified as obese class III (BMI 40.0-59.9 kg/m2) compared with those classified as normal weight (BMI 18.5-24.9 kg/m2). Participants reporting ever smoking cigarettes or a history of chronic disease (heart disease, cancer, stroke, or emphysema) on baseline questionnaires were excluded. Among 9,564 class III obesity participants, mortality rates were 856.0 in men and 663.0 in women during the study period (1976-2009). Among 304,011 normal-weight participants, rates were 346.7 and 280.5 in men and women, respectively. Deaths from heart disease contributed largely to the excess rates in the class III obesity group (rate differences?=?238.9 and 132.8 in men and women, respectively), followed by deaths from cancer (rate differences?=?36.7 and 62.3 in men and women, respectively) and diabetes (rate differences?=?51.2 and 29.2 in men and women, respectively). Within the class III obesity range, multivariable-adjusted hazard ratios for total deaths and deaths due to heart disease, cancer, diabetes, nephritis/nephrotic syndrome/nephrosis, chronic lower respiratory disease, and influenza/pneumonia increased with increasing BMI. Compared with normal-weight BMI, a BMI of 40-44.9, 45-49.9, 50-54.9, and 55-59.9 kg/m2 was associated with an estimated 6.5 (95% CI: 5.7-7.3), 8.9 (95% CI: 7.4-10.4), 9.8 (95% CI: 7.4-12.2), and 13.7 (95% CI: 10.5-16.9) y of life lost. A limitation was that BMI was mainly ascertained by self-report.
Class III obesity is associated with substantially elevated rates of total mortality, with most of the excess deaths due to heart disease, cancer, and diabetes, and major reductions in life expectancy compared with normal weight. Please see later in the article for the Editors' Summary.
Notes
Cites: Healthy People 2000 Stat Notes. 1995 Mar;(6):1-1011762384
Cites: Lancet. 2009 Mar 28;373(9669):1083-9619299006
Cites: Cancer. 2002 May 1;94(9):2490-50112015775
Cites: Obes Rev. 2001 Aug;2(3):141-712120099
Cites: Public Health Nutr. 2002 Aug;5(4):561-512186665
Cites: Cancer Causes Control. 2002 Sep;13(7):625-3512296510
Cites: Natl Vital Stat Rep. 2002 Sep 16;50(15):1-11912382630
Cites: IARC Sci Publ. 2002;156:69-7012484128
Cites: Am J Epidemiol. 2004 Jan 1;159(1):83-9314693663
Cites: Obes Surg. 2004 May;14(5):589-60015186624
Cites: Cancer Epidemiol Biomarkers Prev. 2004 Jul;13(7):1121-715247122
Cites: J Chronic Dis. 1982;35(6):437-437042727
Cites: Cancer. 1989 Aug 1;64(3):570-812743251
Cites: JAMA. 1993 Jan 27;269(4):483-78419667
Cites: Cancer Causes Control. 1994 Nov;5(6):491-5007827235
Cites: J Natl Cancer Inst. 1995 Feb 1;87(3):190-77707406
Cites: Environ Health Perspect. 1996 Apr;104(4):362-98732939
Cites: Cancer Epidemiol Biomarkers Prev. 1997 Nov;6(11):907-169367064
Cites: N Engl J Med. 2004 Dec 23;351(26):2694-70315616204
Cites: Int J Obes (Lond). 2005 Mar;29(3):334-915685247
Cites: Int J Obes (Lond). 2006 May;30(5):822-916404410
Cites: Psychol Methods. 2006 Jun;11(2):193-20616784338
Cites: JAMA. 2006 Jul 5;296(1):79-8616820550
Cites: JAMA. 2006 Sep 20;296(11):1371-616985229
Cites: Obesity (Silver Spring). 2007 Jan;15(1):188-9617228047
Cites: Curr Diabetes Rev. 2006 Nov;2(4):367-7318220642
Cites: Health Rep. 2008 Jun;19(2):77-8418642521
Cites: N Engl J Med. 2008 Nov 13;359(20):2105-2019005195
Cites: J Intern Med. 2008 Nov;264(5):442-5118513340
Cites: Arch Intern Med. 2010 Jan 25;170(2):146-5420101009
Cites: South Med J. 2010 Apr;103(4):323-3020224489
Cites: Eur J Endocrinol. 2010 Nov;163(5):735-4520798226
Cites: JAMA. 2010 Oct 27;304(16):1795-80220935337
Cites: N Engl J Med. 2010 Dec 2;363(23):2211-921121834
Cites: Am J Epidemiol. 2010 Dec 15;172(12):1442-5420952596
Cites: Circulation. 2011 Apr 19;123(15):1683-70121403092
Cites: Diabetes Care. 2011 Oct;34(10):2152-721836103
Cites: Am J Forensic Med Pathol. 2011 Dec;32(4):372-721490499
Cites: JAMA. 2012 Feb 1;307(5):491-722253363
Cites: PLoS One. 2012;7(7):e3947122848355
Cites: Expert Rev Cardiovasc Ther. 2012 Jul;10(7):933-922908926
Cites: Med Clin North Am. 2013 Jan;97(1):59-7423290730
Cites: Prev Chronic Dis. 2013;10:E7723680506
Cites: Acta Diabetol. 2013 Jun;50(3):443-923447004
Cites: Int J Obes (Lond). 2013 Jun;37(6):889-9122986681
Cites: Mayo Clin Proc. 2014 Mar;89(3):335-4524582192
Cites: BMC Public Health. 2013;13:29023547911
Cites: Ann Epidemiol. 2000 Feb;10(2):125-3410691066
Cites: J Womens Health Gend Based Med. 2000 Jan-Feb;9(1):19-2710718501
Cites: Am J Epidemiol. 2000 Aug 1;152(3):264-7110933273
Cites: Control Clin Trials. 2000 Dec;21(6 Suppl):349S-355S11189687
Cites: JAMA. 2001 Sep 26;286(12):1494-711572743
Cites: Am J Epidemiol. 2001 Dec 15;154(12):1119-2511744517
PubMed ID
25003901 View in PubMed
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Association of Genetic and Environmental Factors With Autism in a 5-Country Cohort.

https://arctichealth.org/en/permalink/ahliterature310272
Source
JAMA Psychiatry. 2019 10 01; 76(10):1035-1043
Publication Type
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Date
10-01-2019
Author
Dan Bai
Benjamin Hon Kei Yip
Gayle C Windham
Andre Sourander
Richard Francis
Rinat Yoffe
Emma Glasson
Behrang Mahjani
Auli Suominen
Helen Leonard
Mika Gissler
Joseph D Buxbaum
Kingsley Wong
Diana Schendel
Arad Kodesh
Michaeline Breshnahan
Stephen Z Levine
Erik T Parner
Stefan N Hansen
Christina Hultman
Abraham Reichenberg
Sven Sandin
Author Affiliation
Jockey Club School of Public Health and Primary Care, The Chinese University of Hong Kong, Hong Kong SAR.
Source
JAMA Psychiatry. 2019 10 01; 76(10):1035-1043
Date
10-01-2019
Language
English
Publication Type
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Keywords
Adolescent
Autism Spectrum Disorder - epidemiology - etiology - genetics
Autistic Disorder - epidemiology - etiology
Child
Cohort Studies
Denmark - epidemiology
Environment
Family
Female
Finland - epidemiology
Genetic Association Studies - methods - standards
Genetic Predisposition to Disease - epidemiology - genetics
Humans
Inheritance Patterns - genetics
Israel - epidemiology
Male
Maternal Inheritance - genetics
Sensitivity and specificity
Sweden - epidemiology
Western Australia - epidemiology
Abstract
The origins and development of autism spectrum disorder (ASD) remain unresolved. No individual-level study has provided estimates of additive genetic, maternal, and environmental effects in ASD across several countries.
To estimate the additive genetic, maternal, and environmental effects in ASD.
Population-based, multinational cohort study including full birth cohorts of children from Denmark, Finland, Sweden, Israel, and Western Australia born between January 1, 1998, and December 31, 2011, and followed up to age 16 years. Data were analyzed from September 23, 2016 through February 4, 2018.
Across 5 countries, models were fitted to estimate variance components describing the total variance in risk for ASD occurrence owing to additive genetics, maternal, and shared and nonshared environmental effects.
The analytic sample included 2?001?631 individuals, of whom 1?027?546 (51.3%) were male. Among the entire sample, 22?156 were diagnosed with ASD. The median (95% CI) ASD heritability was 80.8% (73.2%-85.5%) for country-specific point estimates, ranging from 50.9% (25.1%-75.6%) (Finland) to 86.8% (69.8%-100.0%) (Israel). For the Nordic countries combined, heritability estimates ranged from 81.2% (73.9%-85.3%) to 82.7% (79.1%-86.0%). Maternal effect was estimated to range from 0.4% to 1.6%. Estimates of genetic, maternal, and environmental effects for autistic disorder were similar with ASD.
Based on population data from 5 countries, the heritability of ASD was estimated to be approximately 80%, indicating that the variation in ASD occurrence in the population is mostly owing to inherited genetic influences, with no support for contribution from maternal effects. The results suggest possible modest differences in the sources of ASD risk between countries.
Notes
CommentIn: JAMA Psychiatry. 2019 Oct 1;76(10):1005-1006 PMID 31314055
PubMed ID
31314057 View in PubMed
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