Imperial College London

Professor Alina Rodriguez, CPsychol

Faculty of MedicineSchool of Public Health

Visiting Professor
 
 
 
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Contact

 

+44 (0)20 7594 0941a.rodriguez

 
 
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Location

 

168Medical SchoolSt Mary's Campus

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Summary

 

Publications

Publication Type
Year
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95 results found

Hinney A, Kesselmeier M, Jall S, Volckmar AL, Föcker M, Antel J, GCAN, WTCCC3, Heid IM, Winkler TW, GIANT, Grant SF EGG, Guo Y, Bergen AW, Kaye W, Berrettini W, Hakonarson H, Price Foundation Collaborative Group, Childrens Hospital of PhiladelphiaPrice Foundation, Herpertz-Dahlmann B, de Zwaan M, Herzog W, Ehrlich S, Zipfel S, Egberts KM, Adan R, Brandys M, van Elburg A, Boraska Perica V, Franklin CS, Tschöp MH, Zeggini E, Bulik CM, Collier D, Scherag A, Müller TD, Hebebrand Jet al., 2017, Evidence for three genetic loci involved in both anorexia nervosa risk and variation of body mass index., Mol Psychiatry, Vol: 22, Pages: 192-201

The maintenance of normal body weight is disrupted in patients with anorexia nervosa (AN) for prolonged periods of time. Prior to the onset of AN, premorbid body mass index (BMI) spans the entire range from underweight to obese. After recovery, patients have reduced rates of overweight and obesity. As such, loci involved in body weight regulation may also be relevant for AN and vice versa. Our primary analysis comprised a cross-trait analysis of the 1000 single-nucleotide polymorphisms (SNPs) with the lowest P-values in a genome-wide association meta-analysis (GWAMA) of AN (GCAN) for evidence of association in the largest published GWAMA for BMI (GIANT). Subsequently we performed sex-stratified analyses for these 1000 SNPs. Functional ex vivo studies on four genes ensued. Lastly, a look-up of GWAMA-derived BMI-related loci was performed in the AN GWAMA. We detected significant associations (P-values <5 × 10(-5), Bonferroni-corrected P<0.05) for nine SNP alleles at three independent loci. Interestingly, all AN susceptibility alleles were consistently associated with increased BMI. None of the genes (chr. 10: CTBP2, chr. 19: CCNE1, chr. 2: CARF and NBEAL1; the latter is a region with high linkage disequilibrium) nearest to these SNPs has previously been associated with AN or obesity. Sex-stratified analyses revealed that the strongest BMI signal originated predominantly from females (chr. 10 rs1561589; Poverall: 2.47 × 10(-06)/Pfemales: 3.45 × 10(-07)/Pmales: 0.043). Functional ex vivo studies in mice revealed reduced hypothalamic expression of Ctbp2 and Nbeal1 after fasting. Hypothalamic expression of Ctbp2 was increased in diet-induced obese (DIO) mice as compared with age-matched lean controls. We observed no evidence for associations for the look-up of BMI-related loci in the AN GWAMA. A cross-trait analysis of AN and BMI loci revealed variants at three chromosomal loci with potential joint impact. The chromosome 10 locus is particularly pr

Journal article

Forouzanfar MH, Afshin A, Alexander LT, Anderson HR, Bhutta ZA, Biryukov S, Brauer M, Burnett R, Cercy K, Charlson FJ, Cohen AJ, Dandona L, Estep K, Ferrari AJ, Frostad JJ, Fullman N, Gething PW, Godwin WW, Griswold M, Kinfu Y, Kyu HH, Larson HJ, Liang X, Lim SS, Liu PY, Lopez AD, Lozano R, Marczak L, Mensah GA, Mokdad AH, Moradi-Lakeh M, Naghavi M, Neal B, Reitsma MB, Roth GA, Salomon JA, Sur PJ, Vos T, Wagner JA, Wang H, Zhao Y, Zhou M, Aasvang GM, Abajobir AA, Abate KH, Abbafati C, Abbas KM, Abd-Allah F, Abdulle AM, Abera SF, Abraham B, Abu-Raddad LJ, Abyu GY, Adebiyi AO, Adedeji IA, Ademi Z, Adou AK, Adsuar JC, Agardh EE, Agarwal A, Agrawal A, Kiadaliri AA, Ajala ON, Akinyemiju TF, Al-Aly Z, Alam K, Alam NKM, Aldhahri SF, Aldridge RW, Alemu ZA, Ali R, Alkerwi A, Alla F, Allebeck P, Alsharif U, Altirkawi KA, Martin EA, Alvis-Guzman N, Amare AT, Amberbir A, Amegah AK, Amini H, Ammar W, Amrock SM, Andersen HH, Anderson BO, Antonio CAT, Anwari P, Ärnlöv J, Artaman A, Asayesh H, Asghar RJ, Assadi R, Atique S, Avokpaho EFGA, Awasthi A, Quintanilla BPA, Azzopardi P, Bacha U, Badawi A, Bahit MC, Balakrishnan K, Barac A, Barber RM, Barker-Collo SL, Bärnighausen T, Barquera S, Barregard L, Barrero LH, Basu S, Batis C, Bazargan-Hejazi S, Beardsley J, Bedi N, Beghi E, Bell ML, Bello AK, Bennett DA, Bensenor IM, Berhane A, Bernabé E, Betsu BD, Beyene AS, Bhala N, Bhansali A, Bhatt S, Biadgilign S, Bikbov B, Bisanzio D, Bjertness E, Blore JD, Borschmann R, Boufous S, Bourne RRA, Brainin M, Brazinova A, Breitborde NJK, Brenner H, Broday DM, Brugha TS, Brunekreef B, Butt ZA, Cahill LE, Calabria B, Campos-Nonato IR, Cárdenas R, Carpenter DO, Casey DC, Castañeda-Orjuela CA, Rivas JC, Castro RE, Catalá-López F, Chang J, Chiang PP, Chibalabala M, Chimed-Ochir O, Chisumpa VH, Chitheer AA, Choi JJ, Christensen H, Christopher DJ, Ciobanu LG, Coates MM, Colquhoun SM, Cooper LT, Cooperrider K, Cornaby L, Cortinovis M, Crump JA, Cuevas-Nasu L, Damasceno A, Dandona R, Darby SC, Dargan PIet al., 2016, Global, regional, and national comparative risk assessment of 79 behavioural, environmental and occupational, and metabolic risks or clusters of risks, 1990-2015: a systematic analysis for the Global Burden of Disease Study 2015, The Lancet, Vol: 388, Pages: 1659-1724, ISSN: 0140-6736

SummaryBackground The Global Burden of Diseases, Injuries, and Risk Factors Study 2015 provides an up-to-date synthesis of the evidence for risk factor exposure and the attributable burden of disease. By providing national and subnational assessments spanning the past 25 years, this study can inform debates on the importance of addressing risks in context. Methods We used the comparative risk assessment framework developed for previous iterations of the Global Burden of Disease Study to estimate attributable deaths, disability-adjusted life-years (DALYs), and trends in exposure by age group, sex, year, and geography for 79 behavioural, environmental and occupational, and metabolic risks or clusters of risks from 1990 to 2015. This study included 388 risk-outcome pairs that met World Cancer Research Fund-defined criteria for convincing or probable evidence. We extracted relative risk and exposure estimates from randomised controlled trials, cohorts, pooled cohorts, household surveys, census data, satellite data, and other sources. We used statistical models to pool data, adjust for bias, and incorporate covariates. We developed a metric that allows comparisons of exposure across risk factors—the summary exposure value. Using the counterfactual scenario of theoretical minimum risk level, we estimated the portion of deaths and DALYs that could be attributed to a given risk. We decomposed trends in attributable burden into contributions from population growth, population age structure, risk exposure, and risk-deleted cause-specific DALY rates. We characterised risk exposure in relation to a Socio-demographic Index (SDI). Findings Between 1990 and 2015, global exposure to unsafe sanitation, household air pollution, childhood underweight, childhood stunting, and smoking each decreased by more than 25%. Global exposure for several occupational risks, high body-mass index (BMI), and drug use increased by more than 25% over the same period. All risks jointly evaluated

Journal article

Young SJ, Absoud M, Blackburn C, Branney P, Colley B, Farrag E, Fleisher S, Gudjonsson G, Kim K, O'Malley K, Plant M, Rodriguez A, Ozer S, Takon I, Woodhouse E, Mukherjee Ret al., 2016, Guidelines for identification ad treatment of individuals with Attention Deficit/Hyperactivity Disorder and associated Fetal Alcohol Spectrum disorders based upon expert consensus, BMC Psychiatry, Vol: 16, ISSN: 1471-244X

Background: The association of attention deficit/hyperactivity disorder (ADHD) and fetal alcoholspectrum disorders (FASD) results in a complex constellation of symptoms that complicates thesuccessful diagnosis and treatment of the affected individual. Current literature lacks formal guidelines,randomized control trials, and evidence-based treatment plans for individuals with ADHD and associatedFASD. Therefore, a meeting of professional experts was organized with the aim of producing a 3consensus on identification and treatment guidelines that will aid clinicians in caring for this uniquepatient population.Methods: Experts from multiple disciplines in the fields of ADHD and FASD convened in London, UnitedKingdom, for a meeting hosted by the United Kingdom ADHD Partnership (UKAP; www.UKADHD.com) inJune 2015. The meeting provided the opportunity to address the complexities of ADHD and FASD fromdifferent perspectives and included presentations, discussions, and group work. The attendees workedtowards producing a consensus for a unified approach to ADHD and associated FASD.Results: The authors successfully came to consensus and produced recommended guidelines withspecific regards to identification and assessment, interventions and treatments, and multiagencyliaisons and care management, highlighting that a lifespan approach to treatment needs to be adoptedby all involved. Included in the guidelines are: 1) unique ‘red flags’, which when identified in the ADHDpopulation can lead to an accurate associated FASD diagnosis, 2) a treatment decision tree, and 3)recommendations for multiagency care management.Conclusions: While clinically useful guidelines were achieved, more research is still needed to contributeto the knowledge base about the diagnosis, treatment, and management of those with ADHD andassociated FASD.

Journal article

GBD 2015 Collaborators, Piel FBJ, 2016, Measuring the health-related Sustainable Development Goals in 188 countries: a baseline analysis from the Global Burden of Disease Study 2015, The Lancet, Vol: 388, Pages: 1813-1850, ISSN: 0140-6736

BackgroundIn September, 2015, the UN General Assembly established the Sustainable Development Goals (SDGs). The SDGs specify 17 universal goals, 169 targets, and 230 indicators leading up to 2030. We provide an analysis of 33 health-related SDG indicators based on the Global Burden of Diseases, Injuries, and Risk Factors Study 2015 (GBD 2015).MethodsWe applied statistical methods to systematically compiled data to estimate the performance of 33 health-related SDG indicators for 188 countries from 1990 to 2015. We rescaled each indicator on a scale from 0 (worst observed value between 1990 and 2015) to 100 (best observed). Indices representing all 33 health-related SDG indicators (health-related SDG index), health-related SDG indicators included in the Millennium Development Goals (MDG index), and health-related indicators not included in the MDGs (non-MDG index) were computed as the geometric mean of the rescaled indicators by SDG target. We used spline regressions to examine the relations between the Socio-demographic Index (SDI, a summary measure based on average income per person, educational attainment, and total fertility rate) and each of the health-related SDG indicators and indices.FindingsIn 2015, the median health-related SDG index was 59·3 (95% uncertainty interval 56·8–61·8) and varied widely by country, ranging from 85·5 (84·2–86·5) in Iceland to 20·4 (15·4–24·9) in Central African Republic. SDI was a good predictor of the health-related SDG index (r2=0·88) and the MDG index (r2=0·92), whereas the non-MDG index had a weaker relation with SDI (r2=0·79). Between 2000 and 2015, the health-related SDG index improved by a median of 7·9 (IQR 5·0–10·4), and gains on the MDG index (a median change of 10·0 [6·7–13·1]) exceeded that of the non-MDG index (a median change of 5·5 [2·1–8·

Journal article

Rodriguez A, 2016, Are maternal depression symptoms related to umbilical cord cortisol and neurological integrity in the newborn?, 46th Annual Conference of the International-Society-of-Psychoneuroendocrinology - Personalized Medicine in the Neurosciences - Genetics, Imaging, and Hormones, Publisher: PERGAMON-ELSEVIER SCIENCE LTD, Pages: 37-37, ISSN: 0306-4530

Conference paper

Pappa I, St Pourcain B, Benke K, Cavadino A, Hakulinen C, Nivard MG, Nolte IM, Tiesler CMT, Bakermans-Kranenburg MJ, Davies GE, Evans DM, Geoffroy M-C, Grallert H, Groen-Blokhuis MM, Hudziak JJ, Kemp JP, Keltikangas-Jarvinen L, McMahon G, Mileva-Seitz VR, Motazedi E, Power C, Raitakari OT, Ring SM, Rivadeneira F, Rodriguez A, Scheet PA, Seppala I, Snieder H, Standl M, Thiering E, Timpson NJ, Veenstra R, Velders FP, Whitehouse AJO, Smith GD, Heinrich J, Hypponen E, Lehtimaki T, Middeldorp CM, Oldehinkel AJ, Pennell CE, Boomsma DI, Tiemeier Het al., 2016, A Genome-Wide Approach to Children's Aggressive Behavior: <i>The EAGLE consortium</i>, AMERICAN JOURNAL OF MEDICAL GENETICS PART B-NEUROPSYCHIATRIC GENETICS, Vol: 171, Pages: 562-572, ISSN: 1552-4841

Journal article

Alderete E, Bejarano I, Rodriguez A, 2016, Beverage intake and obesity in early childhood: evidence form primary health care clients in Northwest Argentina, JOURNAL OF DEVELOPMENTAL ORIGINS OF HEALTH AND DISEASE, Vol: 7, Pages: 244-252, ISSN: 2040-1744

Journal article

Kyu HH, Pinho C, Wagner JA, Brown JC, Bertozzi-Villa A, Charlson FJ, Coffeng LE, Dandona L, Erskine HE, Ferrari AJ, Fitzmaurice C, Fleming TD, Forouzanfar MH, Graetz N, Guinovart C, Haagsma J, Higashi H, Kassebaum NJ, Larson HJ, Lim SS, Mokdad AH, Moradi-Lakeh M, Odell SV, Roth GA, Serina PT, Stanaway JD, Misganaw A, Whiteford HA, Wolock TM, Hanson SW, Abd-Allah F, Abera SF, Abu-Raddad LJ, AlBuhairan FS, Amare AT, Antonio CAT, Artaman A, Barker-Collo SL, Barrero LH, Benjet C, Bensenor IM, Bhutta ZA, Bikbov B, Brazinova A, Campos-Nonato I, Castaneda-Orjuela CA, Catala-Lopez F, Chowdhury R, Cooper C, Crump JA, Dandona R, Degenhardt L, Dellavalle RP, Dharmaratne SD, Faraon EJA, Feigin VL, Fuerst T, Geleijnse JM, Gessner BD, Gibney KB, Goto A, Gunnell D, Hankey GJ, Hay RJ, Hornberger JC, Hosgood HD, Hu G, Jacobsen KH, Jayaraman SP, Jeemon P, Jonas JB, Karch A, Kim D, Kim S, Kokubo Y, Defo BK, Bicer BK, Kumar GA, Larsson A, Leasher JL, Leung R, Li Y, Lipshultz SE, Lopez AD, Lotufo PA, Lunevicius R, Lyons RA, Majdan M, Malekzadeh R, Mashal T, Mason-Jones AJ, Melaku YA, Memish ZA, Mendoza W, Miller TR, Mock CN, Murray J, Nolte S, Oh I-H, Olusanya BO, Ortblad KF, Park E-K, Paternina Caicedo AJ, Patten SB, Patton GC, Pereira DM, Perico N, Piel FB, Polinder S, Popova S, Pourmalek F, Quistberg DA, Remuzzi G, Rodriguez A, Rojas-Rueda D, Rothenbacher D, Rothstein DH, Sanabria J, Santos IS, Schwebel DC, Sepanlou SG, Shaheen A, Shiri R, Shiue I, Skirbekk V, Sliwa K, Sreeramareddy CT, Stein DJ, Steiner TJ, Stovner LJ, Sykes BL, Tabb KM, Terkawi AS, Thomson AJ, Thorne-Lyman AL, Towbin JA, Ukwaja KN, Vasankari T, Venketasubramanian N, Vlassov VV, Vollset SE, Weiderpass E, Weintraub RG, Werdecker A, Wilkinson JD, Woldeyohannes SM, Wolfe CDA, Yano Y, Yip P, Yonemoto N, Yoon S-J, Younis MZ, Yu C, Zaki MES, Naghavi M, Murray CJL, Vos Tet al., 2016, Global and National Burden of Diseases and Injuries Among Children and Adolescents Between 1990 and 2013 Findings From the Global Burden of Disease 2013 Study, JAMA PEDIATRICS, Vol: 170, Pages: 267-287, ISSN: 2168-6203

Journal article

Forouzanfar MH, Alexander L, Anderson HR, Bachman VF, Biryukov S, Brauer M, Burnett R, Casey D, Coates MM, Cohen A, Delwiche K, Estep K, Frostad JJ, Astha KC, Kyu HH, Moradi-Lakeh M, Ng M, Slepak EL, Thomas BA, Wagner J, Aasvang GM, Abbafati C, Ozgoren AA, Abd-Allah F, Abera SF, Aboyans V, Abraham B, Abraham JP, Abubakar I, Abu-Rmeileh NME, Aburto TC, Achoki T, Adelekan A, Adofo K, Adou AK, Adsuar JC, Afshin A, Agardh EE, Al Khabouri MJ, Al Lami FH, Alam SS, Alasfoor D, Albittar MI, Alegretti MA, Aleman AV, Alemu ZA, Alfonso-Cristancho R, Alhabib S, Ali R, Ali MK, Alla F, Allebeck P, Allen PJ, Alsharif U, Alvarez E, Alvis-Guzman N, Amankwaa AA, Amare AT, Ameh EA, Ameli O, Amini H, Ammar W, Anderson BO, Antonio CAT, Anwari P, Cunningham SA, Arnlov J, Arsenijevic VSA, Artaman A, Asghar RJ, Assadi R, Atkins LS, Atkinson C, Avila MA, Awuah B, Badawi A, Bahit MC, Bakfalouni T, Balakrishnan K, Balalla S, Balu RK, Banerjee A, Barber RM, Barker-Collo SL, Barquera S, Barregard L, Barrero LH, Barrientos-Gutierrez T, Basto-Abreu AC, Basu A, Basu S, Basulaiman MO, Ruvalcaba CB, Beardsley J, Bedi N, Bekele T, Bell ML, Benjet C, Bennett DA, Benzian H, Bernabe E, Beyene TJ, Bhala N, Bhalla A, Bhutta ZQA, Bikbov B, Bin Abdulhak AA, Blore JD, Blyth FM, Bohensky MA, Basara BB, Borges G, Bornstein NM, Bose D, Boufous S, Bourne RR, Brainin M, Brazinova A, Breitborde NJ, Brenner H, Briggs ADM, Broday DM, Brooks PM, Bruce NG, Brugha TS, Brunekreef B, Buchbinder R, Bui LN, Bukhman G, Bulloch AG, Burch M, Burney PGJ, Campos-Nonato IR, Campuzano JC, Cantoral AJ, Caravanos J, Cardenas R, Cardis E, Carpenter DO, Caso V, Castaneda-Orjuela CA, Castro RE, Catala-Lopez F, Cavalleri F, Cavlin A, Chadha VK, Chang J-C, Charlson FJ, Chen H, Chen W, Chen Z, Chiang PP, Chimed-Ochir O, Chowdhury R, Christophi CA, Chuang T-W, Chugh SS, Cirillo M, Classen TKD, Colistro V, Colomar M, Colquhoun SM, Contreras AG, Cooper C, Cooperrider K, Cooper LT, Coresh J, Courville KJ, Criqui MH, Cuevas-Nasu L, Damsere-Deet al., 2015, Global, regional, and national comparative risk assessment of 79 behavioural, environmental and occupational, and metabolic risks or clusters of risks in 188 countries, 1990-2013: a systematic analysis for the Global Burden of Disease Study 2013, LANCET, Vol: 386, Pages: 2287-2323, ISSN: 0140-6736

Journal article

Rodriguez A, Wang Y, Khan AA, Gissler M, Cartwright R, Jarvelin M-Ret al., 2015, Exposure to antenatal corticosteroid therapy is associated with reduced size at birth: Evidence from Finnish Medical Birth Register of 278,508 births, 45th Annual Meeting of the International-Society-of-Psychoneuroendocrinology (ISPNE) on Stress and the Brain - From Fertility to Senility, Publisher: PERGAMON-ELSEVIER SCIENCE LTD, Pages: 37-37, ISSN: 0306-4530

Conference paper

Newton JN, Briggs ADM, Murray CJL, Dicker D, Foreman KJ, Wang H, Naghavi M, Forouzanfar MH, Ohno SL, Barber RM, Vos T, Stanaway JRD, Schmidt JC, Hughes AJ, Fay DFJ, Ecob R, Gresser C, McKee M, Rutter H, Abubakar I, Ali R, Anderson HR, Banerjee A, Bennett DA, Bernabe E, Bhui KS, Biryukov SM, Bourne RR, Brayne CEG, Bruce NG, Brugha TS, Burch M, Capewell S, Casey D, Chowdhury R, Coates MM, Cooper C, Critchley JA, Dargan PI, Dherani MK, Elliott P, Ezzati M, Fenton KA, Fraser MS, Fuerst T, Greaves F, Green MA, Gunnell DJ, Hannigan BM, Hay RJ, Hay SI, Hemingway H, Larson HJ, Looker KJ, Lunevicius R, Lyons RA, Marcenes W, Mason-Jones AJ, Matthews FE, Moller H, Murdoch ME, Newton CR, Pearce N, Piel FB, Pope D, Rahimi K, Rodriguez A, Scarborough P, Schumacher AE, Shiue I, Smeeth L, Tedstone A, Valabhji J, Williams HC, Wolfe CDA, Woolf AD, Davis ACJet al., 2015, Changes in health in England, with analysis by English regions and areas of deprivation, 1990-2013: a systematic analysis for the Global Burden of Disease Study 2013, Lancet, Vol: 386, Pages: 2257-2274, ISSN: 1474-547X

Journal article

Vos T, Barber RM, Bell B, Bertozzi-Villa A, Biryukov S, Bolliger I, Charlson F, Davis A, Degenhardt L, Dicker D, Duan L, Erskine H, Feigin VL, Ferrari AJ, Fitzmaurice C, Fleming T, Graetz N, Guinovart C, Haagsma J, Hansen GM, Hanson SW, Heuton KR, Higashi H, Kassebaum N, Kyu H, Laurie E, Liang X, Lofgren K, Lozano R, MacIntyre MF, Moradi-Lakeh M, Naghavi M, Nguyen G, Odell S, Ortblad K, Roberts DA, Roth GA, Sandar L, Serina PT, Stanaway JD, Steiner C, Thomas B, Vollset SE, Whiteford H, Wolock TM, Ye P, Zhou M, Avila MA, Aasvang GM, Abbafati C, Ozgoren AA, Abd-Allah F, Aziz MIA, Abera SF, Aboyans V, Abraham JP, Abraham B, Abubakar I, Abu-Raddad LJ, Abu-Rmeileh NME, Aburto TC, Achoki T, Ackerman IN, Adelekan A, Ademi Z, Adou AK, Adsuar JC, Arnlov J, Agardh EE, Al Khabouri MJ, Alam SS, Alasfoor D, Albittar MI, Alegretti MA, Aleman AV, Alemu ZA, Alfonso-Cristancho R, Alhabib S, Ali R, Alla F, Allebeck P, Allen PJ, AlMazroa MA, Alsharif U, Alvarez E, Alvis-Guzman N, Ameli O, Amini H, Ammar W, Anderson BO, Anderson HR, Antonio CAT, Anwari P, Apfel H, Arsenijevic VSA, Artaman A, Asghar RJ, Assadi R, Atkins LS, Atkinson C, Badawi A, Bahit MC, Bakfalouni T, Balakrishnan K, Balalla S, Banerjee A, Barker-Collo SL, Barquera S, Barregard L, Barrero LH, Basu S, Basu A, Baxter A, Beardsley J, Bedi N, Beghi E, Bekele T, Bell ML, Benjet C, Bennett DA, Bensenor IM, Benzian H, Bernabe E, Beyene TJ, Bhala N, Bhalla A, Bhutta ZQ, Bienhoff K, Bikbov B, Bin Abdulhak A, Blore JD, Blyth FM, Bohensky MA, Basara BB, Borges G, Bornstein NM, Bose D, Boufous S, Bourne RR, Boyers LN, Brainin M, Brauer M, Brayne CEG, Brazinova A, Breitborde NJK, Brenner H, Briggs ADM, Brooks PM, Brown J, Brugha TS, Buchbinder R, Buckle GC, Bukhman G, Bulloch AG, Burch M, Burnett R, Cardenas R, Cabral NL, Nonato IRC, Campuzano JC, Carapetis JR, Carpenter DO, Caso V, Castaneda-Orjuela CA, Catala-Lopez F, Chadha VK, Chang J-C, Chen H, Chen W, Chiang PP, Chimed-Ochir O, Chowdhury R, Christensen H, Christophi CA, Chughet al., 2015, Global, regional, and national incidence, prevalence, and years lived with disability for 301 acute and chronic diseases and injuries in 188 countries, 1990-2013: a systematic analysis for the Global Burden of Disease Study 2013, The Lancet, Vol: 386, Pages: 743-800, ISSN: 0140-6736

BackgroundUp-to-date evidence about levels and trends in disease and injury incidence, prevalence, and years lived with disability (YLDs) is an essential input into global, regional, and national health policies. In the Global Burden of Disease Study 2013 (GBD 2013), we estimated these quantities for acute and chronic diseases and injuries for 188 countries between 1990 and 2013.MethodsEstimates were calculated for disease and injury incidence, prevalence, and YLDs using GBD 2010 methods with some important refinements. Results for incidence of acute disorders and prevalence of chronic disorders are new additions to the analysis. Key improvements include expansion to the cause and sequelae list, updated systematic reviews, use of detailed injury codes, improvements to the Bayesian meta-regression method (DisMod-MR), and use of severity splits for various causes. An index of data representativeness, showing data availability, was calculated for each cause and impairment during three periods globally and at the country level for 2013. In total, 35 620 distinct sources of data were used and documented to calculated estimates for 301 diseases and injuries and 2337 sequelae. The comorbidity simulation provides estimates for the number of sequelae, concurrently, by individuals by country, year, age, and sex. Disability weights were updated with the addition of new population-based survey data from four countries.FindingsDisease and injury were highly prevalent; only a small fraction of individuals had no sequelae. Comorbidity rose substantially with age and in absolute terms from 1990 to 2013. Incidence of acute sequelae were predominantly infectious diseases and short-term injuries, with over 2 billion cases of upper respiratory infections and diarrhoeal disease episodes in 2013, with the notable exception of tooth pain due to permanent caries with more than 200 million incident cases in 2013. Conversely, leading chronic sequelae were largely attributable to non-communic

Journal article

Forrester GS, Rodriguez A, 2015, Slip of the tongue: Implications for evolution and language development, COGNITION, Vol: 141, Pages: 103-111, ISSN: 0010-0277

Journal article

GBD 2013 Mortality and Causes of Death Collaborators, 2015, Global, regional, and national age–sex specific all-cause and cause-specific mortality for 240 causes of death, 1990–2013: a systematic analysis for the Global Burden of Disease Study 2013, The Lancet, Vol: 385, Pages: 117-171, ISSN: 0140-6736

SummaryBackground Up-to-date evidence on levels and trends for age-sex-specific all-cause and cause-specific mortality is essential for the formation of global, regional, and national health policies. In the Global Burden of Disease Study 2013 (GBD 2013) we estimated yearly deaths for 188 countries between 1990, and 2013. We used the results to assess whether there is epidemiological convergence across countries. Methods We estimated age-sex-specific all-cause mortality using the GBD 2010 methods with some refinements to improve accuracy applied to an updated database of vital registration, survey, and census data. We generally estimated cause of death as in the GBD 2010. Key improvements included the addition of more recent vital registration data for 72 countries, an updated verbal autopsy literature review, two new and detailed data systems for China, and more detail for Mexico, UK, Turkey, and Russia. We improved statistical models for garbage code redistribution. We used six different modelling strategies across the 240 causes; cause of death ensemble modelling (CODEm) was the dominant strategy for causes with sufficient information. Trends for Alzheimer's disease and other dementias were informed by meta-regression of prevalence studies. For pathogen-specific causes of diarrhoea and lower respiratory infections we used a counterfactual approach. We computed two measures of convergence (inequality) across countries: the average relative difference across all pairs of countries (Gini coefficient) and the average absolute difference across countries. To summarise broad findings, we used multiple decrement life-tables to decompose probabilities of death from birth to exact age 15 years, from exact age 15 years to exact age 50 years, and from exact age 50 years to exact age 75 years, and life expectancy at birth into major causes. For all quantities reported, we computed 95% uncertainty intervals (UIs). We constrained cause-specific fractions within each age-sex-co

Journal article

Solmi F, Sonneville KR, Easter A, Horton NJ, Crosby RD, Treasure J, Rodriguez A, Jarvelin M-R, Field AE, Micali Net al., 2015, Prevalence of purging at age 16 and associations with negative outcomes among girls in three community-based cohorts, JOURNAL OF CHILD PSYCHOLOGY AND PSYCHIATRY, Vol: 56, Pages: 87-96, ISSN: 0021-9630

Journal article

van der Valk RJP, Kreiner-Moller E, Kooijman MN, Guxens M, Stergiakouli E, Saaf A, Bradfield JP, Geller F, Hayes MG, Cousminer DL, Koerner A, Thiering E, Curtin JA, Myhre R, Huikari V, Joro R, Kerkhof M, Warrington NM, Pitkanen N, Ntalla I, Horikoshi M, Veijola R, Freathy RM, Teo Y-Y, Barton SJ, Evans DM, Kemp JP, St Pourcain B, Ring SM, Smith GD, Bergstrom A, Kull I, Hakonarson H, Mentch FD, Bisgaard H, Chawes B, Stokholm J, Waage J, Eriksen P, Sevelsted A, Melbye M, van Duijn CM, Medina-Gomez C, Hofman A, de Jongste JC, Taal HR, Uitterlinden AG, Armstrong LL, Eriksson J, Palotie A, Bustamante M, Estivill X, Gonzalez JR, Llop S, Kiess W, Mahajan A, Flexeder C, Tiesler CMT, Murray CS, Simpson A, Magnus P, Sengpiel V, Hartikainen A-L, Keinanen-Kiukaanniemi S, Lewin A, Alves ADSC, Blakemore AI, Buxton JL, Kaakinen M, Rodriguez A, Sebert S, Vaarasmaki M, Lakka T, Lindi V, Gehring U, Postma DS, Ang W, Newnham JP, Lyytikainen L-P, Pahkala K, Raitakari OT, Panoutsopoulou K, Zeggini E, Boomsma DI, Groen-Blokhuis M, Ilonen J, Franke L, Hirschhorn JN, Pers TH, Liang L, Huang J, Hocher B, Knip M, Saw S-M, Holloway JW, Melen E, Grant SFA, Feenstra B, Lowe WL, Widen E, Sergeyev E, Grallert H, Custovic A, Jacobsson B, Jarvelin M-R, Atalay M, Koppelman GH, Pennell CE, Niinikoski H, Dedoussis GV, Mccarthy MI, Frayling TM, Sunyer J, Timpson NJ, Rivadeneira F, Bonnelykke K, Jaddoe VWVet al., 2014, A novel common variant in DCST2 is associated with length in early life and height in adulthood, Human Molecular Genetics, Vol: 24, Pages: 1155-1168, ISSN: 1460-2083

Common genetic variants have been identified for adult height, but not much is known about the genetics of skeletal growth in early life. To identify common genetic variants that influence fetal skeletal growth, we meta-analyzed 22 genome-wide association studies (Stage 1; N = 28 459). We identified seven independent top single nucleotide polymorphisms (SNPs) (P < 1 × 10−6) for birth length, of which three were novel and four were in or near loci known to be associated with adult height (LCORL, PTCH1, GPR126 and HMGA2). The three novel SNPs were followed-up in nine replication studies (Stage 2; N = 11 995), with rs905938 in DC-STAMP domain containing 2 (DCST2) genome-wide significantly associated with birth length in a joint analysis (Stages 1 + 2; β = 0.046, SE = 0.008, P = 2.46 × 10−8, explained variance = 0.05%). Rs905938 was also associated with infant length (N = 28 228; P = 5.54 × 10−4) and adult height (N = 127 513; P = 1.45 × 10−5). DCST2 is a DC-STAMP-like protein family member and DC-STAMP is an osteoclast cell-fusion regulator. Polygenic scores based on 180 SNPs previously associated with human adult stature explained 0.13% of variance in birth length. The same SNPs explained 2.95% of the variance of infant length. Of the 180 known adult height loci, 11 were genome-wide significantly associated with infant length (SF3B4, LCORL, SPAG17, C6orf173, PTCH1, GDF5, ZNFX1, HHIP, ACAN, HLA locus and HMGA2). This study highlights that common variation in DCST2 influences variation in early growth and adult height.

Journal article

Pillas D, Kaakinen M, Tzoulaki I, Netuveli G, Rodriguez A, Fung E, Tammelin TH, Blane D, Millwood IY, Hardy R, Sovio U, Pouta A, Hopstock LA, Hartikainen A-L, Laitinen J, Vaara S, Khan AA, Chong R, Elliott P, Jarvelin M-Ret al., 2014, Infant locomotive development and its association with adult blood pressure, EUROPEAN JOURNAL OF PEDIATRICS, Vol: 173, Pages: 1309-1317, ISSN: 0340-6199

Journal article

St Pourcain B, Cents RAM, Whitehouse AJO, Haworth CMA, Davis OSP, O'Reilly PF, Roulstone S, Wren Y, Ang QW, Velders FP, Evans DM, Kemp JP, Warrington NM, Miller L, Timpson NJ, Ring SM, Verhulst FC, Hofman A, Rivadeneira F, Meaburn EL, Price TS, Dale PS, Pillas D, Yliherva A, Rodriguez A, Golding J, Jaddoe VWV, Jarvelin M-R, Plomin R, Pennell CE, Tiemeier H, Smith GDet al., 2014, Common variation near ROBO2 is associated with expressive vocabulary in infancy, Nature Communications, Vol: 5, ISSN: 2041-1723

Twin studies suggest that expressive vocabulary at ~24 months is modestly heritable. However, the genes influencing this early linguistic phenotype are unknown. Here we conduct a genome-wide screen and follow-up study of expressive vocabulary in toddlers of European descent from up to four studies of the EArly Genetics and Lifecourse Epidemiology consortium, analysing an early (15–18 months, ‘one-word stage’, NTotal=8,889) and a later (24–30 months, ‘two-word stage’, NTotal=10,819) phase of language acquisition. For the early phase, one single-nucleotide polymorphism (rs7642482) at 3p12.3 near ROBO2, encoding a conserved axon-binding receptor, reaches the genome-wide significance level (P=1.3 × 10−8) in the combined sample. This association links language-related common genetic variation in the general population to a potential autism susceptibility locus and a linkage region for dyslexia, speech-sound disorder and reading. The contribution of common genetic influences is, although modest, supported by genome-wide complex trait analysis (meta-GCTA h215–18-months=0.13, meta-GCTA h224–30-months=0.14) and in concordance with additional twin analysis (5,733 pairs of European descent, h224-months=0.20).

Journal article

Cousminer DL, Stergiakouli E, Berry DJ, Ang W, Groen-Blokhuis MM, Koerner A, Siitonen N, Ntalla I, Marinelli M, Perry JRB, Kettunen J, Jansen R, Surakka I, Timpson NJ, Ring S, Mcmahon G, Power C, Wang C, Kahonen M, Viikari J, Lehtimaki T, Middeldorp CM, Pol HEH, Neef M, Weise S, Pahkala K, Niinikoski H, Zeggini E, Panoutsopoulou K, Bustamante M, Penninx BWJH, Murabito J, Torrent M, Dedoussis GV, Kiess W, Boomsma DI, Pennell CE, Raitakari OT, Hyppoenen E, Smith GD, Ripatti S, McCarthy MI, Widen Eet al., 2014, Genome-wide association study of sexual maturation in males and females highlights a role for body mass and menarche loci in male puberty, HUMAN MOLECULAR GENETICS, Vol: 23, Pages: 4452-4464, ISSN: 0964-6906

Journal article

Buxton JL, Das S, Rodriguez A, Kaakinen M, Couto Alves A, Sebert S, Millwood IY, Laitinen J, OReilly PF, Jarvelin M, Blakemore AIFet al., 2014, Multiple Measures of Adiposity Are Associated with Mean Leukocyte Telomere Length in the Northern Finland Birth Cohort 1966, PLOS One, Vol: 9, ISSN: 1932-6203

Studies of leukocyte telomere length (LTL) and adiposity have produced conflicting results, and the relationship between body mass index (BMI) and telomere length throughout life remains unclear. We therefore tested association of adult LTL measured in 5,598 participants with: i) childhood growth measures (BMI and age at adiposity rebound (AR)); ii) change in BMI from childhood to adulthood and iii) adult BMI, waist-to-hip ratio (WHR), body adiposity index (BAI). Childhood BMI at AR was positively associated with LTL at 31 years in women (P = 0.041). Adult BMI and WHR in both men (P = 0.025 and P = 0.049, respectively) and women (P = 0.029 and P = 0.008, respectively), and BAI in women (P = 0.021) were inversely associated with LTL at 31 years. An increase in standardised BMI between early childhood and adulthood was associated with shorter adult LTL in women (P = 0.008). We show that LTL is inversely associated with multiple measures of adiposity in both men and women. Additionally, BMI increase in women from childhood to adulthood is associated with shorter telomeres at age 31, potentially indicating accelerated biological ageing.

Journal article

Khalife N, Kantomaa M, Glover V, Tammelin T, Laitinen J, Ebeling H, Hurtig T, Jarvelin M-R, Rodriguez Aet al., 2014, Childhood Attention-Deficit/Hyperactivity Disorder Symptoms Are Risk Factors for Obesity and Physical Inactivity in Adolescence, JOURNAL OF THE AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY, Vol: 53, Pages: 425-436, ISSN: 0890-8567

Journal article

Khalife N, Kantomaa M, Glover V, Tammelin T, Laitinen J, Ebeling H, Hurtig T, Jarvelin M-R, Rodriguez Aet al., 2014, Childhood attention-deficit/hyperactivity disorder symptoms are risk factors for obesity and physical inactivity in adolescence., J Am Acad Child Adolesc Psychiatry, Vol: 53, Pages: 425-436

OBJECTIVE: To prospectively investigate the association and directionality between attention-deficit/hyperactivity disorder (ADHD) symptoms and obesity from childhood to adolescence in the general population. We examined whether obesogenic behaviors, namely, physical inactivity and binge eating, underlie the potential ADHD symptom-obesity association. We explored whether childhood conduct disorder (CD) symptoms are related to adolescent obesity/physical inactivity. METHOD: At 7 to 8 years (n = 8,106), teachers reported ADHD and CD symptoms, and parents reported body mass index (BMI) and physically active play. At 16 years (n = 6,934), parents reported ADHD symptoms; adolescents reported physical activity (transformed to metabolic equivalent of task [MET] hours per week) and binge eating; BMI and waist-hip ratio (WHR) were measured via clinical examination. Obesity was defined using the International Obesity Task Force (IOTF) cut-offs for BMI and the 95th percentile cut-off for WHR. RESULTS: Childhood ADHD symptoms significantly predicted adolescent obesity, rather than the opposite. Inattention-hyperactivity symptoms at 8 years were associated with indices of obesity at 16 years (obese BMI: odds ratio [OR] = 1.91, 95% confidence interval [CI] = 1.10-3.33; 95th percentile WHR: OR = 1.71, 95% CI = 1.05-2.78), adjusted for gender, baseline BMI, physical activity, family structure change, and maternal education. Child CD symptoms associated with indices of adolescent obesity. Reduced physically active play in childhood predicted adolescent inattention (OR = 1.61, 95% CI = 1.16-2.24). Childhood ADHD and CD symptoms were linked with physical inactivity in adolescence (inattention-hyperactivity; OR = 1.60, 95% CI = 1.20-2.13), but not binge eating. Physical inactivity mediated the associations. CONCLUSIONS: Children with ADHD or CD symptoms are at increased risk for becoming obese and physically inactive adolescen

Journal article

Chen Q, Sjolander A, Langstrom N, Rodriguez A, Serlachius E, D'Onofrio BM, Lichtenstein P, Larsson Het al., 2014, Maternal pre-pregnancy body mass index and offspring attention deficit hyperactivity disorder: a population-based cohort study using a sibling-comparison design, INTERNATIONAL JOURNAL OF EPIDEMIOLOGY, Vol: 43, Pages: 83-90, ISSN: 0300-5771

Journal article

Khalife N, Glover V, Taanila A, Ebeling H, Jarvelin M-R, Rodriguez Aet al., 2013, Prenatal glucocorticoid treatment and later mental health in children and adolescents, PLOS One, Vol: 8, ISSN: 1932-6203

BackgroundAnimal studies demonstrate a clear link between prenatal exposure to glucocorticoids (GC) and altered offspring brain development. We aim to examine whether prenatal GC exposure programs long-term mental health in humans.MethodsUsing propensity-score-matching, children prenatally exposed to synthetic glucocorticoids (sGC), n=37, and controls, n=185, were balanced on important confounders related to sGC treatment - gestational age and pre-pregnancy BMI. We also used mixed-effects modeling to analyse the entire cohort – matching each sGC case, n=37, to all possible controls, n=6079, on gestational age and sex. We obtained data from the Northern Finland Birth Cohort 1986 at four waves – pregnancy, birth, 8 and 16 years. Data on pregnancy and birth outcomes came from medical records. Mental health was assessed at 8 years by teachers with the Rutter B2 scale, and at 16 years by parents with the Strengths and Weaknesses of ADHD symptoms and Normal behavior (SWAN) scale and adolescents by the Youth Self-Report (YSR) scale.ResultsPrenatal sGC treatment was consistently associated with adverse mental health in childhood and adolescence, as shown by both the propensity-score method and mixed-effects model. Using the propensity-score-matched subsample, linear multiple regression showed prenatal sGC was significantly linked with general psychiatric disturbance (B=8.34 [95% CI: .23-16.45]) and inattention (B= .97 [95% CI: .16-1.80]) at 8 years after control for relevant confounders. Similar findings were obtained at 16 years, but did not reach statistical significance. Mediation by birthweight/placental weight was not detected.ConclusionsThis study is the first to prospectively investigate the long-term associations between prenatal exposure to sGC treatment and mental health in children and adolescents. We report an association between prenatal exposure to sGC and child mental health, supportive of the idea that sGC has a programming effect on the fetal br

Journal article

Nordstrom T, Ebeling H, Hurtig T, Rodriguez A, Savolainen J, Moilanen I, Taanila Aet al., 2013, Comorbidity of disruptive behavioral disorders and attention-deficit hyperactivity disorder-Indicator of severity in problematic behavior?, NORDIC JOURNAL OF PSYCHIATRY, Vol: 67, Pages: 240-248, ISSN: 0803-9488

Journal article

Kantomaaa MT, Stamatakis E, Kankaanpaa A, Kaakinen M, Rodriguez A, Taanila A, Ahonen T, Jarvelin M-R, Tammelin Tet al., 2013, Physical activity and obesity mediate the association between childhood motor function and adolescents' academic achievement, PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, Vol: 110, Pages: 1917-1922, ISSN: 0027-8424

Journal article

Fernandes C, Grayton H, Poston L, Samuelsson A-M, Taylor PD, Collier DA, Rodriguez Aet al., 2012, Prenatal exposure to maternal obesity leads to hyperactivity in offspring, MOLECULAR PSYCHIATRY, Vol: 17, Pages: 1159-1160, ISSN: 1359-4184

Journal article

Patel SP, Rodriguez A, Little MP, Elliott P, Pekkanen J, Hartikainen A-L, Pouta A, Laitinen J, Harju T, Canoy D, Jaervelin M-Ret al., 2012, Associations between pre-pregnancy obesity and asthma symptoms in adolescents, Journal of Epidemiology and Community Health, Vol: 66, Pages: 809-814, ISSN: 1470-2738

Background The high prevalence of children's asthma symptoms, worldwide, is unexplained. We examined the relation between maternal pre-pregnancy weight and body mass index (BMI), and asthma symptoms in adolescents.Methods Data from 6945 adolescents born within the Northern Finland Birth Cohort 1986 were used. Prospective antenatal and birth outcome data, including maternal pre-pregnancy weight and BMI, and asthma symptoms in adolescent offspring at age 15–16 years, were employed. Logistic regression analyses were performed to examine the associations between relevant prenatal factors and asthma symptoms during adolescence.Results Current wheeze (within the past year) was reported by 10.6% of adolescents, and physician-diagnosed asthma by 6.0%. High maternal pre-pregnancy BMI was a significant predictor of wheeze in the adolescents (increase per kilogram per square metre unit; 2.7%, 95% CI 0.9 to 4.4 for ever wheeze; 3.5%, 95% CI 1.3 to 5.8 for current wheeze), and adjusting for potential confounders further increased the risk (2.8%, 95% CI 0.5 to 5.1; 4.7%, 95% CI 1.9 to 7.7, respectively). High maternal pre-pregnancy weight, in the top tertile, also significantly increased the odds of current wheeze in the adolescent by 20% (95% CI 4 to 39), and adjusting for potential confounders further increased the risk (OR=1.52, 95% CI 1.19 to 1.95). Results were similar for current asthma. Furthermore, these significant associations were observed only among adolescents without parental history of atopy but not among those with parental history of atopy.Conclusions The association demonstrated here between maternal pre-pregnancy overweight and obesity, and asthma symptoms in adolescents suggests that increase in asthma may be partly related to the rapid rise in obesity in recent years.

Journal article

Khalife N, Glover V, Hartikainen A-L, Taanila A, Ebeling H, Jarvelin M-R, Rodriguez Aet al., 2012, Placental Size Is Associated with Mental Health in Children and Adolescents, PLOS ONE, Vol: 7, ISSN: 1932-6203

Journal article

Khan AA, Rodriguez A, Sebert S, Kaakinen M, Cauchi S, Froguel P, Hartikainen A-L, Pouta A, Jarvelin M-Ret al., 2012, The Interplay of Variants Near LEKR and CCNL1 and Social Stress in Relation to Birth Size, PLOS One, Vol: 7, ISSN: 1932-6203

Background: We previously identified via a genome wide association study variants near LEKR and CCNL1 and in the ADCY5 genes lead to lower birthweight. Here, we study the impact of these variants and social stress during pregnancy, defined as social adversity and neighborhood disparity, on infant birth size. We aimed to determine whether the addition of genetic variance magnified the observed associations.Methodology/Principal Findings: We analyzed data from the Northern Finland Birth Cohort 1986 (n = 5369). Social adversity was defined by young maternal age (<20 years), low maternal education (<11 years), and/or single marital status. Neighborhood social disparity was assessed by discrepancy between neighborhoods relative to personal socio-economic status. These variables are indicative of social and socioeconomic stress, but also of biological risk. The adjusted multiple regression analysis showed smaller birth size in both infants of mothers who experienced social adversity (birthweight by −40.4 g, 95%CI −61.4, −19.5; birth length −0.14 cm, 95%CI −0.23, −0.05; head circumference −0.09 cm 95%CI −0.15, −0.02) and neighborhood disparity (birthweight −28.8 g, 95%CI −47.7, −10.0; birth length −0.12 cm, 95%CI −0.20, −0.05). The birthweight-lowering risk allele (SNP rs900400 near LEKR and CCNL1) magnified this association in an additive manner. However, likely due to sample size restriction, this association was not significant for the SNP rs9883204 in ADCY5. Birth size difference due to social stress was greater in the presence of birthweight-lowering alleles.Conclusions/Significance: Social adversity, neighborhood disparity, and genetic variants have independent associations with infant birth size in the mutually adjusted analyses. If the newborn carried a risk allele rs900400 near LEKR/CCNL1, the impact of stress on birth size was stronger. These observations give support

Journal article

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