Paul Lichtenstein

Paul Lichtenstein

Professor | Deputy head of department
Telephone: +46852487424
Visiting address: Nobels väg 12a, 17165 Solna
Postal address: C8 Medicinsk epidemiologi och biostatistik, C8 MEB Lichtenstein, 171 77 Stockholm
Part of:

About me

  • I am professor in genetic epidemiology and deputy study director for postgraduate studies at the Department of Medical Epidemiology and Biostatistics. I am also deputy head of department and member of MEB's Executive Group.

Research

  • The work in my group is primarily concerned with using genetically informative samples (twins, families) to understand genetic and environmental influences on both health and behavior. The studies are usually based on the Swedish Twin Registry (located at the Department and comprising more than 140.000 twins) and other Swedish Registries such as the Multigenerational Register (comprising all individuals born in Sweden since 1931).

    My group performs quantitative genetic studies - that is, evaluate the relative importance of genes and environments for a phenotype - and "cotwin-control"-studies, where the importance of an exposure is evaluated after controlling for genetic predisposition for the disease. The research is interdisciplinary and includes, among others, medical, genetic, epidemiological, sociological and psychological research questions.

    THE DEVELOPMENT OF HEALTH AND BEHAVIOURAL PROBLEMS IN CHILDREN
    One focus of the work in the group is to understand how genes and environments influence the development of health and behavior during childhood and adolescence. We have followed a cohort of 1.500 twin pairs longitudinally since they were 8 years old in 1994 with multiple contacts (1994, 1999, 2002, 2006, 2013) with both the parents and the twins themselves. We have studied how genetic and environmental effects contribute to the development of mental health problems over time. For example, we have found that genetic effects are more stable for ADHD (Chang, Lichtenstein et al. 2014) compared to internalizing problems (e.g., fears, anxiety) (Kendler, Gardner et al. 2008).

    THE CHILD AND ADOLESCENT TWIN STUDY IN SWEDEN (CATSS)
    In CATSS-9, we conduct a psychiatric telephone interview with parents of all 1, 400 twin pairs born in Sweden annually since 1992 in connection with their 9th birthdays. By April 2014 we have performed 13, 500 interviews with a very high response rate (≈80%), and we have collected DNA from the twins. We follow the families with questionnaires to parents and twins at age 15 and 18. The aim is to understand how genes and environment affect different diseases and behavior during childhood and also to get information about various types of exposures. We have shown that the heritability for ASD was around 80% and that ASD had a common genetic etiology with other neuropsychiatric disorders (Lichtenstein, Carlstrom et al. 2010), that extreme values of ASD (Lundström, Chang et al. 2012) and ADHD (Larsson, Anckarsäter et al. 2012) have the same genetic etiology as normal variation in the underlying traits, and an association between fetal growth on ASD suggesting that fetal growth is in the causal pathway (Losh, Esserman et al. 2011).

    CAUSES AND CONSEQUENCES OF CRIMINALITY AND PSYCHIATRIC DISORDERS
    To elucidate the mechanisms for the association between early risks and mental health problems as well as intergenerational transmissions of psychiatric problems, we use the large population based registries in Sweden, including, among others, information on all psychiatric care, criminal convictions and suicides in Sweden for all first-degree relatives (>15 million individuals) since 1932. Using different quasi-experimental methods we have shown that smoking during pregnancy is not causally related to offspring criminality (D'Onofrio, Singh et al., 2010), that there is a common genetic etiology between schizophrenia and bipolar disorder (Lichtenstein, Yip et al, 2009), and that ADHD medication protects against criminality (Lichtenstein, Halldner et al, 2012).

    THE TWIN REGISTRY
    I was head of the Swedish Twin Registry during 2006-2013. During this time contacts with all twins not previously contacted in the Registry was completed. Now the Swedish Twin Registry contains of 200 000 twins. In addition, all twins in the Registry have had the opportunity to donate DNA for research purposes (n=40, 000).

    RESEARCHERS AND ASSOCIATE PROFESSORS IN MY GROUP
    Agnieszka Butwicka
    Erik Pettersson
    Zheng Chang
    Márta Radó
    Mark Taylor

    CURRENT POST DOCS
    Lotfi Khemiri

Selected publications

  • Article: JAMA PSYCHIATRY. 2016;73(12):1268-1275
    Latvala A; Kuja-Halkola R; Ruck C; D'Onofrio BM; Jernberg T; Almqvist C; Mataix-Cols D; Larsson H; Lichtenstein P
  • Article: MOLECULAR PSYCHIATRY. 2016;21(5):717-721
    Pettersson E; Larsson H; Lichtenstein P
  • Article: PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA. 2016;113(4):1098-1103
    Reichenberg A; Cederlof M; McMillan A; Trzaskowski M; Kapara O; Fruchter E; Ginat K; Davidson M; Weiser M; Larsson H; Plomin R; Lichtenstein P
  • Article: JAMA PSYCHIATRY. 2014;71(4):432-438
    D'Onofrio BM; Rickert ME; Frans E; Kuja-Halkola R; Almqvist C; Sjolander A; Larsson H; Lichtenstein P
  • Article: JAMA PSYCHIATRY. 2014;71(3):319-325
    Chang Z; Lichtenstein P; D'Onofrio BM; Sjolander A; Larsson H
  • Article: JAMA PSYCHIATRY. 2014;71(3):326-333
    Fazel S; Wolf A; Pillas D; Lichtenstein P; Langstrom N
  • Article: LANCET. 2013;382(9905):1646-1654
    Fazel S; Wolf A; Langstrom N; Newton CR; Lichtenstein P
  • Article: JAMA PSYCHIATRY. 2013;70(11):1231-1240
    D'Onofrio BM; Class QA; Rickert ME; Larsson H; Langstrom N; Lichtenstein P
  • Article: NATURE GENETICS. 2013;45(9):984-994
    Lee SH; Ripke S; Neale BM; Faraone SV; Purcell SM; Perlis RH; Mowry BJ; Thapar A; Goddard ME; Witte JS; Absher D; Agartz I; Akil H; Amin F; Andreassen OA; Anjorin A; Anney R; Anttila V; Arking DE; Asherson P; Azevedo MH; Backlund L; Badner JA; Bailey AJ; Banaschewski T; Barchas JD; Barnes MR; Barrett TB; Bass N; Battaglia A; Bauer M; Bayes M; Bellivier F; Bergen SE; Berrettini W; Betancur C; Bettecken T; Biederman J; Binder EB; Black DW; Blackwood DHR; Bloss CS; Boehnke M; Boomsma DI; Breen G; Breuer R; Bruggeman R; Cormican P; Buccola NG; Buitelaar JK; Bunney WE; Buxbaum JD; Byerley WF; Byrne EM; Caesar S; Cahn W; Cantor RM; Casas M; Chakravarti A; Chambert K; Choudhury K; Cichon S; Cloninger CR; Collier DA; Cook EH; Coon H; Cormand B; Corvin A; Coryell WH; Craig DW; Craig IW; Crosbie J; Cuccaro ML; Curtis D; Czamara D; Datta S; Dawson G; Day R; De Geus EJ; Degenhardt F; Djurovic S; Donohoe GJ; Doyle AE; Duan J; Dudbridge F; Duketis E; Ebstein RP; Edenberg HJ; Elia J; Ennis S; Etain B; Fanous A; Farmer AE; Ferrier IN; Flickinger M; Fombonne E; Foroud T; Frank J; Franke B; Fraser C; Freedman R; Freimer NB; Freitag CM; Friedl M; Frisen L; Gallagher L; Gejman PV; Georgieva L; Gershon ES; Geschwind DH; Giegling I; Gill M; Gordon SD; Gordon-Smith K; Green EK; Greenwood TA; Grice DE; Gross M; Grozeva D; Guan W; Gurling H; De Haan L; Haines JL; Hakonarson H; Hallmayer J; Hamilton SP; Hamshere ML; Hansen TF; Hartmann AM; Hautzinger M; Heath AC; Henders AK; Herms S; Hickie IB; Hipolito M; Hoefels S; Holmans PA; Holsboer F; Hoogendijk WJ; Hottenga J-J; Hultman CM; Hus V; Ingason A; Ising M; Jamain S; Jones EG; Jones I; Jones L; Tzeng J-Y; Kaehler AK; Kahn RS; Kandaswamy R; Keller MC; Kennedy JL; Kenny E; Kent L; Kim Y; Kirov GK; Klauck SM; Klei L; Knowles JA; Kohli MA; Koller DL; Konte B; Korszun A; Krabbendam L; Krasucki R; Kuntsi J; Kwan P; Landen M; Langstrom N; Lathrop M; Lawrence J; Lawson WB; Leboyer M; Ledbetter DH; Lee PH; Lencz T; Lesch K-P; Levinson DF; Lewis CM; Li J; Lichtenstein P; Lieberman JA; Lin D-Y; Linszen DH; Liu C; Lohoff FW; Loo SK; Lord C; Lowe JK; Lucae S; MacIntyre DJ; Madden PAF; Maestrini E; Magnusson PKE; Mahon PB; Maier W; Malhotra AK; Mane SM; Martin CL; Martin NG; Mattheisen M; Matthews K; Mattingsdal M; McCarroll SA; McGhee KA; McGough JJ; McGrath PJ; McGuffin P; McInnis MG; McIntosh A; McKinney R; McLean AW; McMahon FJ; McMahon WM; McQuillin A; Medeiros H; Medland SE; Meier S; Melle I; Meng F; Meyer J; Middeldorp CM; Middleton L; Milanova V; Miranda A; Monaco AP; Montgomery GW; Moran JL; Moreno-De-Luca D; Morken G; Morris DW; Morrow EM; Moskvina V; Muglia P; Muehleisen TW; Muir WJ; Mueller-Myhsok B; Murtha M; Myers RM; Myin-Germeys I; Neale MC; Nelson SF; Nievergelt CM; Nikolov I; Nimgaonkar V; Nolen WA; Noethen MM; Nurnberger JI; Nwulia EA; Nyholt DR; O'Dushlaine C; Oades RD; Olincy A; Oliveira G; Olsen L; Ophoff RA; Osby U; Owen MJ; Palotie A; Parr JR; Paterson AD; Pato CN; Pato MT; Penninx BW; Pergadia ML; Pericak-Vance MA; Pickard BS; Pimm J; Piven J; Posthuma D; Potash JB; Poustka F; Propping P; Puri V; Quested DJ; Quinn EM; Antoni Ramos-Quiroga J; Rasmussen HB; Raychaudhuri S; Rehnstroem K; Reif A; Ribases M; Rice JP; Rietschel M; Roeder K; Roeyers H; Rossin L; Rothenberger A; Rouleau G; Ruderfer D; Rujescu D; Sanders AR; Sanders SJ; Santangelo SL; Sergeant JA; Schachar R; Schalling M; Schatzberg AF; Scheftner WA; Schellenberg GD; Scherer SW; Schork NJ; Schulze TG; Schumacher J; Schwarz M; Scolnick E; Scott LJ; Shi J; Shilling PD; Shyn SI; Silverman JM; Slager SL; Smalley SL; Smit JH; Smith EN; Sonuga-Barke EJS; St Clair D; State M; Steffens M; Steinhausen H-C; Strauss JS; Strohmaier J; Stroup TS; Sutcliffe JS; Szatmari P; Szelinger S; Thirumalai S; Thompson RC; Todorov AA; Tozzi F; Treutlein J; Uhr M; van den Oord EJCG; Van Grootheest G; Van Os J; Vicente AM; Vieland VJ; Vincent JB; Visscher PM; Walsh CA; Wassink TH; Watson SJ; Weissman MM; Werge T; Wienker TF; Wijsman EM; Willemsen G; Williams N; Willsey AJ; Witt SH; Xu W; Young AH; Yu TW; Zammit S; Zandi PP; Zhang P; Zitman FG; Zoellner S; Devlin B; Kelsoe JR; Sklar P; Daly MJ; O'Donovan MC; Craddock N; Sullivan PF; Smoller JW; Kendler KS; Wray NR
  • Article: JAMA PSYCHIATRY. 2013;70(7):709-717
    Mataix-Cols D; Boman M; Monzani B; Ruck C; Serlachius E; Langstrom N; Lichtenstein P
  • Article: SCIENCE. 2013;340(6139):1467-1471
    Rietveld CA; Medland SE; Derringer J; Yang J; Esko T; Martin NW; Westra H-J; Shakhbazov K; Abdellaoui A; Agrawal A; Albrecht E; Alizadeh BZ; Amin N; Bamard J; Baumeister SE; Benke KS; Bielak LF; Boatman JA; Boyle PA; Davies G; De Leeuw C; Eklund N; Evans DS; Ferhmann R; Fischer K; Gieger C; Gjessing HK; Haegg S; Harris JR; Hayward C; Holzapfel C; Ibrahim-Verbaas CA; Ingelsson E; Jacobsson B; Joshi PK; Jugessur A; Kaakinen M; Kanoni S; Karjalainen J; Kolcic I; Kristiansson K; Kutalik Z; Lahti J; Lee SH; Lin P; Lind PA; Liu Y; Lohman K; Loitfelder M; McMahon G; Vidal PM; Meirelles O; Milani L; Myhre R; Nuotio M-L; Oldmeadow CJ; Petrovic KE; Peyrot WJ; Polasek O; Quaye L; Reinmaa E; Rice JP; Rizzi TS; Schmidt H; Schmidt R; Smith AV; Smith JA; Tanaka T; Terracciano A; van der Loos MJHM; Vitart V; Voelzke H; Wellmann J; Yu L; Zhao W; Allik J; Attia JR; Bandinelli S; Bastardot F; Beauchamp J; Bennett DA; Berger K; Bierut LJ; Boomsma DI; Bueltmann U; Campbell H; Chabris CF; Cherkas L; Chung MK; Cucca F; de Andrade M; De Jager PL; De Neve J-E; Deary IJ; Dedoussis GV; Deloukas P; Dimitriou M; Eiriksdottir G; Elderson MF; Eriksson JG; Evans DM; Faul JD; Ferrucci L; Garcia ME; Groenberg H; Guonason V; Hall P; Harris JM; Harris TB; Hastie ND; Heath AC; Hernandez DG; Hoffmann W; Hofman A; Holle R; Holliday EG; Hottenga J-J; Iacono WG; Illig T; Jaervelin M-R; Kaehoenen M; Kaprio J; Kirkpatrick RM; Kowgier M; Latvala A; Launer LJ; Lawlor DA; Lehtimaeki T; Li J; Lichtenstein P; Lichtner P; Liewald DC; Madden PA; Magnusson PKE; Maekinen TE; Masala M; McGue M; Metspalu A; Mielck A; Miller MB; Montgomery GW; Mukherjee S; Nyholt DR; Oostra BA; Palmer LJ; Palotie A; Penninx BWJH; Perola M; Peyser PA; Preisig M; Raeikkoenen K; Raitakari OT; Realo A; Ring SM; Ripatti S; Rivadeneira F; Rudan I; Rustichini A; Salomaa V; Sarin A-P; Schlessinger D; Scott RJ; Snieder H; St Pourcain B; Starr JM; Sul JH; Surakka I; Svento R; Teumer A; Tiemeier H; van Rooij FJA; Van Wagoner DR; Vartiainen E; Viikari J; Vollenweider P; Vonk JM; Waeber G; Weir DR; Wichmann H-E; Widen E; Willemsen G; Wilson JF; Wright AF; Conley D; Davey-Smith G; Franke L; Groenen PJF; Hofman A; Johannesson M; Kardia SLR; Krueger RF; Laibson D; Martin NG; Meyer MN; Posthuma D; Thurik AR; Timpson NJ; Uitterlinden AG; van Duijn CM; Visscher PM; Benjamin DJ; Cesarini D; Koellinger PD
  • Article: NEW ENGLAND JOURNAL OF MEDICINE. 2012;367(21):2006-2014
    Lichtenstein P; Halldner L; Zetterqvist J; Sjolander A; Serlachius E; Fazel S; Langstrom N; Larsson H
  • Article: ARCHIVES OF GENERAL PSYCHIATRY. 2012;69(11):1140-1150
    D'Onofrio BM; Rickert ME; Langstrom N; Donahue KL; Coyne CA; Larsson H; Ellingson JM; Van Hulle CA; Iliadou AN; Rathouz PJ; Lahey BB; Lichtenstein P
  • Article: ARCHIVES OF GENERAL PSYCHIATRY. 2012;69(11):1099-1103
    Sullivan PF; Magnusson C; Reichenberg A; Boman M; Dalman C; Davidson M; Fruchter E; Hultman CM; Lundberg M; Langstrom N; Weiser M; Svensson AC; Lichtenstein P
  • Article: ARCHIVES OF GENERAL PSYCHIATRY. 2012;69(1):46-52
    Lundstrom S; Chang Z; Rastam M; Gillberg C; Larsson H; Anckarsater H; Lichtenstein P
  • Article: MOLECULAR PSYCHIATRY. 2011;16(10):1039-1047
    Ronald A; Larsson H; Anckarsater H; Lichtenstein P
  • Article: NATURE GENETICS. 2011;43(10):969-976
    Ripke S; Sanders AR; Kendler KS; Levinson DF; Sklar P; Holmans PA; Lin D-Y; Duan J; Ophoff RA; Andreassen OA; Scolnick E; Cichon S; Clair DS; Corvin A; Gurling H; Werge T; Rujescu D; Blackwood DHR; Pato CN; Malhotra AK; Purcell S; Dudbridge F; Neale BM; Rossin L; Visscher PM; Posthuma D; Ruderfer DM; Fanous A; Stefansson H; Steinberg S; Mowry BJ; Golimbet V; De Hert M; Jonsson EG; Bitter I; Pietilainen OPH; Collier DA; Tosato S; Agartz I; Albus M; Alexander M; Amdur RL; Amin F; Bass N; Bergen SE; Black DW; Borglum AD; Brown MA; Bruggeman R; Buccola NG; Byerley WF; Cahn W; Cantor RM; Carr VJ; Catts SV; Choudhury K; Cloninger CR; Cormican P; Craddock N; Danoy PA; Datta S; De Haan L; Demontis D; Dikeos D; Djurovic S; Donnelly P; Donohoe G; Duong L; Dwyer S; Fink-Jensen A; Freedman R; Freimer NB; Friedl M; Georgieva L; Giegling I; Gill M; Glenthoj B; Godard S; Hamshere M; Hansen M; Hansen T; Hartmann AM; Henskens FA; Hougaard DM; Hultman CM; Ingason A; Jablensky AV; Jakobsen KD; Jay M; Juergens G; Kahn R; Keller MC; Kenis G; Kenny E; Kim Y; Kirov GK; Konnerth H; Konte B; Krabbendam L; Krasucki R; Lasseter VK; Laurent C; Lawrence J; Lencz T; Lerer FB; Liang K-Y; Lichtenstein P; Lieberman JA; Linszen DH; Lonnqvist J; Loughland CM; Maclean AW; Maher BS; Maier W; Mallet J; Malloy P; Mattheisen M; Mattingsdal M; McGhee KA; McGrath JJ; McIntosh A; McLean DE; McQuillin A; Melle I; Michie PT; Milanova V; Morris DW; Mors O; Mortensen PB; Moskvina V; Muglia P; Myin-Germeys I; Nertney DA; Nestadt G; Nielsen J; Nikolov I; Nordentoft M; Norton N; Noethen MM; O'Dushlaine CT; Olincy A; Olsen L; O'Neill FA; Orntoft TF; Owen MJ; Pantelis C; Papadimitriou G; Pato MT; Peltonen L; Petursson H; Pickard B; Pimm J; Pulver AE; Puri V; Quested D; Quinn EM; Rasmussen HB; Rethelyi JM; Ribble R; Rietschel M; Riley BP; Ruggeri M; Schall U; Schulze TG; Schwab SG; Scott RJ; Shi J; Sigurdsson E; Silverman JM; Spencer CCA; Stefansson K; Strange A; Strengman E; Stroup TS; Suvisaari J; Terenius L; Thirumalai S; Thygesen JH; Timm S; Toncheva D; van den Oord E; van Os J; van Winkel R; Veldink J; Walsh D; Wang AG; Wiersma D; Wildenauer DB; Williams HJ; Williams NM; Wormley B; Zammit S; Sullivan PF; O'Donovan MC; Daly MJ; Gejman PV
  • Article: NATURE GENETICS. 2011;43(10):977-983
    Psychiatric GWAS Consortium Bipolar Disorder Worki
  • Article: AMERICAN JOURNAL OF PSYCHIATRY. 2010;167(11):1357-1363
    Lichtenstein P; Carlstrom E; Rastam M; Gillberg C; Anckarsater H
  • Article: ARCHIVES OF GENERAL PSYCHIATRY. 2010;67(5):529-538
    D'Onofrio BM; Singh AL; Iliadou A; Lambe M; Hultman CM; Grann M; Neiderhiser JM; Langstrom N; Lichtenstein P
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Articles

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Grants

  • Swedish Research Council
    1 January 2026 - 31 December 2029
    The causes of obsessive-compulsive disorder (OCD) remain largely unknown. While large-scale genetic studies are beginning to identify OCD risk genes, it is equally important to identify non-heritable risk factors, as some may be modifiable. The discordant monozygotic (MZ) twin design is ideally suited to determine whether non-heritable factors are in the causal pathway to OCD while controlling for genetic and shared environmental effects. OCDTWIN is the first cohort of MZ twin pairs discordant for OCD. In Aim 1 (years 1-3), we will recruit at least 80 discordant MZ twin pairs (45 pairs already recruited) through the Swedish and Danish Twin Registries, collecting biological specimens (blood, saliva, urine, stool, hair, nails), MRI scans, and leveraging the phenylketonuria biobank for biological material collected at birth. Data on early-life environmental exposures (e.g., perinatal complications) are available from national registers. In Aim 2 (years 4-5), we will conduct within-pair comparisons to identify post-zygotic mutations and environmentally mediated biological processes contributing to OCD. In Aim 3 (years 4-5), we will relate within-pair differences in brain phenotypes to brain epigenetic mechanisms, using recently available epigenetic atlases. By the end of this project, we anticipate significant progress in our understanding of OCD aetiology. The OCDTWIN biobank will become a global resource, enabling researchers to test novel hypotheses as new methods emerge.
  • Swedish Research Council
    1 January 2026 - 31 December 2029
    Psychosis diagnoses have profound personal and societal costs. Despite 1 in 4 people with psychosis experiencing onset after age 35, the causes of late-onset psychosis (LOP) are not well understood. This study leverages unique Nordic resources to test a comprehensive set of environmental, genetic, and physiological risk factors giving rise to psychosis later in life.First, we will use the Swedish National Registers, containing data across the lifespan for &gt
    10 million people, to investigate exposures experienced by adults which may influence risk for LOP such as divorce, unemployment, childbirth, serious illness, or death of a family member.Almost no genetic research specific to LOP has been conducted so far. Therefore, our 2nd aim will use the Finnish SUPER study of ~10,000 individuals with a range of psychosis diagnoses to explore how specific and aggregated genetic risk factors for the major psychotic disorders differ between early and late onset groups.Finally, in our sample of &gt
    2 million individuals in Stockholm with clinical laboratory test values we will investigate a range of inflammatory, hormonal, and vitamin biomarkers for prospective differences between people who develop a LOP diagnosis and those who do not.Improving our understanding of the causes of LOP may 1) enable identification of high-risk individuals 2) aid development of interventions to prevent conversion to psychosis and 3) facilitate generation of treatment strategies specific to LOP.
  • Swedish Research Council
    1 December 2025 - 31 December 2029
    This project investigates the recent and marked rise in gender dysphoria diagnoses in Sweden—particularly among adolescents registered female at birth—by integrating national register data with detailed clinical records. Using longitudinal, population-based cohorts and quasi-experimental designs (e.g., sibling comparisons, within-individual models), we will examine temporal trends, psychiatric and somatic comorbidities, familial aggregation, and long-term treatment outcomes. A new register linkage will allow identification of hormonal regimens and outcomes not previously assessable, including osteoporosis, hormone-sensitive cancers, and cardiovascular events. Clinical data from over 700 adults treated with gender-affirming hormones at Sahlgrenska University Hospital provide complementary detail on lab values, patient-reported outcomes, and side effects. Together, these data sources offer an unprecedented opportunity to clarify the etiology and clinical trajectories of gender dysphoria and evaluate the risks and benefits of gender identity-affirming interventions. Findings will inform clinical guidelines and health policy, addressing a critical evidence gap in contemporary psychiatric care.
  • Specifying the association between substance abuse and schizophrenia, with a focus on adolescents and young adults
    Swedish research council for health, working life and welfare
    1 January 2025 - 31 December 2027
  • Does it take a village? The role of social networks in socioeconomic fertility differentials
    Stiftelsen Riksbankens Jubileumsfond
    1 January 2024 - 31 December 2026
    In recent years, higher socioeconomic groups started to have more children than lower socioeconomic groups in Sweden and in many other developed countries. Previous research focusing on individuals as independent units had limited power in explaining this polarization in fertility. We will thus use a social network perspective to understand the role of segregated social networks in the fertility behavior of different socioeconomic groups. Using longitudinal population-level social networks consisting of multiple types of relationships (i.e. neighbors, family, and workmates), we will answer (1) how fertility behavior spreads in the social networks for different socioeconomic groups, (2) how use of assisted reproductive techniques spreads in the social networks for the different socioeconomic group, and (3) how family support in someone’s social network influences fertility among different socioeconomic groups. Data will be obtained from several Swedish registers. Quasi-experimental methods (i.e., instrumental variable and small unit analysis) will be applied to distinguish whether people influence each other’s fertility behavior or simply select their relationship based on pre-existing similarities (e.g., fertility intentions). The project will be the first to investigate the role of social networks in forming socioeconomic fertility differentials based on population-level network data, contributing to the understanding of evolving socioeconomic inequalities.
  • Bank of Sweden Tercentenary Foundation
    1 January 2024 - 31 December 2026
    In recent years, higher socioeconomic groups started to have more children than lower socioeconomic groups in Sweden and in many other developed countries. Previous research focusing on individuals as independent units had limited power in explaining this polarization in fertility. We will thus use a social network perspective to understand the role of segregated social networks in the fertility behavior of different socioeconomic groups. Using longitudinal population-level social networks consisting of multiple types of relationships (i.e. neighbors, family, and workmates), we will answer (1) how fertility behavior spreads in the social networks for different socioeconomic groups, (2) how use of assisted reproductive techniques spreads in the social networks for the different socioeconomic group, and (3) how family support in someone’s social network influences fertility among different socioeconomic groups. Data will be obtained from several Swedish registers. Quasi-experimental methods (i.e., instrumental variable and small unit analysis) will be applied to distinguish whether people influence each other’s fertility behavior or simply select their relationship based on pre-existing similarities (e.g., fertility intentions). The project will be the first to investigate the role of social networks in forming socioeconomic fertility differentials based on population-level network data, contributing to the understanding of evolving socioeconomic inequalities.
  • Swedish Research Council
    1 January 2024 - 31 December 2026
    Autism is a common lifelong condition. Autistic individuals are at a high risk of somatic disorders, such as epilepsy, and are at an increased risk for premature mortality. A better understanding of co-occurring somatic disorders in autistic individuals is thus critical from the perspective of improving public health in marginalized groups, yet existing research is limited by a descriptive focus. Our overall aim is to identify risk factors for somatic disorders in autistic individuals. We will optimize Swedish registry data, including linkage with a large genotyped sample, using powerful longitudinal study designs. First, we will test whether genetic factors account for the association between autism and somatic disorders. We will triangulate three family-based designs, and utilize contemporary molecular genetic approaches to assess genetic links between autism and somatic disorders. Second, we will assess whether the psychosocial adversity faced by autistic individuals impact on their health using longitudinal cohort designs. Finally, real-world data will allow us to circumvent the challenges of conducting randomized controlled trials to examine the impact of psychotropic medication use on somatic health in autistic individuals. This project will guide the field of somatic health in autistic individuals from descriptive epidemiology towards a mechanistic understanding, which will ultimately lead to improved prevention, detection, and treatment of these disorders.
  • Swedish Research Council
    1 January 2024 - 31 December 2026
    Purpose and aims: There is so much comorbidity among psychiatric conditions that one can combine them into a single general psychopathology index. Although general psychopathology predicts adverse outcomes, it remains unknown if it responds to intervention. Therefore, we will estimate the causal effect of psychosocial interventions and psychotropic medications on general psychopathology. Method: We will apply casual inference designs (children-of-siblings design
    co-twin control/within-individual design
    instrumental variable
    and front-door criterion) to data from the Swedish Twin Register and Swedish population registers to estimate the effect of childrearing conditions (year 1), psychotherapy (years 2-3), and psychotropic medication (years 1-5) on general psychopathology (derived from self/parent-reported symptoms and psychiatric diagnoses). The principal investigator will devote 50% of his time to this project, and he is supported by experts in epidemiology, psychotherapy, and psychiatry. Importance: Even though comorbidity is the rule rather than exception in psychiatry, most randomized clinical trials exclude individuals with several disorders. Therefore, there is a lack of knowledge of the effect of treatment on comorbidity. By applying innovative causal inference designs to large observational data, we aim to study the effect of treatment on general psychopathology in the best conceivable way. This could open a new area of research into transdiagnostic treatments.
  • Swedish Research Council for Health Working Life and Welfare
    1 January 2024 - 31 December 2027
    Research problem and specific questions: About one quarter of all children have parents with mental health problems. These children are at increased risk for a wide range of adverse outcomes. Nevertheless, despite the importance of reducing this form of inequality, research on the intergenerational transmission of mental health problems is plagued by three important limitations. These include an overreliance on small samples and retrospective (biased) reports
    a failure to address psychiatric comorbidity
    and inadequate control of unmeasured confounding. The aim of this project is to answer three research questions: 1) What are the associations between psychiatric diagnoses in parents and adverse outcomes in their children? 2) Can these be attributed to broad comorbidity? 3) Does treatment of the parents’ psychiatric disorders reduce the risk of adverse outcomes in children?Data and method: We will include all individuals born in Sweden between 1970 and 2000 (N = 2 797 086). The exposures are 6 psychiatric diagnoses in their parents, and the outcomes are 34 adverse events in the offspring recorded until the end of 2019 (e.g., psychiatric disorders, psychotropic medications, criminality, school and employment problems, etc.). We will estimate associations between the exposures and outcomes
    adjust for comorbidity using multiple regression and a general factor model
    and apply causal inference techniques to control for unmeasured confounding.Plan for project realisation: We will hire a PhD student and a postdoc to complete the project. The PI, along with experts in epidemiology and psychiatry, will provide support.Relevance: Our project will contribute to the study of intergenerational transmission of mental health problems in three important ways. First, because psychiatric treatment resources are becoming increasingly scarce as more individuals seek help, parental psychiatric history can help guide treatment allocation by identifying those at higher risk and by screening out low risk persons. Second, we will highlight the importance of focusing on parental comorbidity, which will guide clinicians to additionally focus on the number of parental diagnoses (rather than only type) when predicting patient prognosis. Third, if a parental psychiatric diagnosis appears causally related to an outcome, then it would be beneficial to develop a policy for child and adolescent mental health providers to recommend that the parent also seek treatment.
  • Swedish Research Council for Health Working Life and Welfare
    1 January 2023 - 31 December 2026
    Research problem and specific questions: Intellectual disability (ID) affects 2% of children worldwide. The disability is present throughout the lifespan, leading to significant morbidity and premature deaths. Early-life risk factors and low socioeconomic status (SES) are associated with ID. But the absence of genetically-informative studies prevented researchers from distinguishing between potential causal environmental influences and genetic confounding. In the proposed project, we will study the effect of early-life environmental factors for ID and identify risk groups in need of clinical follow-up.The aim of this project is to answer the following research questions:What is the causal mechanism by which early-life risk factors are associated with risk of ID?What is the mechanism underlying the association between SES and ID? Which early-life risk factors mediate this associations?Which risk groups are mostly likely to benefit from targeted pediatric surveillance and early health interventions?Data and method: We will use large-scale longitudinal linkages of administrative and health registers along with the Swedish Twin and Multi-Generation Registers. We will examine association between exposures to 1) early-life risk factors and 2) low SES with the outcome of ID. The association will be investigated in the overall population (between-family analyses) and, to address potential causality by adjusting for familial confounding in siblings (i) full-siblings, half-siblings, cousins and (ii) twins (within-family analyses). We will apply causal inference methods for mediation and interactions. 3) We will develop a Clinical Risk Score for prediction of ID based on early-life risk factors, SES and familial risk score.Plan for project realization: The project will be carried out over three years in close collaboration with reference group involving representatives from self-advocacy group “Grunden and Inre Ringen” and relevant stakeholders such as Young People and Adults with Intellectual Disability (FUB), the National Board of Health and Welfare, the Swedish Agency for Participation and the Swedish Municipalities and Regions (SKR).Relevance: The project will increase our knowledge on modifiable risk factors for ID, crucial for informing prevention in the population. If we can identify children atrisk of disabilities, we will be able to plan follow-ups and provide the best opportunities for timely diagnosis and early interventions in children and their families.
  • Swedish Research Council
    1 December 2021 - 30 November 2024
  • Swedish Research Council
    1 January 2020 - 31 December 2023
  • Swedish Research Council
    1 January 2020 - 31 December 2022
  • Swedish Research Council for Health Working Life and Welfare
    1 April 2019 - 31 March 2023
  • Swedish Research Council
    1 January 2019 - 31 December 2021
  • Swedish Research Council
    1 January 2018 - 31 December 2020
  • Swedish Research Council
    1 January 2018 - 31 December 2021
  • Swedish Research Council
    1 January 2017 - 31 December 2020
  • Swedish Research Council
    1 January 2017 - 31 December 2019
  • Swedish Research Council
    1 January 2017 - 31 December 2020
  • Show more

Employments

  • Professor, Genetic epidemiology, Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, 2006-

Degrees and Education

  • Docent, Genetic epidemiology, Karolinska Institutet, 1997
  • Dr.Med.Sc., Genetic epidemiology, Institute of Environmental Medicine, Karolinska Institutet, 1993
  • B.A., Sociology, Stockholm University, 1985

Leadership and responsibility assignments

  • Deputy head of department, Department of Medical Epidemiology and Biostatistics, Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, 2022-
  • Director of studies, Postgraduate studies, Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, 2019-
  • Head of department, Department of Medical Epidemiology and Biostatistics, Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, 2014-2017
  • Elected President, Behavior Genetics Association, Behavior Genetics Association, 2012-2014
  • Responsible for a section, The Swedish Twin Registry, Karolinska Institutet, 2006-2013

Distinction and awards

  • James Shields Award For Lifetime Contributions To Twin Research, The International Society for Twin Studies (ISTS), 2011

Supervision

  • Supervision to doctoral degree

    • Vide Ohlsson Gotby, Register-based studies of sex steroid hormones and psychiatric disorders., 2023
    • Jie Song, Bipolar disorder and lithium treatment: etiologies and consequences, 2017
    • Martin Cederlöf, Risks, correlates and consequences of the extended psychosis phenotype., 2016
    • Amir Sariaslan, Exploring the causal nature of neighborhood influences on violent criminality, substance misuse and psychiatric morbidity., 2015
    • Ralf Kuja-Halkola, Twin and family studies on the development of cognitive and externalizing problems., 2014
    • Hans Walum, Genetic and hormonal influences on affiliative behavior in humans., 2012
    • Jurgita Narusyte, Adolescent adjustment: the role of heritability and family environment., 2009
    • Linda Lindström, Familial studies on common cancers – a population based approach, 2008
    • Catherine Tuvblad, Genetic and environmental influences on antisocial behavior from childhood to emerging adulthood, 2006
    • Emma Nilsson, Genetic epidemiological studies of adverse pregnancy outcome and the role of schizophrenia, 2006
    • Henrik Larsson, Genetic and environmental factors in the development of externalizing symptoms from childhood to adolescence, 2005
    • Anastasia Iliadou, Genetic epidemiological approaches to the study of risk factors for cardiovascular diseases., 2003

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