Asian Science Citation Index is committed to provide an authoritative, trusted and significant information by the coverage of the most important and influential journals to meet the needs of the global scientific community.  
ASCI Database
308-Lasani Town,
Sargodha Road,
Faisalabad, Pakistan
Fax: +92-41-8815544
Contact Via Web
Suggest a Journal
Articles by A Hofman
Total Records ( 13 ) for A Hofman
  M. F Engberink , E. G Schouten , A Hofman , J. C Witteman and J. M Geleijnse

Background: Little is known about the effect of different types of dairy food products on the development of hypertension.

Objective: The objective was to determine whether the incidence of hypertension in older Dutch subjects is associated with intake of dairy products.

Design: We examined the relation between dairy intake and incident hypertension in 2245 participants of the Rotterdam Study aged ≥55 y with complete dietary and blood pressure data, who were free of hypertension at baseline (1990–1993). Blood pressure was reexamined in 1993–1995 and in 1997–1999. Hazard ratios (HRs) with 95% CIs for 2- and 6-y incidence of hypertension were obtained in quartiles of energy-adjusted dairy intake, with adjustment for age, sex, BMI, smoking, educational level, dietary factors, and intake of alcohol and total energy.

Results: Risk of hypertension after 2 y of follow-up (664 incident cases) was inversely associated with dairy product intake. After adjustment for confounders, HRs (95% CIs) were 1.00, 0.82 (0.67, 1.02), 0.67 (0.54, 0.84), and 0.76 (0.61, 0.95) in consecutive quartiles of total dairy product intake (P for trend = 0.008). Corresponding HRs for low-fat dairy products were 1.00, 0.75 (0.60, 0.92), 0.77 (0.63, 0.96), and 0.69 (0.56, 0.86) (P for trend = 0.003). Analysis of specific types of dairy products showed an inverse association with milk and milk products (P for trend = 0.07) and no association with high-fat dairy or cheese (P > 0.6). After 6 y of follow-up (984 incident cases), the associations with hypertension were attenuated to risk reductions of 20% for both total and low-fat dairy products between the extreme quartiles of intake (P for trend = 0.07 and 0.09, respectively).

Conclusion: Intake of low-fat dairy products may contribute to the prevention of hypertension at an older age.

  E. E Devore , F. J van Rooij , A Hofman , B Rosner , M. J Stampfer and M. M. Breteler

Background: Greater fish and omega-3 (n–3) polyunsaturated fatty acid (PUFA) intake may reduce dementia risk; however, previous studies have reported conflicting results, which were largely based on short-term follow-up.

Objective: The objective was to study the dietary consumption of fish and omega-3 PUFAs in relation to long-term dementia risk.

Design: We studied 5395 participants aged ≥55 y in the Rotterdam Study who were free of dementia and reported dietary information at baseline. We used age- and sex-adjusted Cox proportional hazard and multivariate-adjusted models to evaluate the relative risk of dementia and Alzheimer disease (AD) across categories of typical fish intake (none, low, and high) and fish type consumed (none, lean, and fatty). We also evaluated dementia and AD risk across tertiles of omega-3 PUFA intake, specifically, total long-chain omega-3 fatty acids: eicosapentaenoic acid (EPA) + docosahexaenoic acid (DHA), -linolenic acid, and EPA and DHA individually.

Results: During an average follow-up of 9.6 y, dementia developed in 465 participants (365 with a diagnosis of AD). In multivariate-adjusted models, total fish intake was unrelated to dementia risk (P for trend = 0.7). Compared with participants who typically ate no fish, those with a high fish intake had a similar dementia risk (hazard ratio: 0.95; 95% CI: 0.76, 1.19), as did those who typically ate fatty fish (hazard ratio: 0.98; 95% CI: 0.77, 1.24). Dietary intakes of omega-3 PUFAs were also not associated with dementia risk, and the results were similar when we considered AD specifically.

Conclusion: In this Dutch cohort, who had a moderate consumption of fish and omega-3 PUFAs, these dietary factors do not appear to be associated with long-term dementia risk.

  R. S Newson , K Hek , H. J Luijendijk , A Hofman , J. C. M Witteman and H. Tiemeier

Context  Depression is a prominent concern for older adults; therefore, it is important to identify causal mechanisms so that prevention and treatment strategies can be developed. The vascular depression hypothesis proposes that vascular factors precede the onset of depression in older adults. However, although cross-sectional associations have been established, owing to a lack of objective assessments and longitudinal data, the validity and temporal nature of this relationship is unclear.

Objective  To examine whether atherosclerosis, an asymptomatic subclinical indicator of vascular burden, increases the risk of developing depression in older adults.

Design  Prospective, population-based study.

Setting  Set within the Rotterdam study, participants were assessed on objective measures of generalized atherosclerosis at baseline (1997-1999) and followed up for an average of 6 years for incident depression.

Participants  The baseline sample consisted of 3564 participants (56% female) with a mean age of 72 years who initially did not have depression or dementia.

Main Outcome Measures  Depression was categorized into symptoms or syndromes and assessed in a multidimensional manner from physician and mental health specialist reports, pharmacy records (antidepressant usage), a clinical interview, and self-report.

Results  During 21 083 person-years, 429 incidents of depressive symptoms and 197 incidents of depressive syndromes occurred. Individual atherosclerotic measures and a composite measure were not predictive of incident depressive symptoms (composite measure hazard ratio, 0.93; 95% confidence interval, 0.83-1.05) or incident depressive syndromes (composite measure hazard ratio, 0.97; 95% confidence interval, 0.81-1.16). An a priori power analysis indicated a sufficient sample size ( = .05; 0.95 power).

Conclusions  Atherosclerosis does not appear to increase the risk of incident depression in older adults. These findings do not support the vascular depression hypothesis and, alternatively, taking findings from prior studies into account, suggest either that depression contributes to vascular burden or that both result from an underlying biological substrate.

  A Lebon , J. A. M Labout , H. A Verbrugh , V. W. V Jaddoe , A Hofman , W. J. B van Wamel , A van Belkum and H. A. Moll

Objective  To study the association between Staphylococcus aureus nasal colonization and atopic dermatitis (AD) in infancy.

Design  Population-based prospective cohort study of pregnant women and their children.

Setting  This project was embedded in the Generation R Study.

Participants  A total of 1079 postnatal Dutch infants/children participated in the focus cohort.

Main Exposures  Nasal swabs for S aureus cultivation were taken at ages 1.5, 6, and 14 months.

Main Outcome Measure  Questionnaires that pertain to AD and confounders (birth weight, gestational age, sex, and parental eczema) were completed prenatally and postnatally. The outcome was AD in the first and second years of life.

Results  A first positive culture for S aureus at age 6 months was associated with AD prevalence in the first and second years of life (adjusted odds ratio [aOR], 2.13; 95% confidence interval [CI], 1.17-3.87; and aOR, 2.88; 95% CI, 1.60-5.19, respectively) and also with severity (aOR, 3.27; 95% CI, 1.30-8.03). Moreover, frequent colonization in the first year of life (≥2 times) held a 4.29-fold (95% CI, 1.03- to 17.88-fold) risk of moderate to severe AD in the second year of life.

Conclusion  Colonization with S aureus at age 6 months and frequent colonization in the first year of life are associated with AD and its severity in young children.

  T den Heijer , F van der Lijn , P. J Koudstaal , A Hofman , A van der Lugt , G. P Krestin , W. J Niessen and M. M. B. Breteler

Hippocampal atrophy is frequently observed on magnetic resonance images from patients with Alzheimer’s disease and persons with mild cognitive impairment. Even in asymptomatic elderly, a small hippocampal volume on magnetic resonance imaging is a risk factor for developing Alzheimer’s disease. However, not everyone with a small hippocampus develops dementia. With the increased interest in the use of sequential magnetic resonance images as potential surrogate biomarkers of the disease process, it has also been shown that the rate of hippocampal atrophy is higher in persons with Alzheimer’s disease compared to those with mild cognitive impairment and the healthy elderly. Whether a higher rate of hippocampal atrophy also predicts Alzheimer’s disease or subtle cognitive decline in non-demented elderly is unknown. We examine these associations in a group of 518 elderly (age 60–90 years, 50% female), taken from the population-based Rotterdam Scan Study. A magnetic resonance imaging examination was performed at baseline in 1995–96 that was repeated in 1999–2000 (in 244 persons) and in 2006 (in 185 persons). Using automated segmentation procedures, we assessed hippocampal volumes on all magnetic resonance imaging scans. All persons were free of dementia at baseline and followed over time for cognitive decline and incident dementia. Persons had four repeated neuropsychological tests at the research centre over a 10-year period. We also continuously monitored the medical records of all 518 participants for incident dementia. During a total follow-up of 4360 person-years, (mean 8.4, range 0.1–11.3), 50 people developed incident dementia (36 had Alzheimer’s disease). We found an increased risk to develop incident dementia per standard deviation faster rate of decline in hippocampal volume [left hippocampus 1.6 (95% confidence interval 1.2–2.3, right hippocampus 1.6 (95% confidence interval 1.2–2.1)]. Furthermore, decline in hippocampal volume predicted onset of clinical dementia when corrected for baseline hippocampal volume. In people who remained free of dementia during the whole follow-up period, we found that decline in hippocampal volume paralleled, and preceded, specific decline in delayed word recall. No associations were found in this sample between rate of hippocampal atrophy, Mini Mental State Examination and tests of executive function. Our results suggest that rate of hippocampal atrophy is an early marker of incipient memory decline and dementia, and could be of additional value when compared with a single hippocampal volume measurement as a surrogate biomarker of dementia.

  N. L Smith , M. H Chen , A Dehghan , D. P Strachan , S Basu , N Soranzo , C Hayward , I Rudan , M Sabater Lleal , J. C Bis , M. P. M de Maat , A Rumley , X Kong , Q Yang , F. M. K Williams , V Vitart , H Campbell , A Malarstig , K. L Wiggins , C. M Van Duijn , W. L McArdle , J. S Pankow , A. D Johnson , A Silveira , B McKnight , A. G Uitterlinden , Aleksic Wellcome Trust Case Control Consortium; , J. B Meigs , A Peters , W Koenig , M Cushman , S Kathiresan , J. I Rotter , E. G Bovill , A Hofman , E Boerwinkle , G. H Tofler , J. F Peden , B. M Psaty , F Leebeek , A. R Folsom , M. G Larson , T. D Spector , A. F Wright , J. F Wilson , A Hamsten , T Lumley , J. C. M Witteman , W Tang and C. J. O'Donnell

Background— Plasma levels of coagulation factors VII (FVII), VIII (FVIII), and von Willebrand factor (vWF) influence risk of hemorrhage and thrombosis. We conducted genome-wide association studies to identify new loci associated with plasma levels.

Methods and Results— The setting of the study included 5 community-based studies for discovery comprising 23 608 European-ancestry participants: Atherosclerosis Risk In Communities Study, Cardiovascular Health Study, British 1958 Birth Cohort, Framingham Heart Study, and Rotterdam Study. All subjects had genome-wide single-nucleotide polymorphism (SNP) scans and at least 1 phenotype measured: FVII activity/antigen, FVIII activity, and vWF antigen. Each study used its genotype data to impute to HapMap SNPs and independently conducted association analyses of hemostasis measures using an additive genetic model. Study findings were combined by meta-analysis. Replication was conducted in 7604 participants not in the discovery cohort. For FVII, 305 SNPs exceeded the genome-wide significance threshold of 5.0x10–8 and comprised 5 loci on 5 chromosomes: 2p23 (smallest P value 6.2x10–24), 4q25 (3.6x10–12), 11q12 (2.0x10–10), 13q34 (9.0x10–259), and 20q11.2 (5.7x10–37). Loci were within or near genes, including 4 new candidate genes and F7 (13q34). For vWF, 400 SNPs exceeded the threshold and marked 8 loci on 6 chromosomes: 6q24 (1.2x10–22), 8p21 (1.3x10–16), 9q34 (<5.0x10–324), 12p13 (1.7x10–32), 12q23 (7.3x10–10), 12q24.3 (3.8x10–11), 14q32 (2.3x10–10), and 19p13.2 (1.3x10–9). All loci were within genes, including 6 new candidate genes, as well as ABO (9q34) and VWF (12p13). For FVIII, 5 loci were identified and overlapped vWF findings. Nine of the 10 new findings were replicated.

Conclusions— New genetic associations were discovered outside previously known biological pathways and may point to novel prevention and treatment targets of hemostasis disorders.

  A Dehghan , Q Yang , A Peters , S Basu , J. C Bis , A. R Rudnicka , M Kavousi , M. H Chen , J Baumert , G. D.O Lowe , B McKnight , W Tang , M de Maat , M. G Larson , S Eyhermendy , W. L McArdle , T Lumley , J. S Pankow , A Hofman , J. M Massaro , F Rivadeneira , M Kolz , K. D Taylor , C. M van Duijn , S Kathiresan , T Illig , Y. S Aulchenko , K. A Volcik , A. D Johnson , A. G Uitterlinden , G. H Tofler , C Gieger , Psaty Wellcome Trust Case Control Consortium , D. J Couper , E Boerwinkle , W Koenig , C. J O`Donnell , J. C Witteman , D. P Strachan , N. L Smith and A. R. Folsom

Background— Fibrinogen is both central to blood coagulation and an acute-phase reactant. We aimed to identify common variants influencing circulation fibrinogen levels.

Methods and Results— We conducted a genome-wide association analysis on 6 population-based studies, the Rotterdam Study, the Framingham Heart Study, the Cardiovascular Health Study, the Atherosclerosis Risk in Communities Study, the Monitoring of Trends and Determinants in Cardiovascular Disease/KORA Augsburg Study, and the British 1958 Birth Cohort Study, including 22 096 participants of European ancestry. Four loci were marked by 1 or more single-nucleotide polymorphisms that demonstrated genome-wide significance (P<5.0x10–8). These included a single-nucleotide polymorphism located in the fibrinogen β chain (FGB) gene and 3 single-nucleotide polymorphisms representing newly identified loci. The high-signal single-nucleotide polymorphisms were rs1800789 in exon 7 of FGB (P=1.8x10–30), rs2522056 downstream from the interferon regulatory factor 1 (IRF1) gene (P=1.3x10–15), rs511154 within intron 1 of the propionyl coenzyme A carboxylase (PCCB) gene (P=5.9x10–10), and rs1539019 on the NLR family pyrin domain containing 3 isoforms (NLRP3) gene (P=1.04x10–8).

Conclusions— Our findings highlight biological pathways that may be important in regulation of inflammation underlying cardiovascular disease.

  A. C Morrison , J. F Felix , L. A Cupples , N. L Glazer , L. R Loehr , A Dehghan , S Demissie , J. C Bis , W. D Rosamond , Y. S Aulchenko , Y. A Wang , T Haritunians , A. R Folsom , F Rivadeneira , E. J Benjamin , T Lumley , D Couper , B. H Stricker , C. J O'Donnell , K. M Rice , P. P Chang , A Hofman , D Levy , J. I Rotter , E. R Fox , A. G Uitterlinden , T. J Wang , B. M Psaty , J. T Willerson , C. M van Duijn , E Boerwinkle , J. C. M Witteman , R. S Vasan and N. L. Smith

Prognosis and survival are significant concerns for individuals with heart failure (HF). To better understand the pathophysiology of HF prognosis, the association between 2 366 858 single-nucleotide polymorphisms (SNPs) and all-cause mortality was evaluated among individuals with incident HF from 4 community-based prospective cohorts: the Atherosclerosis Risk in Communities Study, the Cardiovascular Health Study, the Framingham Heart Study, and the Rotterdam Study.

Methods and Results—

Participants were 2526 individuals of European ancestry and 466 individuals of African ancestry who experienced an incident HF event during follow-up in the respective cohorts. Within each study, the association between genetic variants and time to mortality among individuals with HF was assessed by Cox proportional hazards models that included adjustment for sex and age at the time of the HF event. Prospective fixed-effect meta-analyses were conducted for the 4 study populations of European ancestry (N=1645 deaths) and for the 2 populations of African ancestry (N=281 deaths). Genome-wide significance was set at P=5.0x10–7. Meta-analytic findings among individuals of European ancestry revealed 1 genome-wide significant locus on chromosome 3p22 in an intron of CKLF-like MARVEL transmembrane domain containing 7 (CMTM7, P=3.2x10–7). Eight additional loci in individuals of European ancestry and 4 loci in individuals of African ancestry were identified by high-signal SNPs (P<1.0x10–5) but did not meet genome-wide significance.


This study identified a novel locus associated with all-cause mortality among individuals of European ancestry with HF. This finding warrants additional investigation, including replication, in other studies of HF.

  N. L Smith , J. F Felix , A. C Morrison , S Demissie , N. L Glazer , L. R Loehr , L. A Cupples , A Dehghan , T Lumley , W. D Rosamond , W Lieb , F Rivadeneira , J. C Bis , A. R Folsom , E Benjamin , Y. S Aulchenko , T Haritunians , D Couper , J Murabito , Y. A Wang , B. H Stricker , J. S Gottdiener , P. P Chang , T. J Wang , K. M Rice , A Hofman , S. R Heckbert , E. R Fox , C. J O'Donnell , A. G Uitterlinden , J. I Rotter , J. T Willerson , D Levy , C. M van Duijn , B. M Psaty , J. C. M Witteman , E Boerwinkle and R. S. Vasan

Although genetic factors contribute to the onset of heart failure (HF), no large-scale genome-wide investigation of HF risk has been published to date. We have investigated the association of 2 478 304 single-nucleotide polymorphisms with incident HF by meta-analyzing data from 4 community-based prospective cohorts: the Atherosclerosis Risk in Communities Study, the Cardiovascular Health Study, the Framingham Heart Study, and the Rotterdam Study.

Methods and Results—

Eligible participants for these analyses were of European or African ancestry and free of clinical HF at baseline. Each study independently conducted genome-wide scans and imputed data to the 2.5 million single-nucleotide polymorphisms in HapMap. Within each study, Cox proportional hazards regression models provided age- and sex-adjusted estimates of the association between each variant and time to incident HF. Fixed-effect meta-analyses combined results for each single-nucleotide polymorphism from the 4 cohorts to produce an overall association estimate and P value. A genome-wide significance P value threshold was set a priori at 5.0x10–7. During a mean follow-up of 11.5 years, 2526 incident HF events (12%) occurred in 20 926 European-ancestry participants. The meta-analysis identified a genome-wide significant locus at chromosomal position 15q22 (1.4x10–8), which was 58.8 kb from USP3. Among 2895 African-ancestry participants, 466 incident HF events (16%) occurred during a mean follow-up of 13.7 years. One genome-wide significant locus was identified at 12q14 (6.7x10–8), which was 6.3 kb from LRIG3.


We identified 2 loci that were associated with incident HF and exceeded genome-wide significance. The findings merit replication in other community-based settings of incident HF.

  E Grundberg , T Kwan , B Ge , K. C.L Lam , V Koka , A Kindmark , H Mallmin , J Dias , D. J Verlaan , M Ouimet , D Sinnett , F Rivadeneira , K Estrada , A Hofman , J. M van Meurs , A Uitterlinden , P Beaulieu , A Graziani , E Harmsen , O Ljunggren , C Ohlsson , D Mellstrom , M. K Karlsson , O Nilsson and T. Pastinen

The common genetic variants associated with complex traits typically lie in noncoding DNA and may alter gene regulation in a cell type-specific manner. Consequently, the choice of tissue or cell model in the dissection of disease associations is important. We carried out an expression quantitative trait loci (eQTL) study of primary human osteoblasts (HOb) derived from 95 unrelated donors of Swedish origin, each represented by two independently derived primary lines to provide biological replication. We combined our data with publicly available information from a genome-wide association study (GWAS) of bone mineral density (BMD). The top 2000 BMD-associated SNPs (P < ~10–3) were tested for cis-association of gene expression in HObs and in lymphoblastoid cell lines (LCLs) using publicly available data and showed that HObs have a significantly greater enrichment (threefold) of converging cis-eQTLs as compared to LCLs. The top 10 BMD loci with SNPs showing strong cis-effects on gene expression in HObs (P = 6 x 10–10 – 7 x 10–16) were selected for further validation using a staged design in two cohorts of Caucasian male subjects. All 10 variants were tested in the Swedish MrOS Cohort (n = 3014), providing evidence for two novel BMD loci (SRR and MSH3). These variants were then tested in the Rotterdam Study (n = 2090), yielding converging evidence for BMD association at the 17p13.3 SRR locus (Pcombined = 5.6 x 10–5). The cis-regulatory effect was further fine-mapped to the proximal promoter of the SRR gene (rs3744270, r2 = 0.5, P = 2.6 x 10–15). Our results suggest that primary cells relevant to disease phenotypes complement traditional approaches for prioritization and validation of GWAS hits for follow-up studies.

  A. D Johnson , M Kavousi , A. V Smith , M. H Chen , A Dehghan , T Aspelund , J. P Lin , C. M van Duijn , T. B Harris , L. A Cupples , A. G Uitterlinden , L Launer , A Hofman , F Rivadeneira , B Stricker , Q Yang , C. J O'Donnell , V Gudnason and J. C. Witteman

Variation in serum bilirubin is associated with altered cardiovascular disease risk and drug metabolism. We aimed to identify genetic contributors to variability in serum bilirubin levels by combining results from three genome-wide association studies (Framingham heart study, n = 3424; Rotterdam study, n = 3847; Age, Gene, Environment and Susceptibility-Reykjavik, n = 2193). Meta-analysis showed strong replication for a genetic influence on serum bilirubin levels of the UGT1A1 locus (P < 5 x 10–324) and a 12p12.2 locus. The peak signal in the 12p12.2 region was a non-synonymous SNP in SLCO1B1 (rs4149056, P = 6.7 x 10–13), which gives rise to a valine to alanine amino acid change leading to reduced activity for a hepatic transporter with known affinity for bilirubin. There were also suggestive associations with several other loci. The top variants in UGT1A1 and SLCO1B1 explain ~18.0 and ~1.0% of the variation in total serum bilirubin levels, respectively. In a conditional analysis adjusted for individual genotypes for the top UGT1A1 variant, the top SLCO1B1 variant remained highly significant (P = 7.3 x 10–13), but no other variants achieved genome-wide significance. In one of the largest genetic studies of bilirubin to date (n = 9464), we confirm the substantial genetic influence of UGT1A1 variants, consistent with past linkage and association studies, and additionally provide strong evidence of a role for allelic variation in SLCO1B1. Given the involvement of bilirubin in a number of physiological and disease processes, and the roles for UGT1A1 and SLCO1B1 in drug metabolism, these genetic findings have potential clinical importance. In analyses for association with gallbladder disease or gallstones, top bilirubin SNPs in UGT1A1 and SLCO1B1 were not associated.

  L Ay , V. A. A Van Houten , E. A. P Steegers , A Hofman , J. C. M Witteman , V. W. V Jaddoe and A. C. S. Hokken Koelega

Objectives: The objectives of the study was to examine which parental, fetal, and postnatal characteristics are associated with fat and lean mass at the age of 6 months and examine the effect of growth (catch-down, catch-up) in fetal life and early infancy on fat and lean mass.

Design: This study was embedded in the Generation R Study, a prospective cohort study from early fetal life onward. Body composition was measured by dual-energy X-ray absorptiometry in 252 infants at 6 months. Parental, fetal, and postnatal data were collected by physical and fetal ultrasound examinations and questionnaires.

Results: Children with fetal catch-up in weight (gain in weight sd score >0.67) in the second trimester tended to have a higher fat mass percentage [FM(%)] at 6 months of age, whereas children with fetal catch-down in weight had a lower FM(%) compared with nonchangers. In the third trimester, both catch-up and catch-down in weight were associated with an increase in FM(%) at 6 months. Children with catch-down in the third trimester had a greater risk for postnatal catch-up in weight greater than 0.67 sd score. Birth weight and weight at 6 wk were positively associated with fat mass at 6 months. Postnatal catch-up in weight within 6 wk after birth had the highest association with total and truncal FM(%) at 6 months. Total and truncal FM were higher in girls.

Conclusion: Catch-down in weight in the third trimester was strongly associated with postnatal catch-up within 6 wk after birth, and both were associated with an increase in fat mass at the age of 6 months. Our study shows that fetal as well as postnatal growth patterns are associated with body composition in early childhood.

  N Wolff , A. S Darlington , J Hunfeld , F Verhulst , V Jaddoe , A Hofman , J Passchier and H. Tiemeier

Objective To investigate the effect of child temperament, maternal psychologic symptoms, maternal chronic pain, and parenting stress on children's somatic complaints. Methods The study was embedded in the Generation R Study, a population-based cohort study. Child somatic complaints were assessed via mother-report in 5,171 children of 18 months of age. Questionnaires assessed maternal somatic symptoms, symptoms of depression, anxiety during pregnancy and 2 months after delivery, maternal chronic pain during pregnancy, parenting stress 18 months after birth, and mother-reported child temperament 6 months after birth, as the determinants. Results Fearful temperament, temperamental falling reactivity, maternal somatic symptoms, anxiety symptoms, and parenting stress each independently and prospectively increased the likelihood of children's somatic complaints at 18 months of age. Conclusions In toddlers, temperament, maternal stress, and maternal somatic symptoms seem particularly important for the development of somatic complaints, but long-term research is needed to establish causality and predictive value of these factors.

Copyright   |   Desclaimer   |    Privacy Policy   |   Browsers   |   Accessibility