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Stephen Buka

Stephen Buka

· Professor of EpidemiologyVerified

Brown University · Microbiology and Immunology

Active 1987–2025

h-index101
Citations42.3k
Papers59357 last 5y
Funding$17.8M1 active
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About

Stephen L. Buka, ScD, is a Professor and was the Founding Chair of the Department of Epidemiology at the Brown University School of Public Health. His work centers on the causes and prevention of neuropsychiatric disorders, with extensive research in neuropsychology and psychiatric epidemiology. Dr. Buka has directed several major longitudinal studies examining the impact of birth complications, environmental hazards, and socioeconomic conditions on behavioral and intellectual development. He originated and directs the New England Family Study, a prospective, three-generation study involving over 5000 participants, which combines a family design, discordant sibling sets, molecular genetics, biological assays, psychiatric, neuropsychological, and functional imaging assessments. Additionally, Dr. Buka has served as Principal Investigator for the National Children’s Study at multiple sites and has been involved in the NCS Executive Steering Committee for seven years. He has served on several Institute of Medicine expert committees and in advisory roles to multiple federal and state agencies.

Research topics

  • Medicine
  • Internal medicine
  • Psychology
  • Environmental health
  • Obstetrics
  • Biology
  • Psychiatry
  • Statistics
  • Developmental psychology
  • Physiology
  • Pediatrics
  • Physics
  • Social psychology
  • Genetics
  • Mathematics
  • Medical emergency
  • Pathology
  • Demography

Selected publications

  • The impact of early childhood adversity on adult cognitive performance: The mediating roles of childhood cognitive ability and educational attainment

    Social Science & Medicine · 2025-07-21

    article
  • Functional redundancy of the posterior hippocampi is selectively disrupted in non-demented older adults with β-amyloid deposition

    Neuroimage Reports · 2025-03-23

    articleOpen access

    deposition. Further, our findings indicate that functional redundancy may underscore a network metric different from global functional connectivity of the LFC.

  • MIR137 polygenic risk for schizophrenia and ephrin-regulated pathway: Role in lateral ventricles and corpus callosum volume

    International Journal of Clinical and Health Psychology · 2024-04-01 · 4 citations

    articleOpen access

    Background/Objective. Enlarged lateral ventricle (LV) volume and decreased volume in the corpus callosum (CC) are hallmarks of schizophrenia (SZ). We previously showed an inverse correlation between LV and CC volumes in SZ, with global functioning decreasing with increased LV volume. This study investigates the relationship between LV volume, CC abnormalities, and the microRNA MIR137 and its regulated genes in SZ, because of MIR137’s essential role in neurodevelopment. Methods. Participants were 1224 SZ probands and 1466 unaffected controls from the GENUS Consortium. Brain MRI scans, genotype, and clinical data were harmonized across cohorts and employed in the analyses. Results. Increased LV volumes and decreased CC central, mid-anterior, and mid-posterior volumes were observed in SZ probands. The MIR137-regulated ephrin pathway was significantly associated with CC:LV ratio, explaining a significant proportion (3.42 %) of CC:LV variance, and more than for LV and CC separately. Other pathways explained variance in either CC or LV, but not both. CC:LV ratio was also positively correlated with Global Assessment of Functioning, supporting previous subsample findings. SNP-based heritability estimates were higher for CC central:LV ratio (0.79) compared to CC or LV separately. Discussion. Our results indicate that the CC:LV ratio is highly heritable, influenced in part by variation in the MIR137-regulated ephrin pathway. Findings suggest that the CC:LV ratio may be a risk indicator in SZ that correlates with global functioning.

  • Mir137 Polygenic Risk for Schizophrenia and Ephrin-Regulated Pathway: Role in Lateral Ventricles and Corpus Callosum Volume

    SSRN Electronic Journal · 2024-01-01

    preprintOpen access
  • Prenatal immune origins of brain aging differ by sex

    Molecular Psychiatry · 2024-11-21 · 5 citations

    articleOpen access

    With an increasing aging population and Alzheimer's disease tsunami, it is critical to identify early antecedents of brain aging to target for intervention and prevention. Women and men develop and age differently, thus using a sex differences lens can contribute to identification of early risk biomarkers and resilience. There is growing evidence for fetal antecedents to adult memory impairments, potentially through disruption of maternal prenatal immune pathways. Here, we hypothesized that in utero exposure to maternal pro-inflammatory cytokines will have sex-dependent effects on specific brain circuitry regulating offspring's memory and immune function that will be retained across the lifespan. Using a unique prenatal cohort, we tested this in 204 adult offspring, equally divided by sex, who were exposed/unexposed to an adverse in utero maternal immune environment and followed into early midlife (~age 50). Functional magnetic resonance imaging results showed exposure to pro-inflammatory cytokines in utero (i.e., higher maternal IL-6 and TNF-α levels) was significantly associated with sex differences in brain activity and connectivity underlying memory circuitry and performance and with a hyperimmune state, 50 years later. In contrast, the anti-inflammatory cytokine, IL-10 alone, was not significantly associated with memory circuitry in midlife. Predictive validity of prenatal exposure was underscored by significant associations with age 7 academic achievement, also associated with age 50 memory performance. Results uniquely demonstrated that adverse levels of maternal in utero pro-inflammatory cytokines during a critical period of the sexual differentiation of the brain produced long-lasting effects on immune function and memory circuitry/function from childhood to midlife that were sex-dependent, brain region-specific, and, within women, reproductive stage-dependent.

  • Quality of parental emotional care and calculated risk for coronary heart disease

    UNC Libraries · 2024-04-05

    articleOpen accessSenior author

    Objective: To evaluate associations between perceived quality of parental emotional care and calculated 10-year risk for coronary heart disease (CHD). Little is understood about the role of parental emotional care in contributing to the risk for CHD. Methods: The study sample was composed of 267 participants from the New England Family Study. Quality of parental emotional care was measured, using a validated short version of the Parental Bonding Instrument (PBI) as the average care scores for both parents (range = 0-12), with higher scores indicating greater care. Ten-year CHD risk was calculated, using the validated Framingham Risk Algorithm that incorporates the following prevalent CHD risk factors: age, sex, diabetes, smoking, total cholesterol, high-density lipoprotein cholesterol, and blood pressure. Multiple linear regression assessed associations of PBI with calculated CHD risk after adjusting for childhood socioeconomic status, depressive symptomatology, educational attainment, and body mass index. Results: Among females, a 1-unit increase in the parental emotional care score resulted in a 4.6% (p =.004) decrease in the 10-year CHD risk score, after adjusting for covariates. There was no association between parental emotional care score and calculated CHD risk score in males (p =.22). Conclusion: Quality of parental emotional care was inversely associated with calculated 10-year CHD risk in females, and not males. Although the gender differences need further investigation and these findings require replication, these results suggest that the early childhood psychosocial environment may confer risk for CHD in adulthood.

  • Mother's affection at 8 months predicts emotional distress in adulthood

    UNC Libraries · 2024-04-05

    articleOpen access

    Background Long-standing theory suggests that quality of the mother's (or primary caregiver's) interaction with a child is a key determinant of the child's subsequent resilience or vulnerability and has implications for health in adulthood. However, there is a dearth of longitudinal data with both objective assessments of nurturing behaviour during infancy and sustained follow-up ascertaining the quality of adult functioning. Methods We used data from the Providence, Rhode Island birth cohort of the National Collaborative Perinatal Project (mean age 34 at follow-up, final N=482) to conduct a prospective study of the association between objectively measured affective quality of the mothereinfant interaction and adult mental health. Infantemother interaction quality was rated by an observer when infants were 8 months old, and adult emotional functioning was assessed from the Symptom Checklist-90, capturing both specific and general types of distress. Results High levels of maternal affection at 8 months were associated with significantly lower levels of distress in adult offspring (1/2 standard deviation; b=-4.76, se=1.7, p<0.01). The strongest association was with the anxiety subscale. Mother's affection did not seem to be on the pathway between lower parental SES and offspring distress. Conclusion These findings suggest that early nurturing and warmth have long-lasting positive effects on mental health well into adulthood.

  • Religious service attendance and spiritual well-being are differentially associated with risk of major depression

    UNC Libraries · 2024-04-05

    articleOpen access

    Background: The complex relationships between religiosity, spirituality and the risk of DSM-IV depression are not well understood. Method: We investigated the independent influence of religious service attendance and two dimensions of spiritual well-being (religious and existential) on the lifetime risk of major depression. Data came from the New England Family Study (NEFS) cohort (n=918, mean age=39 years). Depression according to DSM-IV criteria was ascertained using structured diagnostic interviews. Odds ratios (ORs) for the associations between high, medium and low tertiles of spiritual well-being and for religious service attendance and the lifetime risk of depression were estimated using multiple logistic regression. Results: Religious service attendance was associated with 30% lower odds of depression. In addition, individuals in the top tertile of existential well-being had a 70% lower odds of depression compared to individuals in the bottom tertile. Contrary to our original hypotheses, however, higher levels of religious well-being were associated with 1.5 times higher odds of depression. Conclusions: Religious and existential well-being may be differentially associated with likelihood of depression. Given the complex interactions between religiosity and spirituality dimensions in relation to risk of major depression, the reliance on a single domain measure of religiosity or spirituality (e.g. religious service attendance) in research or clinical settings is discouraged.

  • Involuntary tobacco smoke exposures from conception to 18 years increase midlife cardiometabolic disease risk: a 40-year longitudinal study

    Journal of Developmental Origins of Health and Disease · 2023-12-01 · 2 citations

    articleOpen access

    Abstract Few population studies have sufficient follow-up period to examine early-life exposures with later life diseases. A critical question is whether involuntary exposure to tobacco smoke from conception to adulthood increases the risk of cardiometabolic diseases (CMD) in midlife. In the Collaborative Perinatal Project, serum-validated maternal smoking during pregnancy (MSP) was assessed in the 1960s. At a mean age of 39 years, 1623 offspring were followed-up for the age at first physician-diagnoses of any CMDs, including diabetes, heart disease, hypertension, or hyperlipidemia. Detailed information on their exposure to environmental tobacco smoke (ETS) in childhood and adolescence was collected with a validated questionnaire. Cox regression was used to examine associations of in utero exposure to MSP and exposure to ETS from birth to 18 years with lifetime incidence of CMD, adjusting for potential confounders. We calculated midlife cumulative incidences of hyperlipidemia (25.2%), hypertension (14.9%), diabetes (3.9%), and heart disease (1.5%). Lifetime risk of hypertension increased by the 2 nd -trimester exposure to MSP (adjusted hazard ratio: 1.29, 95% confidence interval: 1.01–1.65), ETS in childhood (1.11, 0.99–1.23) and adolescence (1.22, 1.04–1.44). Lifetime risk of diabetes increased by joint exposures to MSP and ETS in childhood (1.23, 1.01–1.50) or adolescence (1.47, 1.02–2.10). These associations were stronger in males than females, in never-daily smokers than lifetime ever smokers. In conclusion, early-life involuntary exposure to tobacco smoke increases midlife risk of hypertension and diabetes in midlife.

  • Adverse birth outcomes related to concentrations of per- and polyfluoroalkyl substances (PFAS) in maternal blood collected from pregnant women in 1960–1966

    Environmental Research · 2023-09-09 · 22 citations

    articleSenior authorCorresponding

Recent grants

Frequent coauthors

  • Jill M. Goldstein

    Harvard University

    359 shared
  • Larry J. Seidman

    Beth Israel Deaconess Medical Center

    311 shared
  • Ming T. Tsuang

    230 shared
  • William J. Culpepper

    Veterans Health Administration

    171 shared
  • Lorene M. Nelson

    171 shared
  • Nicholas G. LaRocca

    National Multiple Sclerosis Society

    171 shared
  • Laurie Wagner

    McKing Consulting (United States)

    171 shared
  • Helen Tremlett

    University of British Columbia

    171 shared

Education

  • Other, Epidemiology

    Brown University School of Public Health

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