Idan Shalev, Ph.D.

Projects

Biological embedding of early-life experiences: How early-life experiences impact childhood development and can accelerate aging

A project funded by the Sara van Dam Foundation (Roseriet Beijers, Radboud University, Netherlands PI, Shalev Co-I). Its aim is to test early-life factors associated with children’s socio-emotional development, cognition, and pubertal development. This includes biological-embedding mechanisms underlying this link. These research questions are being investigated in the Dutch BIBO-study (Basal Influences on the Baby Development): a prospective study in which 193 mothers and their children are followed from pregnancy until the last assessment at age 10. My lab is conducting all telomere length testing in children at both age 6 and 10.

Complex interactions of behavior, genes, and environment in the multi-system characterization of the effects of sleep loss on health, cardio-metabolic disease risk, cognition, and the epigenome

The aim of this project is to comprehensively characterize cardio-metabolic, cognitive, genomic, and epigenetic effects of sleep insufficiency in a controlled laboratory setting. My lab assist with the collection and sorting of blood samples for DNA methylation and whole-genome expression analysis. For this study, we are further investigating specific type of cells including monocytes and lymphocytes.

Intergenerational transmission of trauma? Testing cellular aging in mothers exposed to sexual abuse and their children

The overarching goal is to test the hypothesis of intergenerational transmission of trauma by measuring cellular aging in both mothers and children, members of the Female Growth and Development Study. Specifically, we are testing telomere length in mothers exposed to sexual abuse, control mothers, and their children.

Temporal genomics mechanisms underlying disease and aging

The goal of this project is to identify genomic mechanisms involved in young adults’ response to stress, as moderated by early adversity. Specifically, we are testing whether individuals exposed to early-life adversity show dysregulated changes in gene expression in response to a well-established laboratory stressor, compared with a no-stress condition, and compared with individuals without exposure to early adversity.

Child Maltreatment and Cardiovascular Disease Risk

This grant (R01HL158577; PI: Schreier) takes advantage of a large, well-characterized, prospective cohort of youth who were recently investigated for child maltreatment and comparison youth without a maltreatment history to better understand the physiological mechanisms between early adversity and cardiovascular diseases risk. By taking advantage of detailed assessments of immune function coupled with administrative health care records and thorough behavioral and psychosocial assessments, we will prospectively examine links between child maltreatment and cardiovascular disease risk, with the hopes of informing future prevention and intervention efforts.

Selected Publications

• Shalev, I. (2012). Early life stress and telomere length: investigating the connection and possible mechanisms: a critical survey of the evidence base, research methodology and basic biology. Bioessays, 34(11), 943-952.

• Shalev, I., Moffitt, T. E., Sugden, K., Williams, B., Houts, R. M., Danese, A., ... & Caspi, A. (2013). Exposure to violence during childhood is associated with telomere erosion from 5 to 10 years of age: a longitudinal study. Molecular Psychiatry, 18(5), 576.

• Shalev, I., Moffitt, T. E., Braithwaite, A. W., Danese, A., Fleming, N. I., Goldman-Mellor, S., ... & Robertson, S. P. (2014). Internalizing disorders and leukocyte telomere erosion: a prospective study of depression, generalized anxiety disorder and post-traumatic stress disorder. Molecular Psychiatry, 19(11), 1163.

• Shalev, I., & Belsky, J. (2016). Early-life stress and reproductive cost: a two-hit developmental model of accelerated aging? Medical Hypotheses, 90, 41-47.

• Shalev, I., Heim, C. M., & Noll, J. G. (2016). Child maltreatment as a root cause of mortality disparities: a call for rigorous science to mobilize public investment in prevention and treatment. JAMA Psychiatry, 73(9), 897-898.