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My main research interest is to study gene-environment interactions that have implications on maternal, foetal and child health. I'm a PhD student registered at the Dept. of Environmental Medicine, Karolinska Institutet, but I work full-time at CHESS.
Chronic diseases are a severe public health problem worldwide. The available evidence on the aetiology of chronic diseases indicates an important role for interactions between genes and the environment, including lifestyle and socio-economic circumstances, often leading to intergenerational health effects. Socioeconomic inequalities in health are observed within both high and low income countries as well as across regions globally. Even in industrialised nations with little absolute poverty, health inequalities that span the socioeconomic spectrum exist. So far, very little is known about the genetic contributions to health inequalities. Genetic factors can contribute to health inequalities if 1. Socioeconomic position (SEP), gender and/or ethnicity are associated with one or more genotypes and 2. These genotypes are themselves causally involved in the occurrence of health problems. Both conditions must be fulfilled. Genetic factors can also contribute to social inequalities in health if genotypes interact with risk factors in the social or physical environment, even when no genetic differences between socioeconomic groups exist. A more specific hypothesis concerning possible role of genetic factors in health inequalities is through personal attributes and gene-environmental interactions influencing social mobility.
A relatively new area of research, aptly termed 'life course epidemiology' studies the long-term biological, behavioural and psychosocial processes that link adult health and disease susceptibility to physical and social exposures acting during prenatal and early life. A number of published studies, many rooted in life course epidemiological models have suggested that impaired foetal growth is likely to increase the risk of several diseases including type 2 diabetes, stroke, hypertension, coronary heart disease and osteoporosis later in life. Sometimes, diseases may arise through developmental plasticity which results in a 'mismatch' between foetal expectation of its postnatal environment and the actual postnatal environment. In-utero or early life environment may affect gene expression and lead to physiological or morphological phenotypes associated with disease. While research on the 'developmental origins of health and disease' (DOHaD) has provided many new insights into pathogenesis of disease, the significance of DOHaD for aetiology of health inequalities has not been fully explored.
Life course models and intergenerational studies provide a good framework to study the role of the environment and its interactions with genetic factors contributing to health inequalities. In such a framework, genetic factors predisposing to health problems can be considered as a disadvantage that accumulates or interacts with other disadvantages over the life course.
The projects included in my thesis are aimed at bridging a key knowledge gap in further studying and identifying markers of inappropriate developmental pathways set in utero. The main approach will be to study gene-environment interactions, and possible modifiers and confounders. The diseases chosen as outcomes in the studies have large health impacts in various strata of populations the world over. Better understanding of the mechanistic pathways and the intricate interplay between genes and the environment can help in timely intervention and reducing the burden of these diseases in the modern world.
Briefly, some of our research projects are focused on:
Studying if socioeconomic position is associated with serum levels of Apo A, Apo B, cholesterol and adiponectin in males and females, children and adults. (Study I)
If size at birth is associated with the above biomarkers in unrelated subjects and in sibling pairs. The strength of associations between size at birth and biomarkers under study differs between socioeconomic groups. (Study II)
Are associations of size at birth with glucose metabolism/insulin sensitivity and type 2 diabetes mediated by adiponectin serum levels and/or its genotypes and modified by socioeconomic position? (Study III)
Do offspring of women of immigrant origin residing in Sweden with a lower socioeconomic position and education, face greater risks of impaired foetal growth than the corresponding offspring of Swedish-born mothers? Does this difference in foetal growth leads to differences in blood pressure in the offspring during adolescence? (Study IV)
Main Supervisor: Prof. Ilona Koupil, CHESS, Stockholm.
Prof. Pär Sparen, Dept. of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm.
Dr. Sara Wedren, Dept. of Environmental Medicine, Karolinska Institutet, Stockholm.
Main Collaborators: Liisa Byberg, at the Dept. of Surgical Sciences, Uppsala University. Bianca De Stavola, Medical Statistics, Non-communicable Disease Epidemiology, both at the London School of Tropical Medicine and Hygiene, UK.
MSc in Molecular Biology, 2004. Umeå University, Sweden.
BSc in Biology and Chemistry, 2003. St. Joseph's College of arts and sciences, India.
2004 Project student at the Dept. of Neurovirology, Department of Neurovirology, National Institute of Mental Health and Neuroscience (NIMHANS), Bangalore, India (5 months). The construction and characterisation of a recombinant Baculovirus expressing the HIV p24 protein.
2005-2006 Project student, Department of Medical Biochemistry and Microbiology, Uppsala University. Project Title: Effects of deletions of Plasmodium falciparum HPPK-DHPS on protein activity. Studying the effects of deletions of the Plasmodium falciparum HPPK- DHPS gene on protein activity with the aim of accessing it as a potential drug target for the treatment of malaria.
2006 Project trainee, IMBIM, Uppsala University. Project Title: Cloning and generation of PilT and PilC1. Fusion proteins of Neisseria gonorrhoeae (6 months). My project dealt with the study of the pili genes of Neisseria gonnorhoeae that are important for bacterial adhesion and motility during infection.
2006-2007 Research assistant, Dept. of Clinical Chemistry, University Hospital, Uppsala, Sweden (5 months).
2007-2008 Stipendiate/research assistant, Department of Medical Epidemiology and Biostatistics, Karolinska Istitutet (9 months). "Genetic signature of response to adjuvant therapy in Breast Cancer".
November 15, 2011
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