Unravelling the Genetic and Environmental Factors in Early-Life Development and Future Disease Risk

Current therapeutic strategies for common diseases, such as cardiometabolic, immunological, and psychiatric diseases, primarily address symptoms after they manifest. The Developmental Origins of Health and Disease (DOHaD) hypothesis proposes that adverse prenatal or early-life environments increase the risk of diseases later in life. While early adverse environmental exposures are associated with long-term health effects, the mechanisms linking these early risk factors to offspring health are not fully understood. Recent genetic epidemiological methods, e.g. Mendelian randomization and discordant twin studies, are exploring this potential causal relationship. Additionally, evidence suggests that genetic pleiotropy, where genes influence both early exposures and disease risk, may underlie this link.

Understanding the genetics of early risk factors is vital for uncovering the link between prenatal or early postnatal environments and future disease risk. Employing statistical genetic models to assess causality will provide a clearer understanding of modifiable risk factors in early life. This comprehension can guide preventive strategies aimed at early-life stages to reduce long-term disease risk, potentially transitioning focus from symptom management post-onset to early intervention and personalized medicine.

Scope:

1. Genetic and environmental determinants of fetal growth and development.
2. Mechanisms linking adverse prenatal and early-life environments to long-term health outcomes.
3. Genetic pleiotropy and its role in the relationship between early-life exposures and disease risk.
4. Application of genetic epidemiological methods—including instrumental variables (such as Mendelian randomization), family-based studies, cross-contextual designs, negative controls, and natural experiments—can effectively elucidate causal relationships. Mendelian randomization studies, in particular, must include appropriate validation. Acceptable forms of validation include: independent clinical or patient cohorts, or biological validation, either in vitro or in vivo. Moreover, Mendelian Randomization studies need to be accompanied by a completed STROBE-MR checklist to ensure rigor and transparency (https://www.strobe-mr.org/).
5. Intervention strategies targeting early-life stages to mitigate future disease risk.
6. Personalized medicine approaches based on genetic and environmental risk factors in early life.

Types of Manuscripts:
1. Original research articles
2. Review
3. Brief Research Report
4. Correction
5. Editorial
6. General Commentary
7. Methods
8. Mini Review
9. Opinion
10. Systematic Review