Developmental origins of adult disease

The “developmental origins of adult disease” model (also called “fetal origins of adult disease” hypothesis or "developmental origins of adult disease" hypothesis) postulates links between fetal growth and the development of other diseases in adult life, including hypertension, type 2 diabetes, obesity, osteoporosis, depression, and schzophrenia (Gluckman et al, 2005). According to this hypothesis, stressors (including malnutrition, overnutrition, and glycemic variance related to gestational diabetes mellitus) at critical periods of development lead to “fetal programming,” or permanent metabolic and structural changes. One mechanism proposed for this "fetal programming" is epigenic modifications to the underlying genes that impact phenotype without a change in genotype (Bianco-Miotto et al, 2017).

It is now widely accepted that the intrauterine environment influences fetal development and has long-lasting effects on health and disease. Infants that are exposed to stressors in utero are predisposed to develop noncommunicable diseases later in life and expose the next generation to similar stressors creating a cycle that contributes to the spread of metabolic diseases worldwide. (El Hajj et al, 2014)