Cellular commitment to a specific lineage is controlled by differential 
silencing of genes, which in turn depends on epigenetic processes such as DNA 
methylation and histone modification. During early embryogenesis, the mammalian 
genome is 'wiped clean' of most epigenetic modifications, which are 
progressively re-established during embryonic development. Thus, the epigenome 
of each mature cellular lineage carries the record of its developmental history. 
The subsequent trajectory and pattern of development are also responsive to 
environmental influences, and such plasticity is likely to have an epigenetic 
basis. Epigenetic marks may be transmitted across generations, either directly 
by persisting through meiosis or indirectly through replication in the next 
generation of the conditions in which the epigenetic change occurred. 
Developmental plasticity evolved to match an organism to its environment, and a 
mismatch between the phenotypic outcome of adaptive plasticity and the current 
environment increases the risk of metabolic and cardiovascular disease. These 
considerations point to epigenetic processes as a key mechanism that underpins 
the developmental origins of chronic noncommunicable disease. Here, we review 
the evidence that environmental influences during mammalian development lead to 
stable changes in the epigenome that alter the individual's susceptibility to 
chronic metabolic and cardiovascular disease, and discuss the clinical 
implications.