Abstract The Barker hypothesis asserts that stressful events early in the life history of an individual have negative health consequences later in adulthood. The hypothesis initially focused on prenatal stressors as indicated by birth weight and related outcomes. This initial concern with the fetal phase of development led to its description as the “fetal programming” or “fetal origins” hypothesis. The realization that stressors in the postnatal phase had similar impacts on adult health has led to its latest characterization as the Developmental Origins of Health and Disease Hypothesis (DOHaD). In this paper, we review the history and evidence in support of the DOHaD hypothesis. We then introduce an untapped source of information on early life stress: enamel hypoplasias and other developmental defects of enamel. Enamel defects are nearly indelible records of physiological perturbations, or stress, to developing ameloblasts (enamel‐forming cells). Furthermore, the location of the defects translates to specific periods of growth, providing a permanent temporal record of early life stressors from in utero to approximately twelve years of age. As we discuss, a handful of studies of different populations reveals that individuals with enamel defects that developed in utero and early in infant‐childhood development tend to be subject to earlier adolescent or adult mortality.
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