Developmental origins of metabolic disease

8 pillars according to Kent L. Thornburg, MS, PhD, FAPS, Oregon Health & Science University

Pillar 1: We all carry a genetic burden from our parents and grandparents, with most money spent on late-stage prevention rather than early-stage prevention.

Pillar 2: Birthweight associations reveal that average-term births are least associated with disease, while high- and low-birth-weight babies have an increased risk of obesity, forming a U-shaped curve.

Pillar 3: While birthweight can serve as a proxy for development, other parental influences, such as maternal body profile, can also be significant. Paternal effects, including epigenetic changes, should not be overlooked.

Pillar 4: Gestational stresses are linked to adverse events in offspring, including fetal hypoxia, toxic chemicals, social stress, malnutrition, and other stressors.

Pillar 5: Environmental stressors can impact genes through epigenetic modifications, such as DNA methylation, histone modifications, and microRNAs. DNA methylation is the most easily studied of these mechanisms.

Pillar 6: The effects of stressors during pregnancy can last at least a century, with trans-generational effects on pregnancy since the fetal germline will also be affected beyond its impact on the fetus.

Pillar 7: Stressors in the womb contribute significantly to chronic disease prevalence in the US, exacerbating the increased incidence of chronic diseases.

Pillar 8: While stressors in utero increase the incidence of chronic disease, reversing these stressors can help alleviate the occurrence of disease.

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