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It is well documented that maternal environment is a key regulator of offspring development. The thrifty phenotype hypothesis put forth by Hales and Barker in 1992 states that suboptimal nutrition in early life leads to adverse metabolic consequences in adulthood (Hales and Barker 1992, Locke et al. 2015). They went on to show that fetal nutrient restriction results in increased cardiovascular risk, type 2 diabetes mellitus, and elevated cholesterol (Barker et al. 1993, Fall et al. 1995, Hales et al. 1991). These studies resulted in the broader developmental origins of health and disease hypothesis, which encompasses the idea that early life environment can result in long-term changes to the offspring (Gluckman and Hanson 2004), independent of genetics.
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