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      Perinatal Origins of Adult Disease and Opportunities for Health Promotion: A Narrative Review

      , ,
      Journal of Personalized Medicine
      MDPI AG

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          Abstract

          The “developmental origins of health and disease” (DOHaD) hypothesis refers to the influence of early developmental exposures and fetal growth on the risk of chronic diseases in later periods. During fetal and early postnatal life, cell differentiation and tissue formation are influenced by several factors. The interaction between genes and environment in prenatal and early postnatal periods appears to be critical for the onset of multiple diseases in adulthood. Important factors influencing this interaction include genetic predisposition, regulation of gene expression, and changes in microbiota. Premature birth and intrauterine growth restriction (IUGR) are other important factors considered by the DOHaD hypothesis. Preterm birth is associated with impaired or arrested structural or functional development of key organs/systems, making preterm infants vulnerable to cardiovascular, respiratory, and chronic renal diseases during adulthood. Growth restriction, defined as impaired fetal growth compared to expected biological potential in utero, is an additional negative factor increasing the risk of subsequent diseases. Environmental factors implicated in the developmental programming of diseases include exposure to pollution, stress, drugs, toxic agents, nutrition, and exercise. The DOHaD may explain numerous conditions, including cardiovascular, metabolic, respiratory, neuropsychiatric, and renal diseases. Potential antenatal and postnatal preventive measures, interventions, and future directions are discussed.

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          Abdominal visceral and subcutaneous adipose tissue compartments: association with metabolic risk factors in the Framingham Heart Study.

          Visceral adipose tissue (VAT) compartments may confer increased metabolic risk. The incremental utility of measuring both visceral and subcutaneous abdominal adipose tissue (SAT) in association with metabolic risk factors and underlying heritability has not been well described in a population-based setting. Participants (n=3001) were drawn from the Framingham Heart Study (48% women; mean age, 50 years), were free of clinical cardiovascular disease, and underwent multidetector computed tomography assessment of SAT and VAT volumes between 2002 and 2005. Metabolic risk factors were examined in relation to increments of SAT and VAT after multivariable adjustment. Heritability was calculated using variance-components analysis. Among both women and men, SAT and VAT were significantly associated with blood pressure, fasting plasma glucose, triglycerides, and high-density lipoprotein cholesterol and with increased odds of hypertension, impaired fasting glucose, diabetes mellitus, and metabolic syndrome (P range < 0.01). In women, relations between VAT and risk factors were consistently stronger than in men. However, VAT was more strongly correlated with most metabolic risk factors than was SAT. For example, among women and men, both SAT and VAT were associated with increased odds of metabolic syndrome. In women, the odds ratio (OR) of metabolic syndrome per 1-standard deviation increase in VAT (OR, 4.7) was stronger than that for SAT (OR, 3.0; P for difference between SAT and VAT < 0.0001); similar differences were noted for men (OR for VAT, 4.2; OR for SAT, 2.5). Furthermore, VAT but not SAT contributed significantly to risk factor variation after adjustment for body mass index and waist circumference (P < or = 0.01). Among overweight and obese individuals, the prevalence of hypertension, impaired fasting glucose, and metabolic syndrome increased linearly and significantly across increasing VAT quartiles. Heritability values for SAT and VAT were 57% and 36%, respectively. Although both SAT and VAT are correlated with metabolic risk factors, VAT remains more strongly associated with an adverse metabolic risk profile even after accounting for standard anthropometric indexes. Our findings are consistent with the hypothesized role of visceral fat as a unique, pathogenic fat depot. Measurement of VAT may provide a more complete understanding of metabolic risk associated with variation in fat distribution.
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            WEIGHT IN INFANCY AND DEATH FROM ISCHAEMIC HEART DISEASE

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              Long-term consequences of breastfeeding on cholesterol, obesity, systolic blood pressure and type 2 diabetes: a systematic review and meta-analysis.

              To systematically review the evidence on the associations between breastfeeding and overweight/obesity, blood pressure, total cholesterol and type 2 diabetes.
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                Author and article information

                Contributors
                (View ORCID Profile)
                Journal
                JPMOB3
                Journal of Personalized Medicine
                JPM
                MDPI AG
                2075-4426
                February 2022
                January 25 2022
                : 12
                : 2
                : 157
                Article
                10.3390/jpm12020157
                35207646
                dd1b0b26-9ee5-4829-aeb6-91264838b5f6
                © 2022

                https://creativecommons.org/licenses/by/4.0/

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