“Extension of the “Fetal Origin Hypothesis of Barker” towards the “Fetal Origin Hypothesis of Mental Diseases”

Vincent Van Ginneken,Clemens Löwik

doi:10.31579/2637-8892/033

Abstract

In this editorial we will first describe most common information about the intriguing “traditional” fetal origin hypothesis of Barker for physiological, endocrine and cardiovascular diseases (CVDs). The ‘developmental origins of adult disease’ hypothesis, often called the ‘Barker hypothesis’, states that adverse inﬂuences early in development, and particularly during intrauterine life, can result in permanent changes in physiology and metabolism, which result in increased disease risk in adulthood.

Highlights

In this editorial we will first describe most common information about the intriguing “traditional” fetal origin hypothesis of Barker for physiological, endocrine and cardiovascular diseases (CVDs)
This hypothesis originally evolved from observations by Barker and colleagues that the regions in England that had the highest rates of infant mortality in the early twentieth century had the highest rates of mortality from coronary heart disease decades later [1]
As the most commonly registered cause of infant death at the start of the twentieth century was low birthweight, these observations led to the hypothesis that low birthweight babies who survived infancy and childhood might be at increased risk of coronary heart disease later in life

Summary

Introduction

In this editorial we will first describe most common information about the intriguing “traditional” fetal origin hypothesis of Barker for physiological, endocrine and cardiovascular diseases (CVDs). The theory of fetal origins or prenatal programming of later at adult age life developing diseases was based on in utero nutritional deficiencies.

Results

Conclusion