Fetal Origins Hypothesis

The fetal origins hypothesis (differentiated from the developmental origins of health and disease hypothesis, which emphasizes environmental conditions both before and immediately after birth) proposes that the period of gestation has significant impacts on the developmental health and wellbeing outcomes for an individual ranging from infancy to adulthood. The effects of fetal origin are marked by three characteristics: latency, wherein effects may not be apparent until much later in life; persistency, whereby conditions resulting from a fetal effect continue to exist for a given individual; and genetic programming, which describes the 'switching on' of a specific gene due to prenatal environment. Research in the areas of economics, epidemiology, and epigenetics offer support for the hypothesis.

The fetus was once believed to be a "perfect parasite," immune to harmful environmental toxins passed from the mother via the placenta. Stemming from this belief, pregnant women of the early to mid 20th century freely drank alcohol, ingested medications, smoked cigarettes, and were largely ignorant of any nutritional needs for a developing fetus. This easy going attitude about pregnancy was challenged, however, by findings relating substances ingested by a mother to tragic outcomes for a fetus. The birth defects crisis due to the medication thalidomide in the 1960s, where thousands of children were born with defects ranging from brain damage to truncated and missing arms and legs is an example of how a seemingly miracle medication supposed to prevent morning sickness instead had disastrous consequences. Similarly, in 1971, a drug known as DES, diethylstilbestrol, when taken by pregnant women, was found to be causing an incredibly rare vaginal cancer known as clear-cell aadenocarcinoma in young girls when the cancer was traditionally only found to affect those of post-menopausal age. This finding, in particular, demonstrates that events occurring during gestation are capable of impacting future health into adulthood. As perhaps the most well-known fetal risk, It wasn't until 1973 that fetal alcohol syndrome was first formally diagnosed, and not until 1989 that the United States government began requiring warning labels directed at pregnant women to be in place on all alcoholic beverages for sale. While the risks associated with certain substances have been well documented during pregnancy, the fetal origins hypothesis goes beyond medical substances to expand upon the effects of maternal stress, obesity, influenza, nutrition, and pollution on a developing fetus.

Epidemiologist David Barker was the earliest proponent of the theory of fetal origins of adult disease, prompting the theory to be denoted as "Barker's hypothesis". In 1986, Barker published findings proposing a direct link between prenatal nutrition and late-onset coronary heart disease. He had noticed that the poorest areas of England were the same areas with the highest rates of heart disease, unearthing the predictive relationship between low birth weight and adult disease. His findings were met with criticism, mainly because at the time heart disease was considered to be predominantly determined by lifestyle and genetic factors. Since Barker's initial findings, the results have been replicated in diverse populations of Europe, Asia, North American, Africa, and Australia. In explanation of such findings, Barker suggests that fetuses learn to adapt to the environment they expect to enter into once outside of the womb. Essentially, all transmissions entering the placenta act as "postcards" giving the fetus clues as to the outside world, preparing its physiology appropriately. This can be an adaptive mechanism, when fetal conditions accurately represent the world of birth; alternatively, it can be a harmful mechanism, when fetal conditions of plenitude or scarcity do not match the world of birth and the child has been physiologically predisposed to inhabit an environment where expected resources are drastically different from reality.

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