Fetal Origins Hypothesis: Mother's Environment May Cause COPD

Health Professional

Researchers are working overtime to learn what causes COPD. The Fetal Origins Hypothesis suggests it all begins in the uterus as the fetus adjusts to its environment. Such adjustments may predispose the fetus to chronic diseases like asthma and COPD later in life.

During the 1950s and 1960s, physicians thought the placenta was a natural barrier that protected unborn babies from the mother’s environment; that it protected the fetus from anything bad ingested or inhaled; that it only allowed good substances, such as essential nutrients, to get to the fetus.

It was based on this old theory that caused physicians, or at least many of them, to remain indifferent to a mother’s nutritional status.  If anything, it was prefered they didn’t gain too much weight. Physicians also remained unconcerned about mothers having a few drinks or inhaling cigarette smoke. In fact, during the 1960s, about half of expectant mothers reported smoking cigarettes.

However, by the 1990s an abounding amount of evidence started to show that this theory was probably poppycock, that the placenta was not a natural barrier, and that anything the mother inhaled or ingested could have a major impact on the growth and development of the fetus, especially during the first trimester.

In 1992, Dr. David J. Barker became the first person to seriously consider this new evidence. He postulated that undernourished infants tended to have small birth weights and were likely to have trouble with obesity later in life. This became known as Barker’s Hypothesis. This hypothesis was later expanded upon to include other chronic diseases, and is now referred to as the Fetal Origins Hypothesis.

Barker believed inadequate nutrition programmed the fetus’s to develop metabolic changes that would predispose the unborn baby to chronic diseases later in life. Others suspected gene mutations leading to physiologic and metabolic changes that prevent the child from reaching a healthy birth weight.

A good example here is COPD. The hypothesis suggest that changes made in utero as fetus’s attempt to adapt to their mother’s environments cause airway changes that prevent these children from obtaining peak lung function by early adulthood.  It is these children who are most likely to develop COPD when chronically exposed to harmful substances in the air.

Subsequent studies have linked small birth weights with decreased lung function and increased risk for respiratory symptoms (wheezing, shortness of breath) in childhood.  Other studies have small birth weights with the development of asthma later in life. It should also be understood here that researchers suspect up to 15 links between asthma and COPD.

There exist other interesting facets of this hypothesis. For instance, it suggests that the nine months in utero are the most critical in a person’s life.  It suggests that the mother’s environment may have a significant impact not just on the development of chronic diseases later in life, but also on a child’s future life, maybe even determining the child’s level of intelligence and future abilities.

While it’s just one hypothesis, it seems to be well accepted by the scientific and medical communities. It shows the importance of ingesting a healthy diet and inhaling healthy air on the future health and abilities of unborn babies. Perhaps future research in this regard will lead to an end to diseases like asthma and COPD.

Here are my references and some further reading you may enjoy:

15 Links Between Asthma and COPD

Impact of Genes on COPD

Links Between Asthma and Genetics

NCBI:  Killing Me Softly: The Fetal Origins Hypothesis

NCBI: Early Life Influences on the Development of COPD

NCBI: Early Origins Or Chronic Pulmonary Disease

NCBI: The Fetal Origins of Adult Disease: A Narrative Review of the Epidemiological Literature

NCBI: Effects of Low Birth Weight on Childhood Asthma