The Prenatal Environment Influences Adulthood Disease

A developing fetus.

The maternal environment affects prenatal development. Many of the effects are not seen until the onset of adulthood diseases such as hypertension. Telomere length may be one potential way to measure prenatal stress and predict the adulthood diseases implicated.


A bounty of new research suggests that stresses placed on an embryo during development can play a factor in disease development up to two generations away.  A team of researchers in the Development, Health and Disease Research Program at the University of California, Irvine have been studying the role that prenatal stress plays in disease risk as well as the part that telomeres play in signaling the subsequent disease risk. Their research appeared in Science Signaling as a presentation (Prenatal Stress, Telomere Biology, and Fetal Programming of Health and Disease Risk, 2012.  Sonja Entringer, et al.). Furthermore, an article appearing in the January 2013 issue of Hypertension found that mice predisposed to hypertension through a maternal low protein diet during pregnancy had higher blood pressure during sympathetic nervous system activation of the cardiovascular system (Prenatal Programming of Hypertension Induces Sympathetic Overactivity in Response to Physical Stress, 2013. Masaki Mizuno, et al.).

Determining the causations of disease alone is challenging.  However, identifying causations of disease during fetal development is particularly challenging because of the interactions between the developing fetus and maternal environment. This is called reciprocal determinism. The two interacting genotypes that result in reciprocal determinism are the maternal genotype and fetal genotype. Stresses that factor into the health outcome of the developing fetus can be categorized by nutrition, infection and psychosocial. They interact with the endocrine and immune systems to affect fetal development. Stress during prenatal development may cause a variety of diseases in adulthood including hypertension, coronary artery disease and diabetes. Studies have previously observed an association between abnormal birth phenotype (i.e. low birthweight) and adulthood diseases. Stresses during fetal development may explain this association. A model of the prenatal environment effects on birth phenotype and adulthood disease is shown in the figure below.

model of effects of prenatal environment.  Explains a correlation observed between abnormal birth phenotype and development of disease later in adulthood.

A plethora of recent human studies have implicated prenatal stress with detrimental affects on cognitive, immune, endocrine and metabolic function.  Researchers are now looking at the role telomeres may play. Telomeres are non-coding DNA sequences capping the ends of chromosomes for chromosomal stability and protection. Telomeres shorten with aging and, as previously reported on ExerciseMed, respond to stress and physical activity. Telomerase is the protein responsible for lengthening telomeres and has recently been found to play a variety of roles in keeping the cell healthy and functioning properly. 

Telomeres.  Telomeres are highlighted in red in on the chromosomes and are responsible for stabilizing and protecting the chromosomal DNA.

Telomeres may be used as a signal for prenatal stress. A newborn with short telomeres may signify prenatal stress and allow doctors to predict adulthood disease and health status later in life. A number of human and animal studies have found a link between shortened telomeres and prenatal stress.  Furthermore, telomere length is correlated to aging. Humans who age prematurely generally have shorter telomeres. Thus, a newborn with shorter telomeres would be expected to see a younger onset of age-related diseases.

Researchers are currently looking into how maternal nutrition, sleep pattern, physical activity and psychological emotions play a role in causing and preventing prenatal stress. Maternal lifestyle choices affect more than just one generation. Humans begin producing their germ cells during fetal development. Therefore, the maternal environment affects not only fetal development, but the development of the fetuses future children as well. 

The aforementioned Hypertension paper showed that prenatal stress caused by low protein intake during pregnancy in rat models causes hypertension via the sympathetic nervous system.  

Pregnant rats were fed a low protein (6% of calories from protein) diet to produce prenatally stressed offspring. At rest, blood pressure of the prenatally stressed rats was not significantly higher. However, when the sympathetic nervous system was activated by stimulating the exercise pressor reflex, blood pressure was found to be significantly higher (see figure below). The exercise pressor reflex activates the cardiovascular system through the sympathetic nervous system using sensors (called proprioceptors) in the muscle during exercise. Patients with hypertension often exhibit high blood pressure during exercise before showing a significantly higher baseline blood pressure. This study implicates sympathetic nervous system development in hypertension generated by stresses during prenatal development.

Sympathetic Nervous System Activation Causes Increased Blood Pressure Change in Prenatal Stressed Rats.

To further determine the role that prenatal development has on adulthood disease and health, future studies may need to enable pregnant women to  monitor their nutritional, psychological, and physical states in real time to develop a more accurate picture of the maternal environment and the health outcome of the developing embryo. 

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