Fetal Stress Exposure Linked to Adult Mood Disorders
Mood Disorder Basics
There are two main categories of mood disorders: depressive disorders and bipolar disorders. People with depressive disorders experience life-disrupting forms of the despondent emotional state known as depression, while (generally speaking) people with bipolar disorders experience life-disrupting swings between periods of depression and an unusually energized, aroused state known as mania. Examples of the depressive disorders include major depression, minor depression, a condition known alternately as dysthymia or dysthymic disorder, and a catchall category called depressive disorders not otherwise specified (DD-NOS). Examples of the bipolar disorders include bipolar I disorder, bipolar II disorder, a condition known alternately as cyclothymia or cyclothymic disorder, and a catchall category called bipolar disorders not otherwise specified (BD-NOS).
Stress reactions in the human body are powered by changes in two different systems: the nervous system and the endocrine (hormone) system. Stress-related changes in the nervous system begin when two key chemicals, called epinephrine (adrenaline) and norepinephrine (noradrenaline), boost the rate of activity in the sympathetic nervous system, a segment of the larger system that functions without conscious control. Elevated activity in the sympathetic nervous system manifests largely as physical reactions in the body’s “fight-or-flight” response, including such things as rapid breathing, a rapid heartbeat and an increased flow of blood to the muscles.
Stress-related changes in the endocrine system begin when a structure in the brain called the hypothalamus produces a substance called corticotrophin-releasing hormone or CRH. After it’s produced, this substance passes to another brain structure called the pituitary gland, where its chemical actions encourage the production of a second hormone, known as adrenocorticotropic hormone (ACTH). ACTH then enters the bloodstream and travels to the adrenal glands in the kidney region, where its chemical actions encourage the production of cortisol (and other secondary stress hormones). When cortisol levels in the body rise, they trigger anxious or fearful emotional states, and also make a variety of physical changes that contribute to the “fight-or-flight” response.
When a pregnant woman is exposed to significant stress, the cortisol in her bloodstream crosses the placental barrier and enters the bloodstream of her developing fetus. Once it’s inside the fetal bloodstream, cortisol reduces the fetus’s overall rate of growth and alters the development rate of specific tissues. It also apparently alters the ways in which the fetus’s genetic code lays out the long-term blueprints that determine a wide variety of personal characteristics during childhood and adulthood. Doctors refer to this alteration in the expression of the genetic code as fetal programming.
One of the potential long-term outcomes of cortisol-related fetal programming is the onset of some form of mood disorder in childhood or adulthood. In a study published in 2008 in the journal Neuropsychopharmacology, a group of Belgian researchers linked fetal exposure to elevated cortisol levels to the presence of medically serious depression symptoms in postpubescent teenage girls. Similarly, a variety of sources (including the Handbook of Clinical Gender Medicine) identify fetal programming as an important underlying mechanism for a range of mood disorders in adults.
In the study presented to the British Neuroscience Association, a team of Scottish researchers identified a specific substance in the body (an enzyme called 11 beta-hydroxysteroid dehydrogenase type 2) that normally breaks down the cortisol from a pregnant mother and prevents it from producing significant fetal programming. Preliminary evidence gathered during the study indicates that people with high risks for fetal stress-related mood disorders lack sufficient amounts of this substance, and therefore accumulate unusually high levels of cortisol in their bloodstreams during fetal development.
The authors of the study presented to the British Neuroscience Association listed several sources of stress that can potentially trigger the onset of cortisol-related fetal programming in the womb. These sources include malnutrition, grief or bereavement, and various forms of physical and/or sexual abuse.