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Biology 202, Spring 2005
First Web Papers
On Serendip

Increased Incidence of Depression in Women


Beverly Burgess


Among psychiatric disorders, depression is one of the most prevalent. Studies conducted on worldwide populations suggest that women are two to three times as likely as men to become depressed in their lifetime (1). While there are similarities in the factors contributing to depression in both sexes, depression in women is subject to the influence of additional factors such as environmental and hormonal changes.


In general, depression is a psychiatric disorder caused by biochemical alterations in the brain. This description of the disease is useful in the broad view of the ailment, however, it is not completely understood what causes the changes that influence the disorder. The most common symptoms of depression include unexplained feelings of sadness, worthlessness, guilt, loss of interest in pleasurable activities, loss of appetite, anxiety, insomnia, inability to concentrate and thoughts of suicide (4). It is estimated that of those that suffer from depression, 15 percent commit suicide (2).


An understanding of how depression develops may be approached by examining some aspects of brain function, beginning with brain composition. The brain is made up of nerve cells called neurons that participate in an intricate form of communication via biochemicals called neurotransmitters. Many different neurotransmitters exist in the brain, but there is a class of three specific neurotransmitters called monoamines that play a role in of some of the drives and moods that we experience: serotonin, norepinephrine, and dopamine. These chemicals are generated within neuron cell bodies found in the brain stem and distributed to other parts of the brain via a branched system that spans many regions of the brain (3). Delivery of neurotransmitters takes place across a space between neurons called the synaptic cleft. One group of neurons, the presynaptic cells, sends neurotransmitters while another group of neurons, the postsynaptic cells, receives neurotransmitters. The signals from the presynaptic cells are responsible for activating or inhibiting a reaction in the postsynaptic cells. A malfunction of the presynaptic cells (the cells that generate monoamines) can prevent the proper functioning of brain regions such as the amygdala, the hypothalamus and the cortical areas all parts of the limbic system that control emotions, libido, appetite, sleep and cognition resulting in the symptoms defined as depression (2). For example, the excessive reuptake of serotonin and/or norepinephrine by the presynaptic cells can create chemical imbalances and has been implicated in most cases of depression. Further imbalances of monoamines may also be the result of monoamine oxidase, an enzyme that degrades neurotransmitters (2). Causes of monoamine insufficiency differ among individuals, but current treatment methods focus on inhibiting enzymes that degrade these neurotransmitters as well as blocking the presynaptic uptake of norepinephrine and/or serotonin. Ultimately, these treatments seek so maintain elevated levels of monoamines, specifically norepinephrine and/or serotonin as they are critical to the function of the limbic system (1).


Additional sources of depressed moods may also result from hormonal responses to stress. When an individual receives a stimulus that elicits the fight or flight mechanism within the body, a cascade of hormonal events follows which ultimately produces symptoms of depression such as appetite reduction, anxiety, and insomnia. The hypothalamic-pituitary-adrenal axis (HPA) is the control center for this physiological reaction to stress and hyperactivity in the HPA axis has been identified as the most likely source of stress related depression (2). While short term exposure to the HPA axis response may be beneficial in life threatening situations, the long term effects of HPA axis hyperactivity can be detrimental to the body's delicate sense of equilibrium.


Aside from the above mentioned factors that influence depression in both men and women, there are additional factors that influence the incidence of depression in women. The continuous yet fluctuating presence of estrogen in the system of a woman is believed to contribute to depression due to its varying effects on different biochemical substances and physiological processes. One substance that is generated in the HPA axis system is cortisol, a hormone that heightens the metabolic and immune system response to stress. Excessive levels of cortisol can result in a burn out of these systems. Estrogen has been found to indirectly increase cortisol levels by interfering with feedback mechanisms that naturally regulate its secretion thereby generating a more enduring and powerful stress response than that found in men (1). Estrogen levels are also believed to cause reductions in serotonin levels resulting in premenstrual syndrome (PMS). These findings suggest that the state of depression, agitation and irritability that characterize PMS is not simply a mentally fabricated ailment as was once believed by physicians (1).


Seasonal changes are also at fault for producing symptoms of depression, especially in women. Seasonal affective disorder (SAD) is a form of depression that results from the seasonal changes in the availability of natural light. The human body responds to a decrease in daylight by producing a hormone called melatonin, which creates a sense of sleepiness. As daylight approaches, melatonin levels fall off with a resulting increase in alertness (5). Studies have found that while melatonin levels in men are constant year round, melatonin levels in women decrease in the summer and increase in the winter. This winter time increase in the hormone is believed to be a factor in the higher incidence of SAD among women (1).


The additional contributors to depressive disorders in women such as estrogen and seasonal changes appear to be the differentiating factors between rates of depression among men and women. Although the situations referenced above are examples of the pathological extremes of these differences as they relate to depression, an interesting question that arises from this conclusion is how subtle variations of these differences influence women's behavior and the experience of being a woman in general.


References

1) Leibenluft, Ellen. "Why Are So Many Women Depressed?" Scientific American 1998: 31-35

2) Nemeroff, Charles B. "The Neurobiology of Depression" Scientific American June 1998: 42-49

3) A Brief Overview of Neurotransmitter Distribution and Function (abstracted from Physiology of Behavior 7th Ed, 2001, by Neil Carlson)

4) Depression , National Institutes of Mental Health, National Institutes of Health web site

5) Melatonin: The Basic Facts , The National Sleep Foundation web site




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