James-Lange Theory of Emotions proposes
that emotions are the brain’s interpretation of physiological responses to
emotionally provocative stimuli. Darwin proposed that emotions played a
significant role in the survival of the species and resulted from similar
evolutionary processes as other behaviors and psychological functions did. For
example, Emotions like fear invoke actions that either could attempt to
overcome the source of fear through fight or run from the source through the
flight. In this way, emotions help us process and respond to danger cues that
aid in our survival. However, prolonged stress exposure and the constant
activation of the Fight or Flight responses are associated with negative
effects as well.
Fight or
Flight Response is provided by activity from the sympathetic branch of the
autonomic nervous system. Fight or Flight Response is responsible for this
biological process that prepares us for action in emergencies including
producing stress hormones epinephrine, norepinephrine, and cortisol. In the anticipation of a sudden demand for energy needed to escape danger, a release
of epinephrine induces glucose metabolism which in turn starts to metabolize
nutrients stored within muscles to become accessible to provide energy.
Norepinephrine is also released and increases blood flow to muscles by
increasing the flow of blood from the heart (Carlson, 2009, p. 601).
Norepinephrine
is not just a stress hormone released in the body as it is also found secreted
in the brain as a neurotransmitter (Carlson, 2009, p. 601). The amygdala is
fundamental to emotional processes, especially those relating to fear. The
amygdala is a structure located in the interior of temporal lobes (Argosy
Online Universities Lecture, 2013). When exposed to stressors a stress response
is activated in a pathway from the “central nucleus of the amygdala to the
locus coeruleus”, provoking the release of norepinephrine from the brain. It is
within the nucleus of the brain stem that the norepinephrine-secreting neurons
are located (Carlson, 2009, p. 602). Corticotropin-releasing hormone activates
the secretion of ACTH by the anterior pituitary gland in the brain, where it in
turn also contributes to some of the emotional responses typically seen in
stressful situations (Carlson, 2009, p. 611).
Cortisol,
also called glucocorticoids, is a steroid secreted by the adrenal cortex,
especially during experiences of stress, and is vital to survival (Carlson,
2009, p. 602). Cortisol is vital in the metabolism of protein and carbohydrates
(Carlson, 2009, p. 602). Glucocorticoids have a specific function of helping
with the endogenous decomposition of protein and converting it to glucose. This
makes fats available for “energy, increase blood flow, and stimulates
behavioral responsiveness by affecting the brain” (Carlson, 2009, p. 602).
Glucocorticoids also affect the ability of the gonads to sense luteinizing
hormone (LH) causing less endogenous production of sex steroid hormones
(Carlson, 2009, p. 602). Long-term exposure to stress-induced glucocorticoids
has been demonstrated to destroy neurons located in hippocampal formation which
is largely associated with cognitive functions such as learning and memory
(Carlson, 2009, p. 604). This cell death is caused by the decreases in the
uptake of glucose and decreasing the reuptake of glutamate, causing extracellular
glutamate which permits calcium to pass through NMDA receptors and kill neurons
(Carlson, 2009, p. 604). While Glucocorticoids aid in vital functions prolonged
exposure to stress-induced Glucocorticoids is associated with damage to “muscle
tissue, steroid diabetes, infertility, inhibition of growth, inhibition of the
inflammatory responses and acts to suppress the immune system” (Carlson,
2009).
Prolonged
exposure to glucocorticoids works to suppress the immune system (Carlson, 2009,
p. 610). Immune suppression from stress can put one at risk for upper
respiratory infection and colds (Carlson, 2009, p. 610). Studies indicate that
increases in the number of undesirable events and a decreases the number of
desirable events in one's life lead to medical illness through immune’s
suppression of the immunoglobulin, IgA, in mucous membranes of the nose, mouth,
throat, and lungs (Carlson, 2009, p. 610). Immunoglobulin, IgA, is the primary
defense against infectious microorganisms that enter the nose or mouth and is
affected by mood (Carlson, 2009, p. 610-611). This risk would naturally be
increased if one's immune system was already suppressed either by medication,
illness, or age.
A stimulus that causes us psychological distress causes the emotions and feelings
associated through increases in stress hormones from activation of the “Fight
or Flight Response” (Carlson, 2009). The stress response produces an
increase in epinephrine and cortisol which will assist in our escape, but
escape from certain life events is not always possible. This leaves the person
who is suffering from prolonged exposure to stress at risk for a variety of
psychological symptoms, physical illnesses, and brain damage from stress
hormone toxicity. Prolonged stress is also associated with increased blood
pressure from the increases in stress hormones Norepinephrine and Epinephrine.
Over time contributes to cardiovascular disease and a variety of other
illnesses like stress disorders. While prolonged overexposure to stress-induced
Cortisol or Glucocorticoids is associated with damage to “muscle tissue,
steroid diabetes, infertility, inhibition of growth, inhibition of the
inflammatory responses, and suppression of the immune system” (Carlson, 2009,
p. 603).
Prolonged exposure to stress can cause brain abnormalities, specifically in the hippocampus and amygdala formations, as seen in studies of patients with PTSD and Stress disorders (Carlson, 2009, p. 607). PTSD is a psychological disorder that results from exposure to a situation of extreme danger and stress and includes distressing symptoms like recurrent dreams or intrusive recollections of trauma that interfere with social activities and cause a feeling of hopelessness (Carlson, 2009, p. 606). The hippocampus plays a vital part in contextual learning including participating in the recognition of the context in which traumatic experiences occur and later helping one distinguish safe from dangerous context (Carlson, 2009, p. 607). One hypothesis suggests that after a person is attacked by something a traumatic trigger is created and stored with traumatic stimuli, however, because of the damage to the hippocampus the ability to distinguish actual traumatic stimuli from similar stimuli is impaired resulting in the activation of the amygdala and the trigger of an emotional response in the face of similar stimuli (Carlson, 2009, p. 607). The prefrontal cortex can exert an inhibitory effect on the amygdala and suppress emotional reactions including the loss of conditioned emotional responses like fear (Carlson, 2009, p. 607). Evidence suggests that actions from prefrontal cortex inhibiting the activity of the amygdala may be liable for emotional reactions and psychological symptoms such as difficulty falling or staying asleep, irritability, outbursts of anger, difficulty in concentrating, and heightened reactions to sudden noises or movements found in persons with PTSD (Carlson, 2009, p. 607-608).
The above changes in physiological fight or flight response to stress and
its effects on cognitive or emotional changes would be similar in most persons
who were living under these same stressors, what would likely differ is the
length of duration before the onset of symptoms that impair function. If
the same stressor was being experienced by a person of the opposite sex or
someone much older or younger there might be some differences in how they react
emotionally. For example, men may be less tearful and frightened and react with
more anger and hostility, while an older or wiser person may feel unabashed and
a younger person may be completely depressed and express with hyperactivity and
impulsivity, instead of displaying fear and tears. How someone reacts to a stressor is largely based on their ability and resources to deal with the
problems, how much social support they have, their previous trauma experiences,
personality, temperament, coping skill and lastly, how long the stressor
persists.
The four most important behavioral
strategies I would suggest one implement immediately to reduce the effects of
stress on my body is cared for themselves by making sure they get
adequate sleep, sun, nutrition, and exercise.
Getting proper nutrition is important
because nutrients play a vital role in neurotransmitter metabolism. Vitamin
deficiencies are often found in subjects with depression and being properly
nourished supplies the body with minerals such as calcium, iron, magnesium,
selenium, and zinc that aid in preventing depression, irritability, and mood
swings (Masley, 2013). One of the most important things one can do to combat
stress is to work on making sure they have a stock of healthy ready to eat
items handy.
Exercise has been shown to increase
serotonin function, so exercising can help induce a positive mood (Young,
2007). Several studies have confirmed a relationship between serotonin and
mood, indicating that less serotonin correlates with more negative moods
(Young, 2007). Studies that have researched exercise and the relationship with
mood concluded that exercise has antidepressant and anxiolytic effects, plus
increases brain serotonin function (Young, 2007).
Get more
sunlight, which can help increase serotonin levels and improve mood. A
studied has demonstrated a “positive correlation between serotonin synthesis
and the hours of sunlight received” that day; therefore, increasing my sunlight
can also help me fight feelings of depression (Young, 2007).
Why
exactly the brain needs to sleep is perhaps poorly understood, but it is clear
that decreases in sleep later results in poor cognitive function and
psychological symptoms because sleep deprivation impairs cerebral functioning
(Carlson, 2009, p. 310). As the brain activity utilities glycogen as fuel for
the neural activity it levels drop producing extracellular adenosine chemicals,
which then accumulate prohibiting normal neural activity (Carlson, 2009). This
chemical toxicity produces both the cognitive and emotional effects that are
seen during sleep deprivation and the process that occurs during sleep helps
restock glycogen for tomorrow.
Poor
sleep results in poor cognitive performance because it is during sleep,
particularly during slow-wave and REM state, that our brains restore cognitive
function and process information (Carlson, 2009). Increases in mental activity,
including dealing with stressors, would cause an increased need for slow-wave
sleep to facilitate the consolidation of explicit memories (Carlson, 2009, p.
307). REM sleep is equally important and is believed to play a major role in
the development and learning, particularly the consolidation of long-term
memories and implicit memories (Carlson, 2009, p. 309). Decreased sleep also
causes increases in highly reactive oxidizing agents called free radicals
within the brain (Carlson, 2009, p. 307). During a process called oxidative
stress, free radicals can bind with electrons from other molecules and damage
the cells that they inhabit (Carlson, 2009, p. 307). The decreased metabolic rate
during slow-wave sleep allows for the restorative mechanisms to eliminate free
radicals before damage occurs (Carlson, 2009, p. 307). Clearly, getting enough
regular sleep will improve my cognitive function and emotional well-being.
The most
important skill one must demonstrate to implement these is time management.
References
Carlson, N. R. (2009). Physiology of Behavior, 10th Edition. Pearson
Learning Solutions. VitalBook file.
Mills, H. Reiss, N.
Dombeck, M. (2008). Cognitive Therapy Techniques for Stress Reduction. MentalHelp. Retrieved from
http://www.mentalhelp.net/poc/view_doc.php?type=doc&id=15667&cn=117
Masley, J. (February, March 2005). The
role of exercise, nutrition, and sleep in the battle against depression. Mental
Health Matters. 2(5,6). Gratiot Medical Center: An Affiliate of MidMichigan
Health. http://fhpcc.com/PDFs/RolesAgainstDepression.pdf
Young, S. M. (2007). How To Increase
Serotonin in the Human Brain Without Drugs. Journal
of Psychiatry Neurosci. 2007 November; 32(6): 394–399. Retrieved from http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2077351/
