Stress
is a normal experience of the human body, beneficial to our survival. It is a
reaction to a perceived situation where a person feels threatened or anxious.
Stress will at some point affect anyone and everyone. Things we deal with and
experience every day can cause us huge amounts of stress without even seeming
as if we are subconsciously interpreting them as a threat. In jobs and schools
where employees or students dedicate huge amounts of time to focusing and
worrying about responsibilities, there is little time left for themselves, and
these people will tend to spend more time in an anxious, stressed, state of
mind than they will resting.
There
are two basic ways that stress can affect us. The first is a seemingly simple
physical reaction to stress, the “fight or flight” reaction, a tool for
survival that we used in the past as hunter-gatherers, and even today in the
face of immediate danger. As this reaction occurs, normally to a stressor –
like a cheetah attack or a final exam – stress hormones and chemicals are
released, reading the body for a fight, or a quick flight. In small, infrequent
doses, these chemicals can save lives. When the body is consistently exposed to
stressors, however, the effects can be harmful. The second type of stress is a
quieter type – happening mainly in the mind. The signs of cognitive stress can be
as simple as worrying, and as complicated as introversion or an anxiety
disorder, such as Post Traumatic Stress Disorder. While the prolonged effects
of stress can be dangerous to our health, there are promising methods for
managing both physical and cognitive stress.
The Center for Disease Control defines stress as “a
condition that is often characterized by symptoms of physical or emotional
tension” (CDC.gov). Stress can help develop skills needed to adapt to new and
potentially threatening situations. However, when symptoms of stress are larger
than life or sustained over long periods of time, humans feel overwhelmed and
reduce their ability to cope (CDC.gov). Physical, or Somatic, stress can be
described as a disturbance of the Autonomic Nervous System, specifically the
Sympathetic Nervous System. The autonomic nervous system is comprised mainly of
the heart, digestive system, and lungs. It is the autonomic nervous system that
allows the heart to continue to beat and the lungs to continue to expand and contract
as we breathe without conscious effort. As Laura A. Freberg states in her
textbook, Discovering Biological Psychology, “The sympathetic nervous system
has been elegantly designed to cope with emergencies.” This system is
responsible for reacting to situations which would traditionally put a person
in danger – like a cheetah attack. Activation of the sympathetic nervous system
in times of perceived danger or arousal in response to external stimuli happens
in mere seconds as a domino-like chain of events readies the body for fighting
or fleeing. Pupils dilate, salivation decreases, heartbeat accelerates and
blood pressure rises, airways relax in order to receive more oxygen, activity
in the stomach and bladder is inhibited, and even blood vessels constrict
(Freberg 425 – 428).
The axons involved in the stress reaction are located in
the thoracic and lumbar portions of the spinal cord, and they react with what
is called the “sympathetic chain.” The sympathetic chain is “a string of cell
bodies outside the spinal cord that receive input from sympathetic neurons in
the central nervous system and that communicate with target organs” (Freberg
50-51). At the cellular level, the amygdala receives sensory information about
the threat, which sends signals to the hypothalamus through the pathway stria
terminalis, which forms additional connections with neurons in the bed nucleus
of the stria terminalis. It is through this process that the
hypothalamic-pituitary-adrenal (HPA) axis is activated. Corticotrophin-releasing-hormone
(CRH) and vasopressin are released by the paraventricular neucleus (PVN) of the
hypothalamus. This causes the pituitary gland to release adrenocorticotropic
hormone (ACTH) which diffuses into the blood stream, eventually reaching the
adrenal glands where it stimulates the release of cortisol. Cortisol then moves
to the brain, causing an increased release of neurotransmitters (Freberg 425 –
428). One of the reasons why cortisol can be harmful to mental functioning is
the time cortisol remains in the bloodstream, approximately three hours after
the threat is addressed, before breaking down.
When there is no longer a threatening stimulus to react
to, the body returns to the “rest and digest” state – the Parasympathetic
Nervous System. In small doses, this reaction to stressors can help achieve
goals and save lives. When prolonged, however, stress can interfere with
judgment, lead to depression, and adversely affect concentration, objectivity, and
memory retention, among other common cognitive functions. The stress response
is a priority-based system, and cognitive functioning above a bare minimum
necessary for survival is not always deemed necessary. Prolonged stress can
also contribute to health problems such as high blood pressure – due to the increased
heart rate experienced with a stressor – heart disease, obesity, and even
diabetes. Both short and long term stress affect the body substantially, even
to the point of a drastic increase in visible aging.
Interestingly, even the mental effects of stress
originate chemically in the brain. The limbic system is primarily responsible
for dealing with perceived stressors, among other functions it is responsible
for – like the regulation of emotions and memory. The limbic system is
comprised of several very different structures in the brain that are fairly
spread out. Several of these systems in the brain are impacted or shut down in
response to a stressful event. For example, in an article written for TIME
Magazine, Michael Lemonick interviews Frank Vocci, the director of
pharmacotherapies at the National Institute of Drug Abuse. “The part of the
prefrontal cortex that is involved in deliberate cognition is shut down by
stress,” Vocci states. When a threat is perceived, it is the limbic system, specifically
the hypothalamus that sends the signal to the autonomic nervous system to begin
the sympathetic reaction. “Chronic over-secretion of stress hormones adversely
affects brain function, especially memory… During a perceived threat the
adrenal glands immediately release adrenalin. If the threat is severe or still
persists after a couple of minutes, the adrenals then release Cortisol. Once in
the brain, cortisol remains much longer than adrenalin, where it continues to
affect brain cells” (Lemonick). It makes sense that in terms of extreme stress,
not only physical processes such as digestion, but mental processes such as
memory formation and retention, would be deemed less important than other
survival-centered processes.
While mere stress will be felt by anyone at some point in
their lifetime, the threshold or level of stress that an individual can cope
with varies from person to person. A study published in The Journal of
Neuroscience found a connection between Brain-Derived-Neurotrophic-Factor
(BDNF), a protein with implications seen in processes within the brain from
drug addiction to epilepsy, and chronic stress in rats. This study found a
connection between chronic stress and abnormalities in the hippocampus and
dentate gyrus. The dentate gyrus, part of the general area that is the
hippocampus, is used mainly for the creation of new memories, which is known to
be affected by the body’s natural stress reaction. “Chronic stress produces
structural changes and neuronal damage especially in the hippocampus… Corticosterone
negative feedback may have contributed in part to the stress-induced decrease
in BDNF and mRNA levels, but stress still decreased BDNF in the dentate gyrus
in adrenalectomized rats suggesting that additional components of the stress
response must also contribute to the observed changes in BDNF” (Smith). BDNF is
a necessary protein that plays an important role in the regeneration and
plasticity of neurons. In cases of chronic stress, it is BDNF that is negatively
affected, leading to the death of neurons in the brain. In a study measuring
the impact of chronic stress on levels of BDNF, researchers found a connection
between BDNF and symptoms of depression and anxiety in rats. The rats were
subject, essentially, to chronic stress, with the behavioral outcome measured
three weeks after the fact. Not
only did this study find a connection between BDNF and depression, but that
chronic stress adversely affected the threshold at which a rat began to be
negatively impacted by the chronic stress. “…hippocampal BDNF expression plays
a critical role in resilience to chronic stress and that reduction of
hippocampal BDNF expression in young, but not adult, rats induces prolonged
elevations in corticosterone secretion” (Taliaz).
Chronic
stress is very different from a short term, fleeting, stressor such as a wild
animal attack. Stress still serves a very necessary evolutionary purpose –
survival. Chronic stress can come from work, school, and even family
obligations. Post-Traumatic Stress Disorder can manifest after a traumatic
event. PTSD is seen frequently in war veterans, and can be difficult to treat.
Many biological factors seem to go into the occurrence of PTSD. Thyroid levels can
be elevated, along with circulating levels of norepinephrine and a higher heart
rate and blood pressure level even weeks after the traumatic event (Yehuda
108-114). PTSD is essentially a case of severe chronic stress. As the person
suffering from PTSD constantly relives the traumatic event, their stress
response is renewed over and over again, leading the body to constantly run
under the influence of the sympathetic nervous system. Similarly to other forms
of chronic stress, a connection between PTSD and reduced hippocampal volume and
function has been found. “A twin study suggested that differences in
hippocampal volume represent familial vulnerability to developing PTSD. A
polymorphism in the coding region (V66M) that reduces trafficking and release
of [BDFN] has been associated with hippocampal deficits and reduced hippocampal
volume” (Amstadter). In addition to the decreased volume and function of the
hippocampus in PTSD patients, the sensitivity of their HPA axis tends to be
increased. A more sensitive HPA axis and lower than normal cortisol level at
the time of the traumatic event could prolong the effects of norepinephrine on
the brain, potentially causing the severe reaction to the event that occurs in
patients with PTSD. Chronic stress, including PTSD, has shown to have severe effects
on the human brain and body, but there are still options for the control of
stress. Because the stress response is a biological reaction, it is possible to
deal with stressors on a similar level.
Exercise,
for example, can do wonders for the physical effects of stress felt every day.
Various studies have been done regarding exercise as a stress management tool.
The De Anza Student health newsletter, for example, cites a study published in
the Journal of Sports Science and Medicine, “…exercise stimulates the release
of a chemical in the body called brain-derived-neurotrophic-factor (BDNF). BDNF
is beneficial to brain function in several ways, it supports neuron growth and
survival, the capacity to learn, and memory function” (Tamm). Yes, one of the many
ways in which exercise has proven to combat the effects of chronic stress is to
increase the levels of the protein that is responsible for the upkeep of
neurons in the brain, as well as the formations of new ones. This is
particularly important in the Hippocampus, specifically the dentate gyrus, for
the formation and retention of new memories. Arthur F. Kramer published a paper
detailing the wide spectrum of positive influences exercise has shown to have
on the brain. “…reported increases in MRI measures of cerebral blood volume
(CBV) in the dentate gyrus of the hippocampus for a group of 11 middle-aged
individuals who participated in a three month aerobic exercise
program…Increases in CBV in a parallel study of exercising mice were found to
be related to enhanced neurogenesis” (Kramer). Kramer then continues on to
speak about the effects of exercise on enhanced learning observed in rodents
performing the Morris water maze. “Enhanced learning on water maze tasks has
been associated with an increased production of neurotrophic molecules, such as
brain-derived neurotrophic factor (BDNF), and a series of molecular and
cellular cascades” (Kramer). Kramer goes
on to highlight the ways in which voluntary exercise increases “both mRNA and
protein levels of BDNF in the hippocampus, cerebellum and frontal
cortex…Therefore, exercise increases BDNF levels, which seem to be inextricably
related to the behavioral improvements observed with an exercise treatment”
(Kramer). The increase in levels of BDNF as a result of exercise leads to the
growth of new capillaries in the hippocampus, cerebellum and motor cortex of
rodents, and may even reduce the amount of cortical damage caused by a manually
administered stroke. (Kramer). Even when rodents were specifically tested for
levels of BDNF after being subject to stressors or even type II diabetes, voluntary
wheel running increased levels of BDNF after as few as six hours. “The characteristic lower levels of hippocampal
BDNF protein and dendritic spine density in type II diabetic mice (db/db) were
significantly enhanced with free access to cage wheels” (Murray). Another
important structure within the hippocampus that appears to be critical in the
stress response is the subiculum, which appears to have a range of functions
and properties beyond memory formation.
The subiculum appears to play a role in spatial
navigation, as well as a control to the response of stress, specifically an
inhibition of the HPA axis. Knowledge of the subiculum is fairly vague, but an
increase in volume in the subiculum has been observed after sedentary patients
engaged in six weeks of aerobic exercise, five days a week, 30 minutes a day
(Thomas). “The subiculum has been shown to have decreased volume in major
depression and provides a major inhibitory input to the
hypothalamic-pituitary-adrenal (HPA) axis, down-regulating stress. Structural
change in the subiculum may therefore be one of the mechanisms by which aerobic
exercise helps alleviate depression and stress” (Thomas). This research has
shown that while it is still within the hippocampus that the benefits of
exercise are found, it is not only in the dentate gyrus that involves memory
retention, but also within the subiculum, which appears to control the body’s
reaction to stress, through the inhibition of the HPA axis.
Although it
appears that damage caused by chronic stress seems to primarily occur in the
limbic system, damage can also be felt in the frontal cortex, the region of the
brain responsible for logic and reasoning. BDNF’s effect is primarily focused
in the dentate gyrus, but it can also be seen in the frontal cortex. In an
article written for the International Journal of Peptides, Patrick S. Murray
speaks of the various roles of BDNF, as well as the effect that exercise may
have on the protein. “Exercise
leads to substantial changes in BDNF and NMDA receptor activity in the
hippocampus, and these changes in large part underlie the effects of exercise
on learning and synaptic plasticity” (Murray). Murray also found that the
increased levels of BDNF remained in the blood of rodents for some time after
the cessation of exercise. Also noted in Kramer’s study, a routine as simple as
walking for about an hour, three days a week, for six months increased gray
matter volume in the prefrontal cortex as well as the temporal cortex, along
with an increase in the volume of anterior white matter.
While exercise has
shown improvements in the somatic, or physical, responses to stress, it has
been found that meditation can also affect the ways the brain responds to
stress. Studies have shown that meditation may improve the emotional regulation
of practitioners, with neuroimaging like PET scans and functional magnetic
resonance imaging providing evidence. Meditation, when practiced regularly for
at least eight weeks, appears to decrease the activation of the amygdala
(Schwartz). The amygdala is, once again, part of the limbic system, which seems
to play an integral role in the interpretation of stressors. The amygdala
specifically plays a role in processing emotions and fear-learning – which can
be very important for evaluating stressors and necessary responses. Meditation
can, essentially, teach the brain which cues to respond to with stress signals,
and which can be ignored. Two types of meditation were employed in a study
conducted at several different facilities in Boston – Mindful Attention
Meditation and Compassion Meditation – with a control group participating in an
eight week health education course. “In the mindful attention group, the
after-training brain scans showed a decrease in activation in the right
amygdala in response to all images, supporting the hypothesis that meditation can
improve emotional stability and response to stress” (Schwartz). The mindfulness meditation
technique showed greater promise in terms of stress response than the
Compassion Meditation technique. The study conducted in Boston found that even
three weeks after completing the training, participants in the study continued
to show decreased activity in the right amygdala – suggesting that the benefits
of meditation for stress management are felt on a long term basis, beyond the
time taken to meditate. Meditation has also shown to increase the release of
dopamine in the brain, acting on the reward pathway similarly to the endorphins
that are released during voluntary exercise (Young). In addition to the release
of dopamine, neuroimaging has shown an increased cortical thickness in patients
that have meditated regularly for at least eight weeks, as well as a decrease
in age-related cortical thinning (Young). Several studies have shown these
effects to be long lasting, even when the participant is not in a meditative
state.
Stress serves an evolutionary purpose – survival. For
some, stress is like a monster lurking in the corner of a room, waiting to
strike. Many presidents – like Abraham Lincoln – have shown the drastic effects
that chronic stress can have on the appearance of natural aging. For others,
stress is a tool they can utilize to complete assignments on time or even run
marathons. Others seek the rush of endorphins that accompanies activities like
roller coaster riding or sky diving. Stress is, at the same time, something
that no one can avoid. One of the scariest aspects of stress can be a feeling
of helplessness that is known to accompany it, particularly in cases of
depression or anxiety disorders such as post-traumatic stress disorder. This
paper has shown, however, that while we cannot simply stop the effects of
chronic stress on the body, there are certainly many ways to curb, or even reverse,
the negative side effects that we feel as a result of the chemical and
biological reactions to stress.
Works
Cited
"Tips for Coping with Stress." CDC.gov. Center for Disease
Control, 20 2012. Web. 26 Nov 2012. <http://www.cdc.gov/violenceprevention/pub/coping_with_stress_tips.html>.
Schwartz, Gary E. "Psychosomatic Medicine
."Psychosomatic Medicine .
40.4 (1978): 321-327. Web. 26 Nov. 2012.
Freberg, Laura A. Discovering Biological Psychology.
2nd ed. San Luis Obispo: Wadsworth, 2010. 425 - 428. Print.
Lemonick, Michael. "How We Get
Addicted." TIME magazine.
05 2007: n.. Print.
Tamm, Stephen. "Exercise Your Way to
Success." Student Health
101. 2012: n. Web. 26 Nov. 2012.
<http://readish101.com/m/1012/03/deanza.html>.
Kramer, Arthur F. "TRENDS in Cognitive
Science."TRENDS in Cognitive Science. 11.8 (2007): .. Web. 26 Nov.
2012. www.sciencedirect.com
Taliaz, Dekel. "The Journal of
Neuroscience." Journal of
Neuroscience. 32.48 (2011): n. Print.
Smith, Mark. "Journal of Neuroscience." Journal of Neuroscience. 15.3
(1995): 1768-1777. Web. 30 Nov. 2012.
<http://www.jneurosci.org/content/15/3/1768.full.pdf>.
Murray, Patrick. "International Journal of
Peptides."International Journal of Peptides. 2011. (2011): 1-12.
Web. 30 Nov. 2012. <http://www.hindawi.com/journals/ijpep/2011/654085/>.
Thomas, Adam. "Rapid changes in brain
structure in response to exercise in sedentary adults." Oxford: 2012.
<http://ww4.aievolution.com/hbm1201/index.cfm?do=abs.viewAbs&abs=5313>.
Baime, Michael. "This Is Your Brain On
Mindfulness."Shambhala Sun. 2007: 44 - 84. Web. 30 Nov. 2012.
Young, Simon. "Journal of Psychiatry and
Neuroscience."Journal of Psychiatry and Neuroscience. 36.2 (2011):
75-77. Web. 30 Nov. 2012.
<http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3044190/>.
Schwartz, Eric. "Meditation Appears to
Produce Enduring Changes in Emotional Processing in the Brain."Science
Daily [Boston] 12 11 2012,
Early Edition n. pag. Web. 30 Nov. 2012. <http://www.sciencedaily.com/releases/2012/11/121112150339.htm>.
Yehuda, Rachel. "New England Journal Of
Medicine." New England
Journal Of Medicine. 346.2 (2002): 108-114. Web. 1 Dec. 2012.
<http://www.impact.arq.org/doc/kennisbank/1000010585-1.pdf>.
