The and H2O2 (Saladin, 2015) as byproductsThe and H2O2 (Saladin, 2015) as byproducts

The dorsal hypothalamus is also a
potential link between stress and cardiac arrhythmia (Fontes, et al., 2017).
The autonomic nervous system increases sympathetic drive to the heart in
response to emotional stress (Saladin, 2015). Animal studies have shown this is
the central pathway involved in stress and cardiac response (Fontes, et al.,

Oxidative Stress

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Oxidative stress is a naturally occurring
mechanism that is largely responsible for the background rate of aging in
cells. ROS are a type of free radical containing oxygen; these free radicals
contain an unpaired electron in the valence shell (Marín, Yubero-Serrano, &
Pérez-Jiménez, 2013), which means the ROS is highly reactive and has the
potential to damage cellular machinery. Oxidative stress is caused by an
imbalance on ROS and an organism’s ability to detoxify the free radical with
antioxidants or repair the damage caused (Marín, Yubero-Serrano, &
Pérez-Jiménez, 2013). Mitochondria under normal physiological conditions
produce O2- and H2O2 (Saladin,
2015) as byproducts in the production of adenosine triphosphate (ATP). These
ROS molecules cause mitochondrial DNA (mtDNA) to be exposed to high levels of
free radicals, which lead to oxidative damage (Marín, Yubero-Serrano, &
Pérez-Jiménez, 2013). This oxidative damage in the mitochondria leads to depletion
of energy supply and dysfunctional proteins. Additionally, oxidative stress
reduces mitochondrial membrane potential and reduces the natural production of
antioxidants by the mitochondria (Baker & Staecker, 2012). This mean that
not only does oxidative stress cause damage, but it simultaneously reduces a
cell’s ability to repair the damage.

Oxidative stress is the major connecting
factor between stress and aging (Baker & Staecker, 2012; Marín, Yubero-Serrano,
& Pérez-Jiménez, 2013; Tomiyama, et al., 2014). Chronic psychological
stress increases rates of oxidative stress through the over production of
glucocorticoids (Liu & Mori, 1999; Tomiyama, et al., 2014). These increased
levels of ROS accelerate the natural rate of aging caused by oxidative stress
(Marín, Yubero-Serrano, & Pérez-Jiménez, 2013).


Aging is the process of growth and
development from infancy to adulthood and the gradual deterioration of organs
and systems after peak functionality (Saladin, 2015). This degradation of organ
functionality becomes obvious when looking at causes of death. From ages 18-34
the main causes of death are accidents, homicide, and suicide. The leading
causes of death of people over the age of 55 are diseases related to senescence
like heart disease, cancer, and stroke (Saladin, 2015). The causes of
senescence are not precisely known, but there are many hypotheses. The leading
hypotheses are related to oxidative stress, cellular inflammation, the length
of telomeres and the activity levels of telomerase (Marín, Yubero-Serrano,
& Pérez-Jiménez, 2013). However, cellular inflammation, telomere length,
and telomerase activity also all have a relationship with oxidative stress that
can amplify the effects of aging (Marín, Yubero-Serrano, & Pérez-Jiménez,

Some studies have shown that race and
gender are an important factor in examining stress (Woods-Giscombé & Lobel,
2008), but they are also important in evaluating rates of aging. African
Americans struggle disproportionately with age-related diseases like
cardiovascular disease (Woods-Giscombé & Lobel, 2008) and they also have
significantly shorter lifespans in comparison to White Americans (Kochanek,
Murphy, & Xu, 2015). In all races, females have a longer lifespan than men
(Kochanek, Murphy, & Xu, 2015). Since oxidative stress is a significant
contributor to age-related diseases, psychological stress may be a contributor
to the decreased lifespans of Black Americans.