Depression Clinical Trial
Official title:
The Effects of Exercise on Depression Symptoms Using Levels of Neurotransmitters and EEG as Markers
The purpose of this study is to examine the effects of exercise on the symptoms of depression
using serum levels of serotonin, catecholamine's, Alpha EEG asymmetry, and self-report of
symptoms as markers.
In an attempt to further understand the mechanisms of improved mood through exercise; this
study will examine the known factors that contribute to depressed mood in a single study
using serotonin and catecholamine levels via blood serum and EEG slow wave asymmetry. Such
information can be useful in understanding the overall neurological components of depression
and the effects of exercise on the brain in depressed individuals that would make the
prescription of exercise a viable treatment option.
There is an increasing demand for clinical effective, safe, and cost conscious forms of
treatment for depression. Research shows depression to account for the largest decrease in
overall health compared to asthma, angina, arthritis, and diabetes (Maussavi, 2007). The cost
of lost productivity at work due to depression is a new focus of research as no current and
accurate numbers exist. Stewart, Ricci, Hahn, & Morganstein (2013) were among the first to
examine this issue and found that lost productivity due to depression cost an estimated $44
billion dollars per year in spite of current medical treatments commonly prescribed. The lost
productivity among those with depression and the low level of treatment suggest that there
may be cost effective opportunities for improving depression outcomes within the general
workforce and society at large.
The question of value regarding the use of exercise as a treatment for depression has
remained a source of investigation in recent years. In cooperation with Centra Health and
Liberty University, this study seeks to understand the mechanisms that make exercise a viable
treatment in depression by examining self-report of symptoms, serum levels of serotonin and
catecholamines (epinephrine, norepinephrin, and dopamine) and frontal slow wave EEG activity
as markers. Although these markers have been examined individually in previous studies, this
is the only known study that examines each of these components in a single study. Such
information can be useful in understanding the overall neurological components of depression
and the effects of exercise on the brain in depressed individuals that would make the
prescription of exercise a viable treatment in depression.
Multiple trials, meta-analyses, and reviews have been conducted in the attempt to clarify the
use of exercise in depressed patients. Research has shown that exercise as a treatment may
result in fewer relapses than sertraline (Strohle, 2009). Similar results are indicated when
exercise is prescribed as an adjunct treatment with psychotherapy (Balon, Sidhu, & Pankhuree,
2009; Blumenthal, Smith, & Hoffman, 2012; Gill, Womack, & Safranek, 2010). Preliminary
characteristics of the ideal dosage of exercise as a treatment have been researched, although
a definitive dose-response curve has yet to be produced (Callaghan, Khalil, Morres, & Carter,
2011; Perraton, Kumar, & Machotka, 2010).
Electroencephalographic (EEG) scans have been shown to demonstrate a left frontal bias in
alpha (8-12 Hz) and theta (4-7 Hz) wave activity (Allen, Urry, Hitt, & Coan, 2004; Demos,
2005; Iosifescu et al., 2008; Nissen et al., 2006). The up-training or down-training of
individual bandwidths in the treatment of depression, anxiety, ADHD, and traumatic brain
injury have long been established (La Vaque, 2002). Although there are no established norms
for neurotransmitter levels, we know through clinical medication trials that the inhibition
of the reuptake of serotonin and or norepinephrine improve mood. Previous studies examining
low levels of serotonin and decreased mood have found a correlation between exercise and
increased serotonin availability without the use of pharmaceuticals (Chaouloff et al., 1985;
Ernst, Olsen, Pinel, Lam, & Christie, 2006; Jacobs & Fornal, 1999). More routine type studies
often use neurotransmitter levels as markers (Lande, Williams, Fileta, 2012; Lidberg, Tuck,
Asberg, Scalia-Tomba, & Bertilsson, 1985; Mann & Stanley, 1984).
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