Exercise Treatment of Sleepiness in Depression Linked to Immune System Chemicals

Exercise Treatment of Sleepiness in Depression Linked to Immune System Chemicals

Posted: October 2, 2015

The impact of exercise on reducing excessive sleepiness in depression is linked to certain chemicals, researchers have found.

Reporting their findings online August 4 in Translational Psychiatry, the research team  looked at sleep quality in depressed people taking antidepressant medication who had not fully recovered. The team was led by Madhukar H. Trivedi, M.D., a 1992 NARSAD Young Investigator grantee and 2002 Independent Investigator grantee, and lead author Chad Rethorst, PhD, of the University of Texas Southwestern Medical Center, Dallas.

As seen in previous studies, they found that high levels of tiredness — called hypersomnia — decreased with exercise. What they discovered for the first time is that these improvements corresponded with reductions in interleukin (IL)-1β, an immune system chemical that influences cell signaling. Reductions were also seen in levels of brain-derived neurotrophic factor (BDNF), a protein that supports neurons and aids the growth of new ones.

Hypersomnia is a common symptom of what is known as atypical depression. Unlike people with typical depression, those with the atypical variety may experience improvements in mood following positive events, an increased appetite and/or weight gain, high sensitivity to social interactions and the feeling their limbs are weighed down. Exercise is known to help reduce hypersomnia among these people. Now, researchers have a clearer picture of how exercise might bring about those changes. While past studies have found BDNF increases to improve sleep quality in a non-depressed group, the new research suggests high BDNF levels contribute to hypersomnia in atypical depression. Similarly, though IL-1β generally improves sleep, the new results indicate that this chemical may be overproduced in atypically depressed people and reduced by exercise, thus lessening symptoms of hypersomnia.

The team did not find any relationship between these chemicals and improvements in insomnia resulting from exercise. This suggests that different biological mechanisms contribute to insomnia — which is more common in typical depression — compared to hypersomnia, the researchers report.

The research team also included Tracy L. Greer, Ph.D., a 2004 Young Investigator grantee, also of UT Southwestern Medical Center.

The team cautioned that they studied only depressed people who were taking antidepressants, specifically selective serotonin reuptake inhibitors (SSRIs). SSRIs can change levels of immune system chemicals and BDNF. They can also disrupt sleep but are not commonly associated with hypersomnia. It is likely that SSRI effects may have shaped the relationship this study found between and the chemical markers. Future work can investigate the possibility of SSRI effects by looking at other groups, including people who are not taking any medication for their depression and those who have recovered from depression but still experience disrupted sleep.

Read the paper.

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Friday, October 2, 2015

The impact of exercise on reducing excessive sleepiness in depression is linked to certain chemicals, researchers have found.

Reporting their findings online August 4 in Translational Psychiatry, the research team  looked at sleep quality in depressed people taking antidepressant medication who had not fully recovered. The team was led by Madhukar H. Trivedi, M.D., a 1992 NARSAD Young Investigator grantee and 2002 Independent Investigator grantee, and lead author Chad Rethorst, PhD, of the University of Texas Southwestern Medical Center, Dallas.

As seen in previous studies, they found that high levels of tiredness — called hypersomnia — decreased with exercise. What they discovered for the first time is that these improvements corresponded with reductions in interleukin (IL)-1β, an immune system chemical that influences cell signaling. Reductions were also seen in levels of brain-derived neurotrophic factor (BDNF), a protein that supports neurons and aids the growth of new ones.

Hypersomnia is a common symptom of what is known as atypical depression. Unlike people with typical depression, those with the atypical variety may experience improvements in mood following positive events, an increased appetite and/or weight gain, high sensitivity to social interactions and the feeling their limbs are weighed down. Exercise is known to help reduce hypersomnia among these people. Now, researchers have a clearer picture of how exercise might bring about those changes. While past studies have found BDNF increases to improve sleep quality in a non-depressed group, the new research suggests high BDNF levels contribute to hypersomnia in atypical depression. Similarly, though IL-1β generally improves sleep, the new results indicate that this chemical may be overproduced in atypically depressed people and reduced by exercise, thus lessening symptoms of hypersomnia.

The team did not find any relationship between these chemicals and improvements in insomnia resulting from exercise. This suggests that different biological mechanisms contribute to insomnia — which is more common in typical depression — compared to hypersomnia, the researchers report.

The research team also included Tracy L. Greer, Ph.D., a 2004 Young Investigator grantee, also of UT Southwestern Medical Center.

The team cautioned that they studied only depressed people who were taking antidepressants, specifically selective serotonin reuptake inhibitors (SSRIs). SSRIs can change levels of immune system chemicals and BDNF. They can also disrupt sleep but are not commonly associated with hypersomnia. It is likely that SSRI effects may have shaped the relationship this study found between and the chemical markers. Future work can investigate the possibility of SSRI effects by looking at other groups, including people who are not taking any medication for their depression and those who have recovered from depression but still experience disrupted sleep.

Read the paper.

Support research now. Donate today!