Abstract
Background
Telomere shortening and alterations of mitochondrial biogenesis are involved in cellular
aging. Childhood adversity is associated with telomere shortening, and several investigations
have shown short telomeres in psychiatric disorders. Recent studies have examined
whether mitochondria might be involved in neuropsychiatric conditions; findings are
limited and no prior work has examined this in relation to stress exposure.
Methods
Two-hundred ninety healthy adults provided information on childhood parental loss
and maltreatment and completed diagnostic interviews. Participants were categorized
into four groups based upon the presence or absence of childhood adversity and the
presence or absence of lifetime psychopathology (depressive, anxiety, and substance
use disorders). Telomere length and mitochondrial DNA (mtDNA) copy number were measured
from leukocyte DNA by quantitative polymerase chain reaction.
Results
Childhood adversity and lifetime psychopathology were each associated with shorter
telomeres (p < .01) and higher mtDNA copy numbers (p < .001). Significantly higher mtDNA copy numbers and shorter telomeres were seen
in individuals with major depression, depressive disorders, and anxiety disorders,
as well as those with parental loss and childhood maltreatment. A history of substance
disorders was also associated with significantly higher mtDNA copy numbers.
Conclusions
This study provides the first evidence of an alteration of mitochondrial biogenesis
with early life stress and with anxiety and substance use disorders. We replicate
prior work on telomere length and psychopathology and show that this effect is not
secondary to medication use or comorbid medical illness. Finally, we show that early
life stress and psychopathology are each associated with these markers of cellular
aging.
Keywords
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Article Info
Publication History
Published online: January 16, 2015
Accepted:
December 31,
2014
Received in revised form:
December 22,
2014
Received:
May 28,
2014
Identification
Copyright
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