Telomere Shortening and Mood Disorders: Preliminary Support for a Chronic Stress Model of Accelerated Aging

Little is known about the biological mechanisms underlying the excess medical morbidity and mortality associated with mood disorders. Substantial evidence supports abnormalities in stress-related biological systems in depression. Accelerated telomere shortening may reflect stress-related oxidative d...

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Published in	Biological psychiatry (1969) Vol. 60; no. 5; pp. 432 - 435
Main Authors	Simon, Naomi M., Smoller, Jordan W., McNamara, Kate L., Maser, Richard S., Zalta, Alyson K., Pollack, Mark H., Nierenberg, Andrew A., Fava, Maurizio, Wong, Kwok-Kin
Format	Journal Article
Language	English
Published	New York, NY Elsevier Inc 01.09.2006 Elsevier Science
Subjects	Adult Adult and adolescent clinical studies Aging Aging - genetics Anxiety - complications Anxiety - genetics Biological and medical sciences bipolar Bipolar Disorder - complications Bipolar Disorder - genetics Case-Control Studies Cellular Senescence - genetics Chromosome Breakage Chronic Disease Depression Female Humans major depressive disorder Male Matched-Pair Analysis Medical sciences Middle Aged Models, Genetic mood disorder Mood disorders Mood Disorders - complications Mood Disorders - genetics Psychology. Psychoanalysis. Psychiatry Psychopathology. Psychiatry Reference Values Statistics, Nonparametric stress Stress, Psychological - etiology Stress, Psychological - genetics Telomere Aging stress bipolar mood disorder major depressive disorder telomere Mood disorder Chronic Senescence Depression Models Stress
Online Access	Get full text
ISSN	0006-3223 1873-2402
DOI	10.1016/j.biopsych.2006.02.004

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Abstract	Little is known about the biological mechanisms underlying the excess medical morbidity and mortality associated with mood disorders. Substantial evidence supports abnormalities in stress-related biological systems in depression. Accelerated telomere shortening may reflect stress-related oxidative damage to cells and accelerated aging, and severe psychosocial stress has been linked to telomere shortening. We propose that chronic stress associated with mood disorders may contribute to excess vulnerability for diseases of aging such as cardiovascular disease and possibly some cancers through accelerated organismal aging. Telomere length was measured by Southern Analysis in 44 individuals with chronic mood disorders and 44 nonpsychiatrically ill age-matched control subjects. Telomere length was significantly shorter in those with mood disorders, representing as much as 10 years of accelerated aging. These results provide preliminary evidence that mood disorders are associated with accelerated aging and may suggest a novel mechanism for mood disorder-associated morbidity and mortality.
AbstractList	Little is known about the biological mechanisms underlying the excess medical morbidity and mortality associated with mood disorders. Substantial evidence supports abnormalities in stress-related biological systems in depression. Accelerated telomere shortening may reflect stress-related oxidative damage to cells and accelerated aging, and severe psychosocial stress has been linked to telomere shortening. We propose that chronic stress associated with mood disorders may contribute to excess vulnerability for diseases of aging such as cardiovascular disease and possibly some cancers through accelerated organismal aging. Telomere length was measured by Southern Analysis in 44 individuals with chronic mood disorders and 44 nonpsychiatrically ill age-matched control subjects. Telomere length was significantly shorter in those with mood disorders, representing as much as 10 years of accelerated aging. These results provide preliminary evidence that mood disorders are associated with accelerated aging and may suggest a novel mechanism for mood disorder-associated morbidity and mortality. Little is known about the biological mechanisms underlying the excess medical morbidity and mortality associated with mood disorders. Substantial evidence supports abnormalities in stress-related biological systems in depression. Accelerated telomere shortening may reflect stress-related oxidative damage to cells and accelerated aging, and severe psychosocial stress has been linked to telomere shortening. We propose that chronic stress associated with mood disorders may contribute to excess vulnerability for diseases of aging such as cardiovascular disease and possibly some cancers through accelerated organismal aging.BACKGROUNDLittle is known about the biological mechanisms underlying the excess medical morbidity and mortality associated with mood disorders. Substantial evidence supports abnormalities in stress-related biological systems in depression. Accelerated telomere shortening may reflect stress-related oxidative damage to cells and accelerated aging, and severe psychosocial stress has been linked to telomere shortening. We propose that chronic stress associated with mood disorders may contribute to excess vulnerability for diseases of aging such as cardiovascular disease and possibly some cancers through accelerated organismal aging.Telomere length was measured by Southern Analysis in 44 individuals with chronic mood disorders and 44 nonpsychiatrically ill age-matched control subjects.METHODSTelomere length was measured by Southern Analysis in 44 individuals with chronic mood disorders and 44 nonpsychiatrically ill age-matched control subjects.Telomere length was significantly shorter in those with mood disorders, representing as much as 10 years of accelerated aging.RESULTSTelomere length was significantly shorter in those with mood disorders, representing as much as 10 years of accelerated aging.These results provide preliminary evidence that mood disorders are associated with accelerated aging and may suggest a novel mechanism for mood disorder-associated morbidity and mortality.CONCLUSIONSThese results provide preliminary evidence that mood disorders are associated with accelerated aging and may suggest a novel mechanism for mood disorder-associated morbidity and mortality. Background Little is known about the biological mechanisms underlying the excess medical morbidity and mortality associated with mood disorders. Substantial evidence supports abnormalities in stress-related biological systems in depression. Accelerated telomere shortening may reflect stress-related oxidative damage to cells and accelerated aging, and severe psychosocial stress has been linked to telomere shortening. We propose that chronic stress associated with mood disorders may contribute to excess vulnerability for diseases of aging such as cardiovascular disease and possibly some cancers through accelerated organismal aging. Methods Telomere length was measured by Southern Analysis in 44 individuals with chronic mood disorders and 44 nonpsychiatrically ill age-matched control subjects. Results Telomere length was significantly shorter in those with mood disorders, representing as much as 10 years of accelerated aging. Conclusions These results provide preliminary evidence that mood disorders are associated with accelerated aging and may suggest a novel mechanism for mood disorder-associated morbidity and mortality.
Author	Maser, Richard S. Pollack, Mark H. Simon, Naomi M. Smoller, Jordan W. Fava, Maurizio Wong, Kwok-Kin McNamara, Kate L. Nierenberg, Andrew A. Zalta, Alyson K.
Author_xml	– sequence: 1 givenname: Naomi M. surname: Simon fullname: Simon, Naomi M. email: NSIMON@Partners.org organization: Department of Psychiatry, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts – sequence: 2 givenname: Jordan W. surname: Smoller fullname: Smoller, Jordan W. organization: Department of Psychiatry, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts – sequence: 3 givenname: Kate L. surname: McNamara fullname: McNamara, Kate L. organization: Department of Medical Oncology, Dana Farber Cancer Institute, Boston, Massachusetts – sequence: 4 givenname: Richard S. surname: Maser fullname: Maser, Richard S. organization: Department of Medical Oncology, Dana Farber Cancer Institute, Boston, Massachusetts – sequence: 5 givenname: Alyson K. surname: Zalta fullname: Zalta, Alyson K. organization: Department of Psychiatry, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts – sequence: 6 givenname: Mark H. surname: Pollack fullname: Pollack, Mark H. organization: Department of Psychiatry, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts – sequence: 7 givenname: Andrew A. surname: Nierenberg fullname: Nierenberg, Andrew A. organization: Department of Psychiatry, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts – sequence: 8 givenname: Maurizio surname: Fava fullname: Fava, Maurizio organization: Department of Psychiatry, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts – sequence: 9 givenname: Kwok-Kin surname: Wong fullname: Wong, Kwok-Kin organization: Department of Medical Oncology, Dana Farber Cancer Institute, Boston, Massachusetts
BackLink	http://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=18107511$$DView record in Pascal Francis https://www.ncbi.nlm.nih.gov/pubmed/16581033$$D View this record in MEDLINE/PubMed
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Snippet	Little is known about the biological mechanisms underlying the excess medical morbidity and mortality associated with mood disorders. Substantial evidence... Background Little is known about the biological mechanisms underlying the excess medical morbidity and mortality associated with mood disorders. Substantial...
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SubjectTerms	Adult Adult and adolescent clinical studies Aging Aging - genetics Anxiety - complications Anxiety - genetics Biological and medical sciences bipolar Bipolar Disorder - complications Bipolar Disorder - genetics Case-Control Studies Cellular Senescence - genetics Chromosome Breakage Chronic Disease Depression Female Humans major depressive disorder Male Matched-Pair Analysis Medical sciences Middle Aged Models, Genetic mood disorder Mood disorders Mood Disorders - complications Mood Disorders - genetics Psychology. Psychoanalysis. Psychiatry Psychopathology. Psychiatry Reference Values Statistics, Nonparametric stress Stress, Psychological - etiology Stress, Psychological - genetics Telomere
Title	Telomere Shortening and Mood Disorders: Preliminary Support for a Chronic Stress Model of Accelerated Aging
URI	https://www.clinicalkey.com/#!/content/1-s2.0-S0006322306001363 https://dx.doi.org/10.1016/j.biopsych.2006.02.004 https://www.ncbi.nlm.nih.gov/pubmed/16581033 https://www.proquest.com/docview/19704687 https://www.proquest.com/docview/68809206
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