HEALTHY LIFESTYLE MAY BUFFER AGAINST STRESS-RELATED CELL AGING
UC San Francisco Study Suggests Healthy Diet, Sleep and Exercise Can Mitigate Negative Impacts of Stress
From the FMS Global News Desk of Jeanne Hambleton Embargo expired: 29-Jul-2014
Source Newsroom: University of California, San Francisco (UCSF) Citations Molecular Psychiatry, July 29, 2014
Newswise — A new study from UC San Francisco is the first to show that while the impact of life’s stressors accumulate overtime and accelerate cellular aging, these negative effects may be reduced by maintaining a healthy diet, exercising and sleeping well.
“The study participants who exercised, slept well and ate well had less telomere shortening than the ones who did not maintain healthy lifestyles, even when they had similar levels of stress,” said lead author Eli Puterman, PhD, assistant professor in the department of psychiatry at UCSF.
“It is very important that we promote healthy living, especially under circumstances of typical experiences of life stressors like death, caregiving and job loss.”
The paper will be published in Molecular Psychiatry, a peer-reviewed science journal by Nature Publishing Group.
Telomeres are the protective caps at the ends of chromosomes that affect how quickly cells age. They are combinations of DNA and proteins that protect the ends of chromosomes and help them remain stable. As they become shorter, and as their structural integrity weakens, the cells age and die quicker. Telomeres also get shorter with age.
In the study, researchers examined three healthy behaviors –physical activity, dietary intake and sleep quality – over the course of one year in 239 post-menopausal, non-smoking women. The women provided blood samples at the beginning and end of the year for telomere measurement and reported on stressful events that occurred during those 12 months.
In women who engaged in lower levels of healthy behaviors, there was a significantly greater decline in telomere length in their immune cells for every major life stressor that occurred during the year. Yet women who maintained active lifestyles, healthy diets, and good quality sleep appeared protected when exposed to stress – accumulated life stressors did not appear to lead to greater shortening.
“This is the first study that supports the idea, at least observationally, that stressful events can accelerate immune cell aging in adults, even in the short period of one year. Exciting, though, is that these results further suggest that keeping active, and eating and sleeping well during periods of high stress are particularly important to attenuate the accelerated aging of our immune cells,” said Puterman.
In recent years, shorter telomeres have become associated with a broad range of aging-related diseases, including stroke, vascular dementia, cardiovascular disease, obesity, osteoporosis diabetes, and many forms of cancer.
Research on telomeres, and the enzyme that makes them, telomerase, was pioneered by three Americans, including UCSF molecular biologist and co-author Elizabeth Blackburn, PhD. Blackburn co-discovered the telomerase enzyme in 1985. The scientists received the Nobel Prize in Physiology for Medicine in 2009 for their work.
“These new results are exciting yet observational at this point. They do provide the impetus to move forward with interventions to modify lifestyle in those experiencing a lot of stress, to test whether telomere attrition can truly be slowed,” said Blackburn.
Co-authors include senior author Elissa Epel, PhD, department of psychiatry, Jue Lin, PhD, department of biochemistry and biophysics, both of UCSF and Jeffrey Krauss, MD, division of physical medicine and rehabilitation at Stanford University. Lin, Epel and Blackburn are the co-founders of Telome Health Inc., a diagnostic company measuring telomere biology.
The study was supported by the Baumann Foundation and the Barney & Barbro Foundation. Puterman is supported by the National Heart, Lung and Blood Institute of the National Institutes of Health.
UCSF is the nation’s leading university exclusively focused on health. Now celebrating the 150th anniversary of its founding as a medical college, UCSF is dedicated to transforming health worldwide through advanced biomedical research, graduate-level education in the life sciences and health professions, and excellence in patient care. It includes top-ranked graduate schools of dentistry, medicine, nursing and pharmacy; a graduate division with world-renowned programs in the biological sciences, a preeminent biomedical research enterprise and two top-tier hospitals, UCSF Medical Center and UCSF Benioff Children’s Hospital San Francisco.
KEY TO AGING IMMUNE SYSTEM IS DISCOVERED
From the FMS Global News Desk of Jeanne Hambleton Released: 31-Jul-2014
Source Newsroom: University of California, San Francisco (UCSF) Nature, July 30, 2014
Newswise — There Is a good reason people over 60 are not donor candidates for bone marrow transplantation. The immune system ages and weakens with time, making the elderly prone to life-threatening infection and other maladies, and a UC San Francisco research team now has discovered a reason why.
“We have found the cellular mechanism responsible for the inability of blood-forming cells to maintain blood production over time in an old organism, and have identified molecular defects that could be restored for rejuvenation therapies,” said Emmanuelle Passegué, PhD, a professor of medicine and a member of the Eli and Edythe Broad Center of Regeneration Medicine and Stem Cell Research at UCSF.
Passegué, an expert on the stem cells that give rise to the blood and immune system, led a team that published the new findings online July 30, 2014 in the journal Nature.
Blood and immune cells are short-lived, and unlike most tissues, must be constantly replenished. The cells that must keep producing them throughout a lifetime are called “hematopoietic stem cells.” Through cycles of cell division these stem cells preserve their own numbers and generate the daughter cells that give rise to replacement blood and immune cells.
But the hematopoietic stem cells falter with age, because they lose the ability to replicate their DNA accurately and efficiently during cell division, Passegué’s lab team determined.
Especially vulnerable to the breakdown, the researchers discovered in their new study of old mice, are transplanted, aging, blood-forming stem cells, which lack the ability to make B cells of the immune system. These B cells make antibodies to help us fight all sorts of microbial infections, including bacteria that cause pneumonia, a leading killer of the elderly.
In old blood-forming stem cells, the researchers found a scarcity of specific protein components needed to form a molecular machine called the mini-chromosome maintenance helicase, which unwinds double-stranded DNA so that the cell’s genetic material can be duplicated and allocated to daughter cells later in cell division.
In their study the stem cells were stressed by the loss of activity of this machine and as a result were at heightened risk for DNA damage and death when forced to divide.
The researchers discovered that even after the stress associated with DNA replication, surviving, non-dividing, resting, old stem cells retained molecular tags on DNA-wrapping histone proteins, a feature often associated with DNA damage. However, the researchers determined that these old survivors could repair induced DNA damage as efficiently as young stem cells.
“Old stem cells are not just sitting there with damaged DNA ready to develop cancer, as it has long been postulated” Passegué said.
But not all was well in the old, surviving stem cells. The molecular tags accumulated on genes needed to make the cellular factories known as ribosomes. The ribosomes make all the cell’s proteins. Passegué will further explore the consequences of reduced protein production as part of her ongoing research.
“Everybody talks about healthier aging,” Passegué added. “The decline of stem-cell function is a big part of age-related problems. Achieving longer lives relies in part on achieving a better understanding of why stem cells are not able to maintain optimal functioning.”
Passegué hopes that it might be possible to prevent declining stem-cell populations by developing a drug to prevent the loss of the helicase components needed to faithfully unwind and replicate DNA, thereby avoiding immune-system failure.
Among the additional study authors are graduate student Johanna Flach and postdoctoral fellow Sietske Bakker, PhD, who performed the experiments in Passegué’s lab at the Eli and Edythe Broad Center of Regeneration Medicine and Stem Cell Research at UCSF.
International collaborators included Juan Méndez, PhD, of the Spanish National Cancer Research Center, in Madrid, and Ciaran Morrison, PhD, of the National University of Ireland, in Galway.
The research was funded by the California Institute for Regenerative Medicine and the National Institutes of Health. Passegué recently was recognized for the research with a prestigious Glenn Award for Research in Biological Mechanisms of Aging.
UC San Francisco (UCSF), now celebrating the 150th anniversary of its founding, is a leading university dedicated to promoting health worldwide through advanced biomedical research, graduate-level education in the life sciences and health professions, and excellence in patient care.
It includes top-ranked graduate schools of dentistry, medicine, nursing and pharmacy, a graduate division with nationally renowned programs in basic, biomedical, translational and population sciences, as well as a preeminent biomedical research enterprise and two top-ranked hospitals, UCSF Medical Center and UCSF Benioff Children’s Hospital San Francisco.
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