Stress, telomeres and CLL, a possible connection

[AussieNeil]

The question of what role stress has in us developing CLL and its rate of progression regularly comes up.  Premature shortening of telomeres provides one possible mechanism behind a disease that is mostly prevalent in the older population, with a median age of diagnosis in the early 70's.  'Elissa Epel is studying how personality, stress processes and environment affect our DNA — and how we might lessen damaging effects.

Money problems, a heavy work load, caregiving — such increasingly common pressures have helped make stress a part of modern American life. According to APA's Stress in America survey, 42 percent of adults in the United States. say their stress level has increased over the past five years. Even teens reported stress rivaling adult levels.

Recent research suggests chronic stress damage starts before we're even conceived and cuts into our very cells. A number of studies have linked stress with shorter telomeres, a chromosome component that's been associated with cellular aging and risk for heart disease, diabetes and cancer.

How do personality and environment play into this phenomenon? Elissa Epel, PhD, has been exploring that question for more than a decade at the University of California, San Francisco, where she directs the Center for Aging, Metabolism and Emotion. She often works with Elizabeth Blackburn, PhD, who won a Nobel Prize in 2009 for her research on telomeres.'

From the American Psychological Association: apa.org/monitor/2014/10/chr...

TEDMED talk in which 'Epel will share insights about how personality, mindset, and lifestyle can accelerate vs. protect us from premature cellular aging':

tedmed.com/speakers/show?id...

Note Elissa Epel's concern about carers of people with chronic health conditions too.

This post provides an overview and references other posts on this very interesting and exciting new research field  :

healthunlocked.com/cllsuppo...

I'll finish with Elissa's closing words:

'One thing to remember about chronic stress is that it's only our thoughts that make it seem so. Viewed mindfully, no situation is truly chronic — there are always calm moments to notice and be present for. Moments that can be lived in with ease.'

Neil

Photo: An 'Everlasting' native flower

[Jill4]

Seems so obvious that the science to validate it should be unnecessary (except when it leads to medical cures).  Stress less to be healthy.  God forbid we should stress less to be happy.  What a concept!

[Kwenda]

Study explains how genetic mutations linked to telomere capping complex contribute to cancers.

Scientists at The Wistar Institute have unveiled part of the protein complex that protects telomeres-;the ends of our chromosomes. The study, published online in Nature Communications, explains how a group of genetic mutations associated with this protein complex contributes to various cancers.

Telomeres are the protective structures at the end of chromosomes and are essential for the faithful replication and protection of our genome. Defects in telomere function can lead to genomic instability in cancer, while the gradual shortening of telomeres is associated with the aging of human cells. A key component of the telomere protecting mechanism is a multi-protein complex called shelterin. Shelterin protects chromosome ends from triggering DNA damage response mechanisms; it also regulates telomere maintenance and replication by the enzyme telomerase.

This new study describes the atomic structure of the protein-protein interaction between two subunits of the shelterin complex, POT1 and TPP1. Several gene mutations have been described as affecting portions of POT1 in familial melanoma, glioma and chronic lymphocytic leukemia. Based on a host of structural, biochemical and cell-based data, the study explains how these mutations may contribute to malignant transformation.

news-medical.net/news/20170...

PHILADELPHIA — (April 10, 2017) — Scientists at The Wistar Institute have unveiled part of the protein complex that protects telomeres—the ends of our chromosomes. The study, published online in Nature Communications, explains how a group of genetic mutations associated with this protein complex contributes to various cancers.

Telomeres are the protective structures at the end of chromosomes and are essential for the faithful replication and protection of our genome. Defects in telomere function can lead to genomic instability in cancer, while the gradual shortening of telomeres is associated with the aging of human cells. A key component of the telomere protecting mechanism is a multi-protein complex called shelterin. Shelterin protects chromosome ends from triggering DNA damage response mechanisms; it also regulates telomere maintenance and replication by the enzyme telomerase.

wistar.org/news-and-media/p...

Dick