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Stress Longevity

Short Stresses Promote Longevity

7 years, 2 months ago

18939  0
Posted on Feb 17, 2017, 6 a.m.

New study reveals why brief periods of bodily stress are good for health and longevity.

"What does not kill you makes you stronger." It's not just a saying. It is a scientific truth. Researchers have pinpointed a cell recycling process tied to the positive effects of moderate stress. This means people shouldn't necessarily fret over those mild stresses. Anything from going for a jog to spending some time in the sauna is beneficial for health as well as longevity

Study Details


Researchers found that the cellular process important for boosting lifespan, known as autophagy, is also important for obtaining benefits from stress. Biologists have known for quite a long time that temporary episodes of moderate stress empower simple organisms as well as cells within human beings to better survive stress at later points in life. The recent research conducted by scientists at the Sanford Burnham Prebys Medical Discovery Institute has shed new light on this truth. These researchers found that autophagy really does benefit the body when stress occurs. Their study was recently published in Nature Communications. The study will likely establish new paths to pursue treatment for various neurological disorders like Huntington's disease.

A Word About Autophagy


Autophagy is best described as a way to recycle cells' broken, aged and unnecessary parts so components can be used to create new molecules or even burned to create energy. Scientists previously linked this process to longevity. The results of the new research connect stress resistance and long life on a cellular level. The study's lead author, staff scientist Caroline Kumsta, Ph.D., states her team made use of C. elegans or diminutive roundworms to analyze fundamental biology.

Roundworms were used to gauge the importance of autophagy for stress resistance. Part of the reason why they were used is the fact that they are translucent so scientists can see exactly what occurs inside of them. Furthermore, the majority of roundworms' molecular signaling pathways and genes are similar to those in human beings. They live a couple of weeks which makes it easier to gauge their lifespans. These worms were incubated at 36 degrees Celsius for a full hour. After this exposure to heat (mild stress), the rate of autophagy heightened across the worms' tissues. The researchers then exposed these heated worms to a lengthy heat source a couple of days later. The worms that were autophagy-deficient did not obtain benefit from the first mild heat shock. Heated worms with intact autophagy obtained benefit from the heat shock.

What It Means


Researchers concluded that a mild source of heat heightens worms' ability to endure another condition that gets worse during the aging process: the accumulation of aggregated proteins. Such a buildup is quite stressful for cells. Kumsta made use of worms that replicate Huntington's disease that causes degeneration in the brain. Exposing worms with sticky neuronal proteins (like those found in patients with Huntington's disease) to a moderate heat shock decreased protein aggregates. This suggests a moderate mount of heat stress can minimize the toxic accumulation of proteins.

The study is a massive breakthrough as it sets the stage for new approaches to mitigating the onset of neurodegenerative diseases like Huntington's. These results might also pertain to Parkinson's and Alzheimer's disease as they are also induced by the accumulation of proteins prone to clumping.

Perhaps the induction of autophagy as a result of moderate heat stress at an early stage allows cells to better survive heat exposure at a later point in time. Questions regarding cellular memory must be explored. In the end, it can be said that heading to the sauna, going for a jog or doing hot yoga might not be a bad idea at all.

Caroline Kumsta, Jessica T. Chang, Jessica Schmalz, Malene Hansen. Hormetic heat stress and HSF-1 induce autophagy to improve survival and proteostasis in C. elegans. Nature Communications, 2017; 8: 14337 DOI: 10.1038/ncomms14337

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