Chronic stress, an individual has consistently over a significant lot of time. It influences mental and emotional wellbeing as well as physical health.
Studies have tied chronic stress to increased cognitive impairment, a higher risk of heart issues, and issues with gut health.
Past research likewise proposes that exposure to stress could accelerate the development of malignant growth through its effect on gene activity.
Presently, analysts from the Dalian Medical University in China — as a team with partners from over the world — have found a key mechanism. This mechanism triggers chronic stress, that fuels the development of malignant growth.
More specifically, scientists have studied this mechanism in mouse models of breast cancer.
Their findings are reported in The Journal of Clinical Investigation. These findings blame the hormone epinephrine. However, they additionally suggest a procedure to counteract the impacts of stress mechanism on cancer cells.
“You can kill all the cells you want in a tumor,” notes co-author Keith Kelley, from the University of Illinois at Chicago, “but if the stem cells, or mother cells, are not killed, then the tumor is going to grow and metastasize.”
He adds, “This is one of the first studies to link chronic stress specifically with the growth of breast cancer stem cells.”
Stress energizes tumor development:
According to principal investigator Quentin Liu, from the Institute of Cancer Stem Cell at Dalian Medical University, “The direct signaling network between stress pathways and a cancer-propagating system remains almost completely unknown.”
He adds, “A better understanding of the biochemistry that causes stress to increase the growth of cancer cells could lead us toward targeted drug interventions, one of which we discovered in this work.”
How does epinephrine help cancer stem cells to flourish?
Researchers investigated how different physiological factors changed in the mice that had encountered chronic stress. The researchers surrounded a hormone called epinephrine.
The stressed mice had more elevated levels of this hormone than the mice in the control group. Likewise, in mice from the experimental group that had gotten a medication that blocked ADRB2 — tumors were littler. The number of cancer stem cells were also lower.
The authors clarify that this hormone binds to ADRB2. This binding supports levels of lactate dehydrogenase. Lactate dehydrogenase is a protein that typically gives muscles an “injection” of energy in a risk circumstance. This enables the individual to either battle the risk or flee from it.
A result of this jolt of energy is the production of an organic compound called lactate. In the case of individuals with cancer, the harmful cells really feed on this compound. It enables them to procure more energy.
This implies if an individual has chronic stress, they will have too much lactate dehydrogenase in their system. This, thus, will activate the genes related to cancer development. This also enables cancer cells to flourish.
Is Vitamin C a cure?
In laboratory tests on breast cancer cell lines, researchers analyzed the impacts of a few FDA approved drugs on lactate dehydrogenase production.
The most encouraging substance that the researchers settled on was actually Vitamin C. It blocked lactate dehydrogenase production in laboratory tests. Researchers tried this methodology in mouse models. They acquired similar outcomes: Stressed mice they’d injected with Vitamin C experienced tumor shrinkage.
“Taken together, these findings show that vitamin C might be a novel and effective therapeutic agent for targeting cancer in patients undergoing chronic stress,” concludes Liu.