New Study Sheds Light on Extending Lifespans
Most of us would love to live forever or at least longer than usual. Scientists have spent centuries attempting to uncover ways of elongating our lives. In fact, new treatments like vaccines or antibiotics and life-saving procedures like heart surgery have doubled our life expectancy over the last 150 years.
More recently, investigators discovered a way to increase the lifespan of mice and even decrease their likelihood of developing diabetes in old age, according to the American Association for the Advancement of Science. The mice need to be raised without a certain pain receptor or sensor in order for this to occur.
Additionally, the researchers uncovered that a molecule found in spicy foods like chili peppers could lead to the same beneficial health outcomes. Instead of losing the pain receptor, human beings may be able to profit from this substance in spicy foods.
Whenever you hurt yourself, pain receptors in your skin usually send signals to your brain via neurons and let you know what has been damaged. Unfortunately, an excess of pain can actually impair your body. For instance, those with chronic pain tend to have shorter lifespans. The exact cause of this has not been found, but aches and spasms tend to be inversely correlated with total years in one’s lifetime.
A research team from The University of California, Berkeley raised mouse models in the lab without the pain receptor TRPV1. Interestingly enough, this receptor is triggered by capsaicin, a compound found in chili peppers. Essentially, the scientists found that mouse models without TRPV1 lived 14 percent longer than the control group of mice. Calorie restriction is another method for lengthening the lifespan of laboratory mice.
The mice without TRPV1 showed better metabolism as they aged. They were able to cleanse the sugars in blood quickly and efficiently. This is called glucose tolerance and often declines as animals age. This shows that mouse models bred without TRPV1 had a much lower likelihood of contracting diabetes. The experimental group also burned more calories while exercising than the standard, aging mouse.
The decreased risk of diabetes and increased longevity may be tied to the TRPV1 receptor’s role in regulating insulin within the pancreas. This receptor triggers the discharge of the CGRP compound, which stops insulin from moving into the blood passageways. When there is less insulin in the bloodstream, it is more difficult to control the amount of sugars moving throughout the arteries.
Lead researcher Andrew Dillin from UC Berkeley explains that drug companies have already been targeting TRPV1 when creating painkillers, but may also benefit from using this type of medications “for treating diabetes and obesity.”
“It is striking that the mice without TRPV1 were protected from some of the ravages of old age, including declines in metabolism, cognition, and physical activity,” Molecular biologist David Sinclair of Harvard Medical School told the news source.
Whether it is to decrease the risk of diabetes or elongate lifespan, the mouse models display that removal of TRPV1 can achieve either goal.
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