The body undergoes many changes as it ages and some of the processes that don’t work as well contribute to a shortened lifespan. New research from the Baylor University College of Medicine found the combination of glycine and N-acetyl cysteine (GlyNAC) was able to extend the life of laboratory mice by 24 percent.
Researchers looking to counter glutathione deficiency, increased oxidative stress, mitochondrial dysfunction and other effects of aging on the body wanted to see if GlyNAC could reverse some of those conditions based on results seen in other work with those two nutrients.
"Just like a car is subject to wear and tear over many years of use, limiting how long it works well, the natural aging process can progressively deteriorate the body and limit lifespan," said researcher Rajagopal Sekhar. "Energy is the currency of life and is generated by mitochondria. However, aging is associated with mitochondrial malfunction, and this could affect energy availability.
"When we discovered that GlyNAC supplementation can correct mitochondrial defects in aging, we asked an important question: Could GlyNAC supplementation from a younger age extend length of life?" Sekhar added. "To answer this question, we worked with healthy, normal laboratory mice."
He and his colleagues started working with a group of mice when they reached the age of 65 weeks because that is when they normally start to show a drop in glutathione levels and develop mitochondrial dysfunction and oxidative stress. At that time they split the group in two and kept them fed the same way with the exception of GlyNAC supplementation for one group. They were then observed for the remainder of their lives.
"We were excited to find that the mice that received GlyNAC lived 24% longer than those that did not receive GlyNAC," Sekhar said. "We next wanted to understand how GlyNAC works."
A second study was conducted to look closer at the effects of aging on the heart, liver and kidneys of the mice. They found all three organs displayed glutathione deficiency, oxidative stress, mitochondrial dysfunction and abnormal mitophagy, which is difficulty disposing of damaged mitochondria. They also showed signed of impaired nutrient sensing and genomic damage.
GlyNAC supplementation was able to improve and correct these conditions in the mice. That is what researchers attribute to the extended life of that subset of mice.
"But mice are not humans," Sekhar said. "Could this happen in people? There is published evidence from our human studies showing that GlyNAC supplementation improves similar defects in people."
In one study, a 24-week supplement routine with GlyNAC showed improvement in glutathione deficiency, oxidative stress, mitochondrial dysfunction and other characteristic defects of aging. It also led to improvements in muscle strength, exercise capacity and cognitive function.
Another study with HIV patients also showed improvements in processes consistent with premature aging.
"There is growing interest in being able to improve both healthy aging and longer life, but this is not an easy task," Sekhar said. "We have investigated aging in mice and in human studies for two decades, and our studies show that GlyNAC supplementation successfully and consistently improves many age-related defects. It is exciting that something as simple as GlyNAC can improve several important defects in aging and also extend life."