Cold stimulates the production of a muscle molecule that slows cellular ageing.
Person running in a cold environment (AI-generated image)
Research led by the University of Cologne and published in the journal Nature has found that low temperatures induce muscles to produce the molecule BH2 (dihydrobiopterin). This metabolite travels to other organs and activates proteostasis, the cellular mechanism responsible for properly maintaining, repairing and eliminating proteins. It was already known that cold temperatures could extend lifespan in animals, but this finding reveals the biochemical machinery that explains this phenomenon beyond the simple slowing down of metabolism.
Experiments carried out with the laboratory worm C. elegans showed an increase of up to 50% in longevity after lowering the temperature from 20°C to 15°C, keeping the specimens young and healthy for longer. The main results were confirmed in human cells: the addition of BH2 prevented protein dysfunction in neurons affected by neurodegenerative disorders such as amyotrophic lateral sclerosis (ALS) or Huntington’s disease, in which failure of proteostasis is a determining factor.
Although the breakthrough will not have immediate applications, the team led by biochemist David Vílchez has patented the results and plans to launch a startup to develop therapies that mimic the benefits of cold without exposing the body to low temperatures. The main long-term goal will be the treatment of neurodegenerative diseases — such as Alzheimer’s or Parkinson’s — and, in the even longer term, the possibility of extending the length of time we live in good health.
