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Cold, muscle and BH2: the molecule behind longer-lived worms (Nature, University of Cologne)
The full story behind my Short: A University of Cologne study in Nature found that mild cold makes C. elegans worms' muscles produce BH2, which travels to other tissues and drives tyrosine production, extending worm lifespan. Lifespan results are in worms, not people.
The short version
Can a little cold slow ageing? In tiny C. elegans worms, at least, scientists at the University of Cologne think they know why it helps. Moving the worms from 20 °C to 15 °C considerably extends their lifespan. The cold makes their muscles produce a molecule called BH2 (dihydrobiopterin); the muscle acts as a 'central factory'. BH2 travels to other tissues, including the gut and neurons, where it is converted into BH4 and used to make the amino acid tyrosine. Boosting BH2 production in muscle, or giving the worms tyrosine, extended their lifespan even at normal temperatures. In human cells in the lab, BH2 or tyrosine reduced the clumping of proteins linked to Huntington's disease and ALS, and BH2 reduced cell death in lab-grown motor neurons carrying an ALS mutation. Caveat: the longer lives were in worms, not people, and the researchers say it is far too early for a pill that copies the effects of cold (Lee et al., Nature, 2026).
15 °Cvs the standard 20 °C: moderate cold considerably extends worm lifespan [2]
BH2produced in muscle, transported to the gut and neurons, converted to BH4 [1][2]
Tyrosinemade with BH4's help; tyrosine supplements extended worm lifespan even at standard temperature [2]
Worms onlyfor lifespan; human results are in cells in the lab [1][2]
What they found
The team led by Professor David Vilchez at the CECAD Cluster of Excellence on Aging, the Centre for Molecular Medicine Cologne and University Hospital Cologne raised C. elegans worms at the standard 20 °C until adulthood, then moved them to 15, 20 or 25 °C. Of the metabolites boosted by cold, BH2 (dihydrobiopterin) was among the most strongly induced [2]. Cold raises the activity of the enzyme CAT-4 (GCH1 in humans), and the muscle acts as a ‘central factory’ producing BH2 [1][2].
BH2 is transported to other tissues, including the intestine and neurons, where the enzyme DHFR-1 converts it into the active cofactor BH4. BH4 helps the enzyme PAH-1 make tyrosine, an amino acid, which promotes longevity and helps maintain proteostasis, the cell's balance of working proteins [2]. Increasing BH2 synthesis in muscle alone extended lifespan at 15, 20 and 25 °C, and tyrosine supplementation extended lifespan at both cold and standard temperature [2].
In human HEK293 cells, BH2 or tyrosine supplementation reduced aggregation of the polyQ-expanded protein associated with Huntington's disease and of mutant TDP-43 and FUS proteins that cause ALS. BH2 also reduced cell death (cleaved caspase-3) in motor neurons carrying the ALS-causing FUS(P525L) mutation [2].
Watch the Short
AI voice note: the narration in this Short is my own voice, cloned with AI.
About this page
All lifespan results described here are in C. elegans worms, not people; the human results are from cells grown in the lab. The paper reports that boosting BH2 production in muscle, and supplementing tyrosine, extended worm lifespan; I have not repeated the press release's wider wording about BH2 supplements extending lifespan, because the paper's lifespan data for BH2 supplements themselves are less clear-cut. Study figures are cropped from Lee et al., Nature 2026 (CC BY 4.0); the other images are illustrative, from Wikimedia Commons.
Why it matters
- One tissue, body-wide effects. Vilchez says targeting a single tissue such as muscle could provide organism-wide protection, opening new avenues for therapies [1].
- Cold without the cold. The team hopes to look for treatments that mimic the beneficial effects of cold without changing body temperature [1].
- Early days. The lifespan results are in worms; the researchers say it is far too early for a ‘pill’ that replicates cold's longevity effects [1].
Full narration (transcript)
Could being a little cold slow ageing? Scientists may have found the molecule behind it. A new Nature study from Cologne used tiny worms called C. elegans. Move them from 20 degrees to 15, and they live considerably longer. But how? Cold makes their muscles produce a molecule called BH2. Muscle acts like a central factory. BH2 travels to the gut and nerves, where it's used to make the amino acid tyrosine. Here's where it gets interesting. Boosting BH2 production in muscle, or giving the worms tyrosine, made them live longer, even without the cold. In human cells in the lab, BH2 or tyrosine reduced protein clumps linked to Huntington's and ALS. BH2 also reduced cell death in lab-grown motor neurons with an ALS mutation. The big caveat: the longer lives were in worms, not people. And the researchers say it's far too early for a pill that copies the effects of cold. It could point to treatments that mimic cold's benefits, without changing body temperature. For the full story, follow the link in the description.
Sources
- [1] University of Cologne (2026). “Mechanism revealed behind the positive effects of cold temperatures on delaying aging and preventing age-related diseases.” Press release, 22 October 2026. uni-koeln.de
- [2] Lee, H.J., Doğan, C., Koyuncu, S., et al. & Vilchez, D. (2026). “Cold activates a BH2 metabolic network promoting longevity and proteostasis.” Nature, published 21 October 2026. Open access, CC BY 4.0. nature.com
Credits
Images: Lee et al., Nature 2026 (CC BY 4.0, cropped) and Wikimedia Commons (illustrative): Hoar frost ice crystals in Tuntorp 13.jpg (W.carter, CC BY-SA 4.0); Adult Caenorhabditis elegans.jpg (Zeynep F. Altun (WormAtlas), uploaded by Kbradnam, CC BY-SA 2.5); Lee et al., Nature (2026), Fig. 1g (cropped) (Hyun Ju Lee, …, David Vilchez (Nature, 2026), CC BY 4.0 (cropped from the original figure)); Muscle Tissue Skeletal Muscle Fibers (28089114338).jpg (Berkshire Community College Bioscience Image Library, CC0); Lee et al., Nature (2026), Fig. 1b (cropped) (Hyun Ju Lee, …, David Vilchez (Nature, 2026), CC BY 4.0 (cropped from the original figure)); Lee et al., Nature (2026), Fig. 5a (cropped) (Hyun Ju Lee, …, David Vilchez (Nature, 2026), CC BY 4.0 (cropped from the original figure)); Lee et al., Nature (2026), Fig. 5e (cropped) (Hyun Ju Lee, …, David Vilchez (Nature, 2026), CC BY 4.0 (cropped from the original figure)); Universitat zu Köln Hauptgebäude ost.jpg (Universität zu Köln (UzK), Public domain). Sketches and animation: my own. Narration: AI clone of Nasper Mushonga's own voice (Chatterbox TTS by Resemble AI, MIT licence), used with his consent.