Orange feathers and red hair have long been viewed as risky evolutionary traits, linked to pigments that can raise cellular stress and, in humans, increase cancer risk.
New research suggests that under certain conditions, that same orange pigment may instead help protect cells by managing specific dietary challenges.
In a controlled study at the Spanish National Research Council (CSIC), biologists studied 65 zebra finches to test whether pigmentation itself can limit metabolic damage.
Led by Dr. Ismael Galvan, the team used this built-in color difference to address a long-standing evolutionary puzzle: why a pigment associated with long-term costs persists so widely.
By manipulating diet and pigment production together, the study explores whether orange coloration serves not just as a signal, but as a cellular strategy for handling sulfur-rich nutrients.
The cost of orange pigment
Scientists call the orange pigment pheomelanin, an orange-to-red pigment built with sulfur that colors red hair and finch feathers.
Yet the same biology that colors red hair has been linked to higher melanoma risk, a pattern that has puzzled evolutionary biologists for decades.
If the pigment only added danger, natural selection would usually favor genetic variants that steer cells toward safer dark melanin.
Dr. Galvan’s team tested a long-standing idea that making pheomelanin can also solve a nutritional problem.
Too much cysteine inside cells
Cells use cysteine, a sulfur amino acid used for protein building, but excess amounts can damage delicate chemical balances.
Under some conditions, cysteine oxidizes into cystine, and disulfidptosis – a form of cell death driven by disulfide stress – can follow.
Because pheomelanin is built from cysteine, producing more pigment can lock excess cysteine into a stable, harmless form.
That idea matters in pigment cells, where cysteine also feeds glutathione, a small molecule that helps neutralize reactive chemicals.
A drug blocks the pigment
To test the cysteine hypothesis, Galván’s group supplemented some birds and blocked pigment synthesis in others during the same period.
Each treated bird drank water containing about 0.013 ounces per gallon (0.1 g/L) of cysteine for one month.
Some males also received ML349, a drug that blocks pheomelanin synthesis by keeping a pigment receptor active.
After the treatments, blood tests tracked malondialdehyde, a byproduct of fat breakdown during oxidation, as a marker of systemic damage.
Damage showed in males
Among males, blocking pheomelanin changed the outcome of the cysteine supplement in a clear direction.
Males given cysteine plus ML349 had higher malondialdehyde levels in plasma than males given cysteine alone, once antioxidant capacity was considered.
The analysis adjusted for antioxidant-control gene activity in melanocytes, pigment-making cells in skin and feathers, before comparing the treatment groups.
Those results support a simple mechanism, pigment production used extra cysteine, leaving fewer reactive byproducts to harm cells.
Females lacked a safety valve
Females offered a natural contrast, since they do not lay down orange pheomelanin in their feathers.
When females drank the cysteine-spiked water, malondialdehyde levels tended to rise compared with controls that received plain water.
ML349 did not change female blood markers, which fit with their lack of pheomelanin production in the first place.
Without the pigment pathway, excess cysteine appeared more like a burden than a useful nutrient in these birds.
Turning amino acids into feathers
Pheomelanin formation can lower free cysteine in cells, since building the pigment uses the same amino acid.
Inside melanosomes – tiny packages where pigment is assembled – melanocytes build pheomelanin and move it into growing feathers.
“These results demonstrate that pheomelanin synthesis avoids cellular damage by excreting excess cysteine to inert keratinous structures such as feathers,” said Galvan.
The catch is that other tissues may not have this pigment pathway, so cysteine handling can differ across the body.
What this means for redheads
For humans, the same orange pigment is most familiar in red hair and very fair skin. A 2012 mouse-model study found that the pheomelanin pathway can increase melanoma risk without ultraviolet radiation.
The finch results suggest diet and metabolism could shape that risk by changing how much cysteine pigment cells need to manage.
Human testing was not part of this work, so it cannot yet determine which foods raise cysteine levels in skin.
Pigment doubles as cellular protection
If pheomelanin helps manage excess cysteine, orange plumage may persist because it solves physiological problems beyond signaling or style.
Natural selection can favor pigment-related genes even when they carry long-term costs, as long as they reduce everyday cellular stress under certain diets or environmental conditions.
That tradeoff could help explain why orange and red color patterns reappear so often across birds, mammals, and reptiles.
It also complicates simple health narratives around pigmentation, suggesting that a pigment’s biological effects may depend as much on environment and diet as on genetics.
Taken together, the CSIC-led finch experiment links orange pigmentation and cysteine regulation to measurable markers of cellular damage in the blood.
Next, the researchers will explore whether human skin relies on a similar pigment-based storage route. The team will also investigate whether shifts in diet or disease alter cysteine levels in ways that change pigment’s protective role.
The study is published in the journal PNAS Nexus.
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