John Dalton, the English chemist better known for his atomic theory, gave the first systematic account of color blindness in 1794 when he described his own inability to tell scarlet from green and pink from blue. He was not the first person ever to notice color confusion, but he was the first to study and document it as a distinct visual condition, earning the phenomenon the lasting name “Daltonism” in many languages. His explanation for why it happened turned out to be completely wrong, and it would take nearly two centuries of science to sort out the real answer.
John Dalton’s Self-Experiment
Dalton presented his observations to the Manchester Literary and Philosophical Society in 1794. He and his brother shared the same color confusions, which gave him an early clue that the condition ran in families. What struck him most was how consistently he and others around him disagreed about everyday colors. A geranium that everyone else called red, he saw as something closer to what he would call blue or dark pink. He could not reliably sort colored threads or identify colored signals the way most people did.
To explain the problem, Dalton proposed that his vitreous humor, the gel filling the eyeball, was tinted blue. He reasoned that this blue filter absorbed longer-wavelength light before it reached his retina, preventing him from seeing reds properly.1PubMed. The chemistry of John Dalton’s color blindness It was a logical guess for the era, and it was testable. Dalton was so committed to the idea that he left instructions for his eyes to be examined after his death.
When Dalton died in 1844, his assistant Joseph Ransome dissected one of his preserved eyes and found the vitreous humor perfectly clear, not blue at all. The tinted-fluid hypothesis was dead. But the eyes were saved, stored in a jar at the Manchester Literary and Philosophical Society. More than 150 years later, in the 1990s, researchers extracted DNA from that preserved tissue and performed genetic analysis. The result confirmed that Dalton had deuteranopia, a specific type of red-green color blindness caused by the absence of functional green-sensitive cone photoreceptors.1PubMed. The chemistry of John Dalton’s color blindness So the man who first described color blindness never understood his own condition’s true cause, but his willingness to study himself set the whole field in motion.
Building the Theory of Color Vision
Dalton’s account placed color blindness on the scientific map, but the deeper question of how color vision works in the first place needed answering before anyone could properly understand color blindness. That work began with Thomas Young, who in the early 1800s proposed that the eye contains just three types of color receptor. Young realized that people could match any visible color by mixing only three lights, which made sense if the retina had three receptor types rather than hundreds. Hermann von Helmholtz later refined and championed Young’s idea, and it became known as the Young-Helmholtz trichromatic theory.2PubMed Central. The evolution of concepts of color vision
Not everyone was convinced. In the mid-1800s, Ewald Hering argued that color perception worked through opponent processes: red versus green, blue versus yellow, and black versus white. For decades, the trichromatic camp and the opponent-process camp treated each other’s views as incompatible. The resolution came much later, when researchers found that both were right at different stages of visual processing. The retina does contain three cone types, just as Young proposed, but neurons further along the visual pathway combine those signals into opponent channels, just as Hering described.2PubMed Central. The evolution of concepts of color vision This layered understanding of color vision finally gave scientists the framework to explain what goes wrong in different forms of color blindness.
A Train Crash That Changed Public Policy
For most of the 1800s, color blindness was a medical curiosity. That changed abruptly in November 1875, when two trains collided head-on near Lagerlunda, Sweden, killing several people. A Swedish physiologist named Alarik Frithiof Holmgren argued publicly that color blindness in railway workers was to blame for the disaster, and the claim gained enormous traction. Within a few years, European and North American railroads introduced mandatory color vision screening for their workers.3PubMed. The Lagerlunda collision and the introduction of color vision testing
Here is the twist: Holmgren was probably wrong about what actually caused the crash. Court records from the investigation show that the collision resulted from the engine driver and the station master acting contrary to operating regulations, not from any failure to distinguish colored signals.4PubMed. A railway accident a hundred years ago as reason for systematic testing of colour vision But Holmgren’s narrative was so persuasive, and the idea that color-blind workers were a safety risk so intuitively alarming, that the myth has been passed along as established fact ever since. The accident itself did not prove that color blindness caused disasters, yet it undeniably triggered a revolution in occupational screening. Methods of color vision testing improved rapidly in the years that followed, giving both clinicians and researchers far better tools than Dalton ever had.
The legacy of Lagerlunda is worth sitting with for a moment, because it illustrates something that recurs throughout the history of color blindness research: a wrong explanation driving a real and lasting change. Dalton’s wrong theory about blue vitreous humor put the condition on the map. Holmgren’s wrong attribution of the train crash created an entire infrastructure of workplace testing. Both errors produced genuine progress.
Finding the Genes
The next great leap came in the 1980s, when molecular biology caught up with color vision. In 1986, Jeremy Nathans and colleagues at Stanford and Johns Hopkins isolated and sequenced the genes encoding the three cone photopigments, the proteins responsible for absorbing light at different wavelengths in the red, green, and blue portions of the spectrum. The red and green pigments turned out to be remarkably similar to each other, sharing about 96 percent of their amino acid sequences, while both were only about 43 percent identical to the blue pigment.5PubMed. Molecular genetics of human color vision: the genes encoding blue, green, and red pigments
That 96-percent similarity between the red and green pigment genes turned out to be the key to understanding why red-green color blindness is so common. Because those genes sit right next to each other on the X chromosome and are nearly identical, they are prone to errors during DNA replication. During cell division, the similar stretches of DNA can misalign and recombine unevenly, deleting or merging gene copies in ways that knock out one pigment or create a hybrid that does not function properly. Nathans’ team tested DNA from 25 men with various red-green color vision deficiencies and confirmed that these genetic rearrangements were exactly what had happened in each case.3PubMed. The Lagerlunda collision and the introduction of color vision testing6Science. Molecular genetics of inherited variation in human color vision
This also explained why red-green color blindness affects roughly 8 percent of men but fewer than 1 percent of women. Because the red and green pigment genes live on the X chromosome, men, who have only one X, are affected if that single copy is altered. Women, with two X chromosomes, have a backup copy, so they are affected only if both copies carry the alteration. The genetics were elegant, and they finally confirmed the suspicion Dalton himself had hinted at over 190 years earlier when he noted that the condition ran through his family’s male members.
Gene Therapy and the Prospect of Restoring Color Vision
The discovery of the genes opened an obvious question: if you know which gene is missing or broken, could you insert a working copy and cure color blindness? In 2009, researchers did exactly that in squirrel monkeys that had been born with only two types of cone pigment, making them red-green color blind from birth. By injecting a virus carrying the gene for a third pigment into the monkeys’ retinas, the team gave the animals trichromatic color vision as adults. The monkeys began passing color discrimination tests they had always failed before.7PubMed Central. Gene therapy for red-green colour blindness in adult primates
This was a surprise because conventional thinking in neuroscience held that the brain’s visual circuitry needed to be wired up during a critical developmental window in early life. Adding a new type of input to an adult brain, the reasoning went, should not work because the neural machinery to process it was never built. The monkey experiments suggested otherwise: the adult visual system was flexible enough to incorporate a new dimension of color information without any special developmental intervention.7PubMed Central. Gene therapy for red-green colour blindness in adult primates
In humans, gene therapy trials have so far focused on achromatopsia, a much rarer and more severe condition in which cones barely function at all, leaving people essentially color-blind and highly sensitive to bright light. Several phase I/II clinical trials have tested viral delivery of working cone genes in patients with specific genetic forms of achromatopsia.8PubMed Central. Gene Therapy for Color Blindness A trial of nine patients who received a subretinal injection of a gene targeting a specific cone channel protein found no serious safety problems over 12 months, and every treated eye showed some improvement in cone-related measures, including a small but real gain in visual acuity and contrast sensitivity.9JAMA Ophthalmology. Safety and Vision Outcomes of Subretinal Gene Therapy Targeting Cone Photoreceptors in Achromatopsia: A Nonrandomized Controlled Trial
These are early-stage results in a rare condition, and no gene therapy for common red-green color blindness has reached human trials yet. But the primate work provides reason to think the basic approach could eventually extend to the millions of people with the garden-variety form of the condition.
Do Color-Filtering Glasses Actually Work?
While gene therapy remains experimental, a more accessible product has generated enormous public interest: tinted glasses marketed to people with color vision deficiency, most prominently those sold by EnChroma. These lenses use notch filters that selectively block narrow bands of light where the red and green cone responses overlap most. In theory, this sharpens the difference between the signals reaching each cone type, letting someone with anomalous trichromacy (a milder form of color deficiency where the cones exist but have shifted sensitivity) perceive more distinct reds and greens.
The evidence is genuinely mixed. One study found that the filters did shift color matches in the predicted direction and enhanced how vivid red-green colors appeared to wearers, providing the first quantitative evidence that the lenses can alter color perception for people with anomalous trichromacy.10PubMed. Empirical tests of the effectiveness of EnChroma multi-notch filters for enhancing color vision in deuteranomaly But the same study found minimal effect on the ability to discriminate colors at threshold, the kind of fine-grained color distinction measured by clinical tests. A separate, larger study of 86 color-deficient observers found no overall improvement on standard clinical color vision tests when wearing the glasses. That study concluded that the lenses improved discrimination for some colors while worsening it for others, with no net benefit.11PubMed. Do EnChroma glasses improve performance on clinical tests for red-green color deficiencies?
So the glasses may make colors look more vivid or saturated in a way that users find emotionally meaningful, which explains the viral reaction videos. But they do not restore normal color vision, and they do not help people pass color vision screening tests. Anyone considering them should understand the distinction between “colors look different” and “I can now distinguish all the colors a typical person can.”
Color Blindness That Is Not Inherited
Most conversations about color blindness focus on the inherited, lifelong kind. But color vision can also be lost later in life through disease or injury. Acquired color vision deficiency occurs as the result of conditions affecting the eyes, the optic nerve, or the brain. Glaucoma, macular degeneration, multiple sclerosis, diabetes, and certain medications can all degrade color perception over time.12PubMed. Acquired color vision deficiency
An even more striking form is cerebral achromatopsia, where color vision is lost because of damage to a specific region of the brain rather than anything wrong with the eyes themselves. The eyes and retina work fine, wavelengths of light are detected normally, but the brain area responsible for constructing color perception, located in the ventromedial occipital and temporal lobes, has been damaged by stroke or trauma.13PubMed. Cerebral achromatopsia: colour blindness despite wavelength processing People with this condition sometimes describe the world as looking like a black-and-white film.
The damage does not always affect the entire visual field. In one documented case, a 24-year-old woman sustained a contusion to her right anterior temporal lobe and afterward noticed that blue objects appeared green, but only in the left half of her visual field. Standard color vision tests came back normal because those tests present stimuli centrally, but specialized testing revealed a clear color distortion limited to one side. Brain imaging showed damage specifically in her right fusiform gyrus.14PubMed Central. Cerebral trauma-induced dyschromatopsia in the left hemifield: case presentation Cases like this reinforce that “seeing color” is not just about the eyes. It is a multi-stage process that depends on intact wiring from the retina through to the cortex, and a failure at any point along that chain can produce its own form of color blindness.
Why Is Red-Green Color Blindness So Common?
Given that roughly one in twelve men has some form of red-green color deficiency, evolutionary biologists have long wondered why natural selection has not weeded out the responsible gene variants. One influential idea is that dichromats, people with two rather than three cone types, actually have visual advantages in certain situations that offset their color limitations.
A classic laboratory study tested this by asking dichromatic and trichromatic observers to find textured targets against a background where color was used as camouflage. The texture elements were randomly colored red or green, making the target hard to spot based on shape alone. Trichromats struggled with the task because the irrelevant color information interfered with their ability to see the texture boundary. Dichromats, however, were not distracted by the color variation at all and performed significantly better in the camouflage condition.15Proceedings of the Royal Society B. Dichromats Detect Colour-Camouflaged Objects that are not Detected by Trichromats
A more recent study extended this idea using a naturalistic egg-finding task, asking participants to spot camouflaged eggs against cluttered backgrounds. Trichromats were generally faster overall, but simulated dichromats showed a particularly interesting advantage: they learned to find targets faster over repeated trials than trichromats did, and their performance improved more dramatically when luminance cues were available.16PubMed Central. Relative advantages of dichromatic and trichromatic color vision in camouflage breaking The interpretation is that dichromats, freed from distracting color information, rely more heavily on texture, shape, and brightness cues, making them better at “seeing through” certain kinds of camouflage.
In an ancestral environment where spotting predators or prey against dappled foliage could mean the difference between eating and starving, having a few dichromats in the group could have been a genuine asset. This does not prove that color blindness was actively selected for, but it suggests the condition was not always a pure disadvantage, which could explain why natural selection tolerated the gene variants rather than eliminating them. Groups with a mix of trichromats and dichromats may have been better at detecting a wider range of visual threats and resources than groups composed entirely of one type.
The Protanopia and Deuteranopia Distinction
Not all red-green color blindness is the same, and the difference matters more than people realize. Protanopia involves the loss of the long-wavelength (red-sensitive) cone, while deuteranopia involves the loss of the medium-wavelength (green-sensitive) cone. Both lead to confusion between reds and greens, but the details of what gets confused differ. Protanopes tend to see reds as darker than deuteranopes do, because they are missing the receptor that normally contributes the most to perceiving brightness in the red part of the spectrum. A red traffic light, for instance, can look quite dim to someone with protanopia, while a deuteranope might see it at roughly normal brightness but struggle to distinguish its color from certain greens or yellows.
Research on the underlying visual mechanisms shows that the two conditions shift color perception in measurably different ways. Protanopes’ neutral point, the wavelength that appears neither warm nor cool but a plain gray, falls at a shorter wavelength than that of deuteranopes, and their chromatic response curves peak at slightly shorter wavelengths as well.17PLoS ONE. Orthogonal Relations and Color Constancy in Dichromatic Colorblindness In practical terms, this means the two conditions are not interchangeable even though they are often lumped together under the casual label “red-green color blind.” Someone designing accessible signage, for example, needs to account for both patterns, not just one.
Dalton himself had deuteranopia, as confirmed by the DNA analysis of his preserved eyes almost two centuries after he first described his symptoms. It is a small irony that the man whose name became synonymous with color blindness in much of the world had the “green-blind” variety, not the “red-blind” one, a distinction he never could have made with the tools available to him.