Color blindness usually comes from inherited differences in the retina’s cone cells. Eye disease, injury, or some medications can also change color vision later in life.
In detail
Color blindness is caused by the cone cells in the retina responding to light differently than usual. In the great majority of cases the cause is inherited: the genes for the red and green cone pigments sit on the X chromosome, so a single altered copy affects men far more often than women.
A smaller share of cases is acquired later in life from eye disease, diabetes, optic nerve damage, injury, or certain medications — and unlike the inherited kind, acquired color vision change can progress and sometimes reverses when its cause is treated.
Most cases
Inherited
X-linked, present from birth
Cones involved
L, M or S
Red, green or blue pigment
Acquired causes
Can progress
Disease, injury, medication
Causes of color blindness, side by side
The split that matters is inherited versus acquired: one is fixed from birth, the other can progress and sometimes reverses when its cause is treated.
Inherited — present from birth
Inherited red-green (X-linked)
What happens
Altered or missing L (red) or M (green) cone pigment gene on the X chromosome
Onset
Present at birth
Does it change?
Stable for life
Inherited blue-yellow (tritan)
What happens
Change in the S (blue) cone pigment gene on chromosome 7 — affects men and women equally
Onset
Present at birth
Does it change?
Stable for life
Achromatopsia
What happens
Cone cells largely non-functional; vision relies on rods
Onset
Present at birth
Does it change?
Stable, with light sensitivity
Acquired — develops later
Cataract
What happens
Clouding and yellowing of the lens filters short-wavelength light before it reaches the retina
Onset
Usually later in life
Does it change?
Often improves after the cataract is treated
Diabetic retinopathy
What happens
Damage to retinal blood vessels and photoreceptors
Onset
Gradual, with diabetes duration
Does it change?
Can progress; managed with the underlying condition
Glaucoma
What happens
Optic nerve damage affecting signal transmission from the retina
Onset
Gradual, often unnoticed
Does it change?
Progressive if untreated
Age-related macular degeneration
What happens
Loss of photoreceptors in the central retina, where cones are densest
Onset
Later in life
Does it change?
Progressive
Optic neuritis (including multiple sclerosis)
What happens
Inflammation of the optic nerve, classically hitting red saturation first
Onset
Often sudden, usually one eye
Does it change?
May partly recover
Medication side effects
What happens
Some drugs affect the retina or optic nerve — hydroxychloroquine and ethambutol are the best-known examples
Onset
During treatment
Does it change?
Sometimes reversible; never stop a prescribed drug on your own
Head or eye injury
What happens
Trauma to the retina, optic nerve, or the visual areas of the brain
Onset
Sudden
Does it change?
Depends on the injury
Causes of color blindness grouped into inherited and acquired, with the mechanism, typical onset, and whether the deficiency can change over time
Cause
What happens
Onset
Does it change?
Inherited — present from birth
Inherited red-green (X-linked)
Altered or missing L (red) or M (green) cone pigment gene on the X chromosome
Present at birth
Stable for life
Inherited blue-yellow (tritan)
Change in the S (blue) cone pigment gene on chromosome 7 — affects men and women equally
Present at birth
Stable for life
Achromatopsia
Cone cells largely non-functional; vision relies on rods
Present at birth
Stable, with light sensitivity
Acquired — develops later
Cataract
Clouding and yellowing of the lens filters short-wavelength light before it reaches the retina
Usually later in life
Often improves after the cataract is treated
Diabetic retinopathy
Damage to retinal blood vessels and photoreceptors
Gradual, with diabetes duration
Can progress; managed with the underlying condition
Glaucoma
Optic nerve damage affecting signal transmission from the retina
Gradual, often unnoticed
Progressive if untreated
Age-related macular degeneration
Loss of photoreceptors in the central retina, where cones are densest
Later in life
Progressive
Optic neuritis (including multiple sclerosis)
Inflammation of the optic nerve, classically hitting red saturation first
Often sudden, usually one eye
May partly recover
Medication side effects
Some drugs affect the retina or optic nerve — hydroxychloroquine and ethambutol are the best-known examples
During treatment
Sometimes reversible; never stop a prescribed drug on your own
Head or eye injury
Trauma to the retina, optic nerve, or the visual areas of the brain
Sudden
Depends on the injury
What causes color blindness?
Normal color vision uses three kinds of cone cell in the retina, each holding a pigment tuned to a different part of the spectrum: long wavelengths (L, loosely "red"), medium (M, "green"), and short (S, "blue"). The brain reads color from the differences between their three signals. Color blindness happens when one of those pigments is shifted along the spectrum, weakened, or absent, which shrinks the difference the brain has to work with.
The L and M pigments already sit close together, so their signals overlap a lot even in normal vision. That is why red-green deficiency is by far the most common form and why a small genetic shift produces a noticeable effect: move the green pigment toward red and the two curves nearly collapse onto each other. The blue S cone sits far away on the spectrum and is coded on a different chromosome, which is part of why blue-yellow deficiency is much rarer.
None of this involves the eye being damaged or unhealthy. Inherited color vision deficiency is a variation in how the retina is built, not an injury to it.
Why is color blindness inherited from the mother?
The L and M cone pigment genes sit next to each other on the X chromosome. Men have one X and one Y, so a single altered copy of that gene is enough to produce a red-green deficiency — there is no second X to compensate. Women have two X chromosomes, so a working copy on the other one usually covers for the altered one; they are far less often affected and much more often carriers.
Because a boy gets his single X from his mother, a red-green deficiency in a son traces back to her side of the family, which is why it often skips visibly from a grandfather to a grandson. It also explains the prevalence gap: roughly 1 in 12 men and about 1 in 200 women of Northern European descent.
Blue-yellow deficiency works differently. Its gene sits on chromosome 7, which is not a sex chromosome, so it is inherited in an autosomal pattern and affects men and women at similar rates.
Can you become color blind later in life?
You cannot develop inherited color blindness — that is set before birth and does not switch on later. But color vision can genuinely change in adulthood, and when it does the cause is acquired: something has altered the light reaching the retina, the health of the photoreceptors, or the nerve carrying their signal.
The pattern usually differs from the inherited kind in three ways. Acquired changes more often hit the blue-yellow axis than red-green. They frequently affect one eye more than the other, so covering each eye in turn and comparing a strongly colored object can reveal them. And they can progress rather than staying fixed.
Some are reversible. Color perception often shifts back after cataract surgery, and drug-related changes can settle when a prescriber adjusts treatment. Others, such as glaucoma or macular degeneration, are managed rather than reversed — which is exactly why a new change in color vision is worth an eye exam rather than a wait-and-see.
What does not cause color blindness
A few explanations come up often and are not supported. Screen time, reading in poor light, and eye strain do not cause color vision deficiency. Neither does looking at the sun briefly, wearing glasses, or a diet low in any particular vitamin. Color vision deficiency is also not a form of blindness: sharpness, field of view, and night vision are all unaffected in the inherited form.
It is likewise not a learning difficulty, though it is frequently mistaken for one in school when a child is graded on color-coded work. And it is not curable. Filter glasses can raise the contrast between confusable colors for some people, which is a real and useful effect, but they do not change the cones or restore normal color vision.
Find out which type you have
A free screening estimates whether a red-green deficiency is present and which family it points to. If you want to understand how it passed through your family, the inheritance calculator works out the odds for sons and daughters.
Color vision that has changed needs an eye exam, not a screening — acquired causes are worth finding early.
Causes of color blindness — frequently asked questions
Is color blindness a disease or damage to the eye?
No. Inherited color vision deficiency is a variation in how the retina is built, not an injury to it: one cone pigment is shifted, weakened or absent, and the eye is otherwise healthy. Acquired color vision loss is different and does come from conditions such as cataract, glaucoma, diabetic retinopathy or optic nerve inflammation.
What is the main reason for color blindness?
Genetics. Around 99% of cases are inherited red-green deficiency caused by an altered L or M cone pigment gene on the X chromosome. Because men have only one X chromosome, one altered copy is enough — which is why about 1 in 12 men and about 1 in 200 women are affected.
Can you become color blind?
You cannot acquire the inherited form, but color vision can change in adulthood. Acquired color vision change is linked to cataract, diabetes, glaucoma, macular degeneration, optic neuritis, head injury, and drugs such as hydroxychloroquine and ethambutol. It typically affects blue-yellow more than red-green and often one eye more than the other, and it should be assessed by an eye-care professional.
Is color blindness dominant or recessive?
Red-green color blindness is X-linked recessive: a woman needs an altered copy on both X chromosomes to be affected, while a man needs only the one he has. Blue-yellow (tritan) deficiency follows an autosomal dominant pattern on chromosome 7, and complete achromatopsia is autosomal recessive.
Can color blindness be cured?
No. Inherited color vision deficiency is part of how the retina is built and there is no treatment that restores normal color vision. Filter glasses can make some confusable colors look more separated for some people without changing the underlying cones. Acquired color vision changes are a different matter — some improve when the condition causing them is treated.
Does color blindness come from the mother or the father?
For red-green deficiency, from the mother. A son inherits his only X chromosome from her, so the altered gene reaches him through her side even when she has normal color vision herself as a carrier. A father passes his X to his daughters, which is why an affected father's daughters become carriers rather than being affected.