There are three main categories of color blindness: red-green, blue-yellow, and complete color blindness. Within those categories, several distinct subtypes exist, each affecting color perception differently. Red-green color blindness is by far the most common, affecting roughly 8% of men and 0.4% of women of European descent.
Red-Green Color Blindness
Red-green color blindness accounts for the vast majority of all color vision deficiency. It has four subtypes, split into two groups: anomalous (weakened) and absent cone function.
Deuteranomaly is the single most common form. Your green-sensing cones are present but don’t work as well as they should, which makes certain shades of green appear more red. Most people with deuteranomaly consider it mild, and it rarely interferes with everyday tasks.
Protanomaly is similar but affects the red-sensing cones instead. Certain reds look more green and less bright. Like deuteranomaly, it’s typically mild.
Protanopia and deuteranopia are the more severe forms. In both cases, one type of cone cell is completely nonfunctional rather than just weakened. People with either condition cannot distinguish red from green at all. The practical difference between the two is which cone is missing: red-sensing cones in protanopia, green-sensing cones in deuteranopia. The day-to-day experience, though, is quite similar for both.
Blue-Yellow Color Blindness
Blue-yellow color blindness is much less common than red-green. It involves the short-wavelength cones, which are responsible for detecting blue light. It also comes in two forms:
- Tritanomaly: Blue-sensing cones are present but underperform, making it harder to distinguish blue from green and yellow from red.
- Tritanopia: Blue-sensing cones are absent entirely, causing a more pronounced inability to tell blue from green and yellow from violet or pink.
One important genetic distinction separates blue-yellow from red-green deficiency. Red-green color blindness is carried on the X chromosome, which is why it overwhelmingly affects men. A man only needs one copy of the gene (on his single X chromosome) to have the condition, while a woman would need the gene on both of her X chromosomes. Blue-yellow color blindness involves a different chromosome entirely, so it affects men and women at equal rates.
Complete Color Blindness
True color blindness, where someone sees no color at all, is rare. The medical term is achromatopsia, sometimes called rod monochromacy. It comes in two forms: complete and incomplete. People with complete achromatopsia see only black, white, and shades of gray. Those with incomplete achromatopsia retain some limited color perception.
Achromatopsia typically comes with additional vision problems beyond the loss of color. Most people with the condition experience significant light sensitivity and glare intolerance, involuntary back-and-forth eye movements, and noticeably reduced visual sharpness. Farsightedness or nearsightedness is also common. A related condition called blue cone monochromacy, where only the blue-sensing cones function, is sometimes classified as a form of incomplete achromatopsia.
Like blue-yellow deficiency, achromatopsia is not X-linked and affects all sexes equally.
Severity Varies Within Each Type
Color blindness isn’t binary. Within any subtype, deficiency can range from mild to severe. Someone with mild deuteranomaly might never notice a problem unless tested, while someone with moderate deuteranomaly could struggle to pick ripe fruit or read color-coded charts. The “anomaly” subtypes (deuteranomaly, protanomaly, tritanomaly) tend to be milder because the relevant cone cells still function partially. The “anopia” subtypes (deuteranopia, protanopia, tritanopia) represent total loss of that cone type and produce more dramatic color confusion.
Color Blindness You Aren’t Born With
Most color blindness is genetic and present from birth, but it can also develop later in life. A range of eye diseases can impair color vision by damaging the retina or optic nerve, including glaucoma, age-related macular degeneration, cataracts, and diabetic retinopathy. Neurological conditions like multiple sclerosis, Parkinson’s disease, and stroke can also cause color vision loss by disrupting the brain’s visual processing pathways.
Certain medications, particularly some used to treat autoimmune conditions and tuberculosis, have been linked to acquired color vision changes. Exposure to industrial chemicals like carbon monoxide and lead can do the same. And natural aging plays a role: color perception often declines gradually after 60 and more noticeably after 70. Unlike inherited color blindness, acquired forms can sometimes improve if the underlying cause is treated.
How Color Blindness Is Diagnosed
The test most people recognize is the Ishihara plate test, where you identify numbers hidden in circles of colored dots. It’s effective for detecting red-green deficiency but cannot identify blue-yellow problems at all.
For a more complete picture, eye care providers use the Hardy-Rand-Rittler test, which uses 24 plates with symbols like crosses and triangles and can diagnose both red-green and blue-yellow deficiency along with severity. The Farnsworth-Munsell 100-Hue test takes a different approach: you arrange colored discs in order, which reveals how precisely you can distinguish between similar shades. A shorter version, the D-15, catches moderate to severe cases but may miss very mild ones.
The most accurate method for diagnosing red-green deficiency is a device called an anomaloscope, which asks you to match two colors by adjusting their mix. It’s considered the gold standard but is primarily used in specialized settings rather than routine eye exams. For young children (ages 3 to 6), a simplified test called Color Vision Testing Made Easy uses shapes instead of numbers to screen for red-green deficiency before kids can reliably read.