Colour Blindness UK: Types, Causes, Testing and Daily Life

Colour blindness — more accurately called colour vision deficiency (CVD) — is a reduced ability to distinguish between certain colours. It is not 'blindness' in the traditional sense — people with CVD can see clearly; they simply perceive certain colours differently. Approximately 1 in 12 men (8%) and 1 in 200 women (0.5%) in the UK have some form of colour vision deficiency. The most common type is red-green colour blindness, which is inherited and present from birth.

The main types are: protanomaly (weakened red sensitivity — the most common mild form); deuteranomaly (weakened green sensitivity); protanopia (complete absence of red cones — reds appear very dark or black); deuteranopia (complete absence of green cones — similar to protanopia in practical terms); tritanomaly/tritanopia (blue-yellow confusion — rare, often acquired); and achromatopsia (complete colour blindness, seeing in greyscale — very rare). Most colour-blind people have anomalous trichromatism (shifted cone function) rather than absent cones.

Inherited colour blindness is caused by mutations in the genes encoding the cone photopigments (opsin genes) on the X chromosome — which explains why it is far more common in men (who have one X chromosome) than women (who have two, with the functional allele usually dominant). Deuteranomaly and protanomaly result from shifted spectral sensitivity; deuteranopia and protanopia result from absent cone types. Blue-yellow CVD and achromatopsia are caused by mutations in other genes. Acquired CVD is caused by eye disease, optic nerve disease or neurotoxic medications.

Approximately 1 in 12 men (8%) and 1 in 200 women (0.5%) in the UK have some form of inherited colour vision deficiency. This means approximately 2.7 million people in the UK — predominantly men — have CVD. Red-green colour blindness (deuteranomaly, deuteranopia, protanomaly, protanopia) accounts for the vast majority. Complete colour blindness (achromatopsia) is very rare, affecting approximately 1 in 33,000 people.

The most common forms of inherited colour blindness — red-green CVD — are caused by mutations in the OPN1LW (L-cone opsin) and OPN1MW (M-cone opsin) genes, which are located on the X chromosome. Inheritance is X-linked recessive: men have one X chromosome and one Y, so a single mutated copy causes CVD. Women have two X chromosomes — they need mutations on both to be colour-blind (rare), but can be carriers (one mutated copy) who pass CVD on to their sons with 50% probability. This is why CVD is approximately 16 times more common in men than women.

The Ishihara colour plate test is the standard screening test for red-green colour vision deficiency. It consists of a series of circular patterns (plates) made up of dots of various sizes and colours. Each plate contains a number or shape that is visible to people with normal colour vision but not to those with certain types of CVD, or vice versa. The full Ishihara test has 38 plates; screening versions have 14 or 24 plates. It is widely used by opticians, GPs and occupational health services. It does not diagnose blue-yellow CVD.

Yes, significantly so. Because the genes causing the most common forms of red-green colour blindness are located on the X chromosome, and because men have only one X chromosome (from their mother), a single mutated copy is sufficient to cause CVD. Women have two X chromosomes — they need mutated copies on both X chromosomes to be colour-blind, which is much rarer. Approximately 1 in 12 men (8%) have some form of red-green CVD, compared with approximately 1 in 200 women (0.5%).

Yes — the vast majority of colour-blind people can see many colours perfectly well. Most have anomalous trichromatism — they have all three cone types but one has shifted sensitivity, meaning they have difficulty distinguishing between specific colours (typically reds and greens), not an inability to see all colour. Only people with achromatopsia (complete cone absence — very rare) see entirely in shades of grey. People with dichromacy (protanopia or deuteranopia) have two functional cone types and can distinguish many colours, but confuse reds and greens.

Almost never. The rare condition called achromatopsia — in which all cone types are absent or non-functional — causes truly greyscale vision, but it affects approximately 1 in 33,000 people and is usually accompanied by other visual problems (photophobia, nystagmus and poor visual acuity). The vast majority of colour-blind people see a full range of colours — they simply have difficulty distinguishing between specific colour pairs (typically red/green or, rarely, blue/yellow) that appear very similar to them but clearly different to people with normal colour vision.

Inherited colour blindness does not worsen over time — it is a stable, lifelong condition caused by the genetic structure of the cone photoreceptors. Most people with inherited CVD are unaware of any change in their colour perception throughout their lives. Acquired colour vision deficiency — caused by eye disease, optic nerve disease or medications — can worsen if the underlying condition progresses. Any perceived change in colour vision (particularly if one eye is more affected than the other) should prompt an ophthalmology assessment.

There is currently no treatment or cure for inherited colour blindness. The cone photoreceptors are structurally normal but with shifted or absent pigment; no approved treatment corrects this. Research into gene therapy for colour blindness is in early experimental stages. For rare achromatopsia caused by CNGB3 or CNGA3 gene mutations, gene therapy clinical trials are under way. Colour-filtering glasses (such as EnChroma or Pilestone) can enhance colour contrast and saturation for some wearers and may be helpful in everyday situations, but they do not restore normal colour vision.

EnChroma glasses use a selective light-filtering lens technology designed to enhance colour discrimination for people with red-green colour vision deficiency. They selectively filter specific wavelengths at the overlap between the red and green cone sensitivity curves, increasing the colour contrast that the wearer perceives. They do not restore 'normal' colour vision and do not work for all types or severities of CVD. Many colour-blind people report enhanced vibrancy and improved discrimination with EnChroma glasses in certain lighting conditions, though responses vary considerably. They are not a medical treatment and cannot be prescribed on the NHS.

Colour-blind children may struggle with colour-coding in teaching materials, colour-coded maps, graphs and diagrams, coloured pens and pencils in art and design, and certain science experiments. Teachers who are unaware of a child's colour vision deficiency may misinterpret difficulties as lack of attention or learning difficulties. The RNIB and Colour Blind Awareness recommend that all children are screened for colour vision deficiency before starting school or in Year 1, so that appropriate adjustments can be made. Adjustments include labelling coloured items, using high-contrast alternatives and digital accessibility tools.

Yes. Colour vision deficiency does not prevent driving in the UK. Standard traffic lights are designed to be distinguishable by colour-blind people — by position (red at top, green at bottom in vertical lights) as well as colour. The DVLA does not require colour vision testing for driving licences. However, people with CVD should be aware that certain road signs and hazard-marking systems (coloured road markings, coloured warning signs) may be more difficult to interpret, and should adapt accordingly.

Certain occupations have specific colour vision requirements for safety reasons. Aviation (commercial pilots, air traffic controllers) requires normal or near-normal colour vision assessed by anomaloscopy. Maritime officers must meet colour vision standards set by the MCA (Maritime and Coastguard Agency). Train drivers require normal colour vision. Some electrical work (colour-coded wiring) requires adequate colour discrimination. Colour vision requirements vary between forces for police and fire services. The RAF and Royal Navy have specific standards. It is worth checking occupational requirements early if colour blindness is suspected.

Acquired colour vision deficiency develops later in life due to damage to the retina, optic nerve or visual cortex — unlike inherited CVD which is present from birth. Common causes include: optic neuritis (often the first sign of multiple sclerosis — causes red-green desaturation in the affected eye); glaucoma (blue-yellow CVD); AMD; diabetic retinopathy; ethambutol toxicity (TB treatment); hydroxychloroquine toxicity; and toxic optic neuropathy from alcohol, tobacco or other substances. Acquired CVD is typically asymmetric and should be investigated urgently.

Yes, though far less commonly than men. For women to have inherited red-green colour blindness, they need to inherit the relevant mutation on both X chromosomes — one from each parent. This happens when the father is colour-blind (and therefore passes a mutated X to all his daughters) and the mother is a carrier. Approximately 0.5% (1 in 200) of women in the UK have some form of colour vision deficiency. Women can also be carriers — they have one normal and one mutated X chromosome, have normal colour vision themselves, but have a 50% probability of passing CVD to their sons.

Colour vision deficiency is equally prevalent across all ethnic groups and populations worldwide — approximately 8% of men globally have some form of CVD. In low-income countries, colour blindness screening is not routinely performed in schools or clinics, so most people are unaware of their condition and receive no information about adaptations. Acquired colour vision loss — a potential sign of serious eye disease — may go unrecognised and untreated. World Aid Network funds eye health services through locally-licensed ophthalmologists, supporting better diagnosis and care in the regions where we operate.