If you have not read our home page, please go back to it now and do so. It will give you a simple explanation of colour vision and the difference ColorView lenses make. Following on from that, this section gives a more in-depth description of the science of colour vision. It is intended for those with a medical or science background, or those that have researched colour vision deficiency to some extent already. It is not necessary to understand the following to benefit from ColorView lenses!
Visible light is energy from the sun that can be absorbed by retinal cells to cause vision. Electromagnetic wavelengths from approx. 400nm to 700nm are visible light for the human retina, and are represented by the colour spectrum or can be seen as a rainbow.
Vision is the interpretation in the brain of light impulses sent from the retina of the eye via the optic nerve. There are many cell layers in the retina but the 2 cell types that collect light impulses are the rods and the cones.
Rods operate in low light conditions and do not detect colour. They are responsible for most of our night vision.
Cones contain a pigment that causes them to fire only when they absorb light from a specific range of wavelengths. Sensitivity varies across this range.
- Tritos cones have peak sensitivity to wavelengths of 420nm, which we perceive as violet, and are called S-cones or blue cones because blue and violet are short wavelengths of light.
- Deuterous cones have peak sensitivity to wavelengths of 534nm, which we perceive as green, and are called M-cones or green cones because green is a medium wavelength of light.
- Protos cones have peak sensitivity to wavelengths of 564nm, which we perceive as yellowish-green. This is also a medium wavelength of light, but protos are called L-cones, or red cones, to distinguish them from M-cones and to signify that they fire for the longer wavelengths of light.
Thus we are able to distinguish different colours in the world around us - in fact it has been estimated that humans can recognise aproximately 10 million different colours!
The graph below shows the wavelengths of light that the S, M and L cones detect.
| Normalized human cone cell responses (S, M and L types) to monochromatic spectral stimuli.
When light reaches the retina, the three types of cones yield three signals based on the extent to which each is stimulated. These values are known as the tristimulus values.
Interpretation of colour vision information by the brain:
One might assume that the tristimulus values would be sent directly to the brain to be computed into colour. However in evolutionary terms, mammals developed a 2-colour (dichromat) colour vision system based on Blue and Yellow -pigment cones. Later the yellow pigment cone diversified through mutation into L and S cones. The original Blue-Yellow path was maintained, and a new Red-Green pathway developed to process the new data of L cone stimulus compared to S cone stimulus.
The modern theory of color vision proposes that color information is transmitted out of the eye by three opponent processes, or opponent channels, each constructed from the raw output of the cones: a blue-yellow channel, a red-green channel, and a black-white "luminance" channel.
- The blue-yellow channel summates the signals from the M and L cones and compares this to the stimulus value of the S cones.
- The red-green channel ignores the S cone signal and compares the stimulus values of the M and L cones. (This pathway is relatively recent in evolutionary terms, and is found in primates but no other mammals).
- The luminance channel summates the signals from the M and L cones and processes it separately to the above (It simply asks ‘How much light?’ rather than ‘What colour?’)
Example: The tristimulus value for a monochromatic light source of wavelength 600nm would be approx: S-cone = 0; M-cone = 0.4; L-cone =0.9. (These values can be read from the graph above).
Blue yellow channel: compares S with (M+L) to get 0 : 1.3
Red-green channel: compares M and L to get 0.4 : 0.9
The brain in effect says “The Blue-Yellow channel tells me that there is no blue in this colour so it’s quite yellow. And the Red-Green channel tells me that there is more long-wavelength than medium-wavelength light, suggesting quite a bit of red, so I will perceive this colour as orange.”
Most light sources are mixtures of various wavelengths of light, but often the eye cannot distinguish them from monochromatic sources. For example, most computer displays reproduce the spectral color orange as a combination of red and green light; it appears orange because the red and green are mixed in the right proportions to allow the eyes’ red and green cones to respond the way they do to orange.
Why does light come to us in different wavelengths?
Light from the sun is a blend of all wavelengths and is known as white light. Light from an object we are looking at is reflected light: only the wavelengths that bounce off that object make it to our eyes. For example, if the object is a red chair, then the chair absorbs all the other wavelengths and only the red ones bounce off and make it to our eyes. So predominantly our protos (L) cones fire and we see the chair as red.
Plants look green because they absorb all the long and short (and some UV) wavelengths for photosynthesis. They don’t use the green light so it is reflected off and predominantly stimulates our deuterous (M) cones.
A white object reflects all the wavelengths, which is why white-painted rooms are brighter. Black objects absorb all the wavelengths, which is why black sand and asphalt get so hot: they absorb more of the sun’s energy than white sand or concrete, which are reflective.
In true colour blindness, no cones are present in the retina. This is extremely rare, and worse than no colour vision is the fact that there is no detailed vision either. The eye operates with rod-vision only and the central, detailed vision that the cones would provide is absent altogether.
Colour vision deficiency
The type of deficiency is determined by which of the 3 cone types is affected, and by whether the cones are present, but functioning abnormally, or absent altogether.
Colour Vision Defect
|Type of cone affected
||Anomalous trichromasy: cones present, but function abnormally
||Dichromasy: Cones absent
| M-cone (deuterous)
| S-cone (tritos)
An S-cone deficiency (tritanomaly or tritanopia) is rare. Almost all colour deficiency in humans is the L-cone or M-cone type.
Dichromasy leads to a much reduced ability to identify colours. Confused colours are: red-yellow-green; white and green; white and yellow.
Anomalous trichromasy occurs when the pigment within one of the types of cone cells (usually L or M) is abnormal, resulting in these cones firing for a different range of light wavelengths (and having a different peak sensitivity) than they normally would. It varies in severity, as the pigment aberration can range from a subtle difference through to quite a marked difference.
Protanomaly and deuteranomaly cause very similar colour confusion. This is because in protanomaly (L-cone anomaly) the pigment absorption is shifted to shorter wavelengths of light, while in deuteranomally (M-cone anomaly), the pigment absorption is shifted to longer wavelengths of light. Thus for both conditions, the faulty cell fires for a colour in between normal protos and deuterous peaks on the colour spectrum. This results in diminished discrimination between L and M cone data in the Red-Green pathway above. (The summation of L and M cone data is virtually unchanged, so the Blue-Yellow channel remains normal).
However, protanomals have reduced sensitivity to red light; while deuteranomals have reduced sensitivity to varying shades of green. Both confuse coral-orange-green shades. Protanomals have difficulty discerning the difference between a raw and a cooked steak, for example, while deuteranopes are intrigued to know what colour purple is - they see it as more of a non, or neutral, colour.
How do ColorView lenses help?
The following graph shows how the ColorView lenses edit the light before it enters the eye, altering the tristimulus values that the brain uses to determine colour. ('Transmitance' is the amount of light getting through the lens to the eye). The success of the ColorView lenses is due to the very precise editing of the light entering the eye, and it varies for different severities of colour deficiency.
Low transmittance in the ‘colour confusion zone’ (in between red and green) filters out the wavelengths that the faulty cell detects.
High transmittance in the red zone enhances red-green discrimination.
Transmittance in the blue zone varies with lens design to maintain the normal Blue-Yellow channel.
How do ColorView lenses work?
- Mirror coat: Reflects away selected wavelengths that would confuse the colour vision picture.
- Anti-reflection coat: prevents reflection of other selected wavelengths to enhance the overall colour vision picture.
- Lens material: For mild colour vision deficiency, the lens is clear. For moderate to severe deficiency, a tint is included to ‘mop up’ the remaining colour wavelengths that cause confusion.
The difficult part of manufacture is the precise control required for the specialized coatings above. If the layers are of the wrong thickness, the wrong wavelength of light will be targeted, reducing the effectiveness. The patented process is the result of seven years of research and development by the manufacturers of ColorView lenses.
The overall effect of ColorView lenses is to re-sculpt the colour-spectrum of light entering the eye so that the M and L cone data is better discriminated by the colour-deficient retina, allowing the brain to discriminate between previously confusing colours. In effect, the spectral absorption peaks of the M and L cones are separated.
How is colour deficient vision inherited?
The inheritance pattern for colour vision deficiency is X-linked recessive. The information for cone pigment is carried on the X-chromosome only. Females have two X chromosomes. If one has normal cone pigment, then colour vision is normal, even if the other X-chromosome has abnormal/absent cone pigment.
However, if a male (XY) inherits the colour deficient chromosome, his Y-chromosome has no colour information to cover for it, and he will be colour deficient.
As a result, one in every twelve men is colour deficient, but it is rare for women to be affected: only one in approx 270.
- A colour deficient man will not pass the condition on to his sons. They inherit their X chromosome from mum. However, his daughters will inherit his X chromosome and be carriers of colour deficiency (although having normal colour vision themselves). In turn, when they have children, their sons have a 50% chance of being colour deficient, depending whether they get the normal or deficient gene from mum. The daughters have a 50% chance of being carriers.
- For a girl to be colour deficient, mum must be a carrier or deficient, and dad must be colour deficient.