By chance, the British scientist discovered that he confused colors. He thought this was due to a defect in the vitreous humor. In order to corroborate or deny his theory, he donated his eyes
If scientific history had to be summed up in one fundamental statement, it could be: “All things are made up of atoms.”
Such a statement, which today seems a truism, would not be possible without the theory proposed by the English naturalist and chemist John dalton in 1808, cornerstone of modern physics.
When he died in 1844, more than 40,000 people marched past the recumbent body and his funeral procession spanned more than two miles, a show of affection and respect for a self-taught schoolmaster who lived up to the modest principles of his Quaker beliefs and that he had spent his entire grim life shunning honors, tributes, medals, and distinctions.
However great Dalton’s scientific work is, for this article we are interested in a small essay he presented in 1794.
In it he described for the first time a visual defect that he suffered, which he discovered accidentally, and in which he deepened during a time in which he devoted himself to the study of flowers.
A convinced Quaker, Dalton wore almost talar clothes, so that his friends were very surprised the day he went out on the street dressed in garish scarlet stockings.
Alerted by the jokes, he confessed that he had bought them thinking they were gray.
In this way he was the first scientist to discover that it was unable to distinguish certain colors, a defect congenital that today we know as dyschromatopsia or color blindness.
Although there are many variants of this defect, the most common is that those who suffer from it confuse the green and red.
Our eyes contain two types of photoreceptors responsible for the vision.
The cotton buds They help us see in low light conditions, but they do not provide information about color.
The cones They work when there is abundant light and divide the world into three colors: blue, green and red.
Color blind people often lack of one of the three types of cones, so they only see some colors.
People who do not have cones, and consequently do not see colors at all, are called acromats.
Their main problem is not that their world is black and white, but that bright light causes them tremendous annoyance and they can be blinded by sunlight.
Color blindness is due to failures in genes that regulate the production of cone pigments.
The genetic defect is hereditary and is transmitted by a recessive allele linked to the X sex chromosome, of which males have one and females two.
It is enough for a man to inherit a defective X chromosome for him to be color blind. Women will only be color blind if both of their X chromosomes are deficient, which is highly unlikely.
Otherwise, as with hemophilia, they will be carriers: they do not have the defect, but they can transmit it to their offspring.
Eyes at the service of science
All this, which is taught in schools today, was absolutely unknown in Dalton’s time, so that his speculations on the causes of its defect were based on the physical laws of optics, a branch of knowledge relatively well developed at that time thanks to the trichromatic theory proposed in 1803 by Thomas Young.
Dalton assumed that the vitreous humor of his eyes, -the gelatinous mass that occupies the space between the lens and the retina- would not be transparent as in a normal eye, but had to be bluish in color and would function as a red filter.
His reasonable hypothesis had the drawback that, to prove and confirm it, he would have to pierce his eye to extract the vitreous humor, something that, as strong as his love of science was and no matter how sure of his hypothesis, he was not willing to do.
But it does not seem that our man was incapable of defending his principles even from beyond.
In his will he ordered that they be extracted eyes to check if the vitreous humor was bluish. He died on July 27, 1844, aged 78, fifty years after he had described his color blindness.
The next day his GP, Joseph Ransome, removed the vitreous humor from one of the eyes, placed it on a lens, and wrote that it was perfectly transparent.
He removed the second eye, left it almost intact except for the opaque back, and found that neither the red nor the green were distorted when looking through it.
In this expeditious manner he discarded the color blind hypothesis that color blindness was due to a “preretinal filter” and concluded (erroneously) that the defect must be in the optic nerve that connects the retina to the brain.
Knowing perhaps that in science what is ignored today can be explained tomorrow, Ransome kept his eyes on a container that happened to be proudly guarded by the Manchester Literary and Philosophical Society.
In 1983, biochemist Kary Mullis developed a novel molecular biology technique – PCR – by which a small fragment of nucleic acid can be cloned several times to obtain sequential copies, something that is very useful in multiple biomedical applications.
The technique became very popular after the 1993 Nobel Prize in Chemistry was awarded to Mullis, so scientists around the world began to delve into it.
To commemorate the second centenary of Dalton’s vision test, in 1994 a group of English geneticists and ophthalmologists applied to the Manchester Society for permission to take a small sample of Dalton’s retina in order to extract and amplify DNA by PCR. and examining the genes of the three types of retinal cones involved in color vision.
Photosensitive compounds contain proteins called opsins. Using the known genetic sequences for the red and green photopigment opsins, the researchers showed that Dalton had the opsin gene for red photopigment, but lacked the homologue for the green photopigment.
Dalton had actually been a “Deuteranope”, with a defect in the optical pigment sensitive to intermediate wavelengths, and not, as Young had postulated in 1807 in a famous compilation of his lectures, a “protanope” lacking the red-sensitive pigment.
For a deuteranope, the red part of the spectrum appears dim because the regions that appear yellow, orange, and red to normal observers are all the same hue to him, but red is less luminous than the yellow and orange regions to which he juxtaposes.
The history of science is like a portrait gallery in which there are many copies and few originals.
A century and a half after his death, the original experiment that the English physicist had begun with just thirty years to inquire about the cause of his visual defect, finally concluded.
* This artThe article was originally published in The Conversation. Click here if you want to read the original version.
**Manuel Peinado Lorca is a university professor. Department of Life Sciences and Researcher at the Franklin Institute for North American Studies, University of Alcalá, Spain. Luis Monje is a biologist and professor of scientific photography at the same university.
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