Why Colin Blakemore shouldn’t get a title
It must be New Year again, Colin Blakemore is moaning again that he hasn’t got a knighthood. The problem is that awards for stitching kittens eyes together are hard to justify. Add to that the fact that Colin’s wasted his career and not actually contributed anything worthwhile to medical knowledge, and it’ not a great start if you’re asking for a knighthood.
Colin claims he researches ambylopia – decrease in eye function, and strabismus (squints). All advances, are thanks to Colin and his like: "...before the animal research began it was not known whether squint could cause amblyopia or whether the existence of poor vision in one eye causes the squint.” He also claims that amblyopia "...was poorly understood until about 25 years ago when experimental research involving animals began to tackle the question of its origin...in the absence of any real knowledge of the cause of the disease there was no single agreed method of treatment."[2]
Woops – big error. Claud Worth, in the 1800s, showed that is was the deficiency in eye function which caused the misalignment, or squint,[3] Not Colin. But Claud Worth wasn’t the first. George Louis Leclerc Comte de Buffon, who did his research in the 1700s, proved it by studying humans.[4] Worth’s research is still the Gold Standard: "It is surprising how little...has been added to the major store of knowledge as he presented it, at least from the practical viewpoint...”[5] He was also aware of the risk that doctors could cause amblyopia in stronger eyes by treating children too young.
Animal experiments
Trying to give animals amblyopia and strabismus have been ineffective. Cats and monkeys have been favourite animals. Cats have a different visual process from humans: we use the fovea and macula to see, cats don’t.[6] The interaction between the brain and eyes is crucial, yet cats are irrelevant to humans in this area. The lack of references in clinical research literature to neuroanatomical research in the cat highlight this.[7]
Monkeys are of similar value. Research shows the poor correlation of experimental monkeys in short-sightedness experiments with human myopia.[8] Animal experimenter Jampolsky has also noted that common forms of strabismus in humans are rarely, if ever, found naturally in monkeys. Strabismus is misalignment of the eyes, and a central part of this research. Conditions typical to humans with strabismus are not found in induced and occurring monkey strabismus.[9] As with all illnesses, today it is studied on a detailed level, yet the differences between animal models and human conditions are just too many. The human visual system is unique at this level.
Further problems exists with the animal models: they rely on taking cell recordings, which don’t identify what the animal can see, or whether it can see at all.[10] Sewing the eyelid shut differs from human blindness in the amount and quality of light reaching the retina.
Experts tend to agree with Colin’s critics, not Colin. One expert says “There has been considerable concern expressed by vision scientists other than just myself that the experimental work is either not relevant or may be misleading with respect to the human condition and its treatment.”[11] Another says he had little faith in animal results, concluding “the morphologic and functional organization of the visual system in cats is substantially different from that in man.” [12]
Who can blame them? Primate experiments have misled us over the critical time at which amblyopia develops.[13] Monkey experiments suggested that getting children to wear eye patches might be harmful, while studies on children showed that it actually helped. A researcher involved described this as a “surprise” and suggested that we should ask whether to believe animal results.[14]
What can we do instead?
This may be an area in which more work is needed, or even it could be appropriate to give awards of some sort. But given the role animal experiments have had in misleading doctors, wasting resources and indeed careers, it’s not practitioners of vivisection that should be encouraged. Modern magnetic resonance imaging technologies can assess visual cortex function with a resolution of 1.4 mm.[15] CAT scans, PET scans, and autopsy studies enable a more complete picture to be built up. The modern neurological research lab is a high-tech, human-centred centre of discovery, where revelations about human conditions will enable new therapies. Low-profile researchers may well be working in these areas, quietly uncovering details with the potential to revolutionise treatment. If honours are due, you can be sure they deserve them, not someone who wastes his time stitching animals’ eyes shut.
1. Colin Blakemore "A reply to criticism of experiments involving visual deprivation," September 1987.
2. Colin Blakemore "A reply to criticism of experiments involving visual deprivation," September 1987.
3. Abraham, S.V.: A tribute to Claud Worth. Ann. Ophthalmol.
4 Marg, E.: Prentice Memorial Lecture: Is the animal model for stimulus deprivation amblyopia in children valid or useful? Am. J. Optometry Physiol. Optics 59: 451-464, 1982.
5. Abraham, S.V.: A tribute to Claud Worth. An n. Ophthalmol. 4: 171-175, 1972.
6. von Noorden, G .K.: Application of basic research data to clinical amblyopia. Ophthalmology 85: 496-504, 1978.
7. “AMBLYOPIA” Nedim C. Buyukmihci, V.M.D.a, http://avar.org/
8. Raviola E, Wiesel TN. An animal model of myopia. New England Journal of Medicine 1985;312: 1609-1615.
9. Jampolsky A. Unequal visual inputs and strabismus management: a comparison of human and animal strabismus, in Transactions of the New Orleans Academy of Ophthalmology, Symposium on Strabismus. St. Louis, CV Mosby, 1978, p 358-492
10. Blakemore, C . and Vital-Durance, F.: Development of the neural basis of visual acuity in monkeys: Speculation on the origin of deprivation amblyopia. Trans. Ophthalmol. Soc. U.K. 99: 363-368, 1979.
11. “AMBLYOPIA” Nedim C. Buyukmihci, V.M.D.a, http://avar.org/
12. von Noorden, G .K. and Maumenee, A .E.: Clinic al observations on stimulus- deprivation amblyopia (amblyopia ex anopsia). Am. J. Ophthalmol. 65: 220-224, 1968.
13. Vaegan TD. Critical period for deprivation amblyopia in children. Transaction of the Ophthalmological Society of the United Kingdom 1979;99:432-439
14. Marg, E.: Prentice Memorial Lecture: Is the animal model for stimulus deprivation amblyopia in children valid or useful? Am. J. Optometry Physiol. Optics 59: 451-464, 1982. Hoyt, C.S .: The long- term visual effects of short-term binocular occlusion of at-risk neonates. Arch . Ophthalmol. 98: 1967-1970, 1980.
15. Engel SE, Rumelhart DE, Wandell BA, et al. fMRI of human visual cortex. Nature 1994:369;525,