Colin Blakemore has managed throughout the years to capitalise on his high
media profile and, despite his years of experiments having yielded nothing
meaningful for the human problem associated with amblyopia and strabismus,
he has become a media personality. Recent years have seen him with his own
television series about the brain and a week seldom passes by without an
appearance from Mr Blakemore on either television or radio. It's surprising
what a careful manipulation of the media can do for ones celebrity status.
So what has Mr Blakemore actually done to enhance the font of medical
knowledge? Mr Blakemore was born in 1944 in Stratford-upon-Avon and, if he
is to be believed, and it's something he never seems to tire of telling us,
into a Labour-supporting working class family. From such humble origins he
has turned into a figure of such status that allowed him last year to
publicly lambast the government for not having given him a knighthood.
Not of course because he has any egotistical tendencies but because he
deserves it! So you must now be asking yourself how many thousands of
people has he managed to help with their eyesight problems in order that he
can exert such a power over both the media and government. The following
article debunks many of the falsehoods surrounding many of Mr Blakemore's
more public pronouncements. We give you the facts and we let you decide the
truth.
Once again SPEAK would like to take this opportunity to offer Mr Blakemore
the chance to publicly put the record straight, an open and public debate
into vivisection. It will give him a wonderful opportunity to tell the
public exactly how vivisection has benefited them and just as importantly,
exactly what he has done to benefit us all?
AMBLYOPIA: The failure of experiments on cats and monkeys
Blakemore's research has been into amblyopia and strabismus. Amblyopia is
decrease in function of one or both eyes, or impairment in the way in which
the eyes interact, for which no cause can be detected in the eyes.
Strabismus is misalignment of the eyes, and can take the form of a squint.
Treatments and how they were discovered
Blakemore has claimed that advances have been due to research such as his:
"...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." [1] 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]
In response to the first point, it should be noted that in the 1800s Claud
Worth identified that is was the deficiency in eye function which caused
the misalignment, or squint.[3] He was preceded by George Louis Leclerc
Comte de Buffon, who did his research in the 1700s. [4]
Regarding treatment of amblyopia, this has changed little over recent
years, and has not benefited from Blakemore's improved knowledge of
blindness in kittens. The recognised pioneer in amblyopia treatment is
Claude Worth, whose work is described thus: "It is surprising how
little...has been added to the major store of knowledge as he presented it,
at least from the practical viewpoint...Worth's emphasis on early treatment
of the error of refraction and the amblyopia is still the keynote of the
most rational approach to the treatment of the strabismic child..."[5]
Worth retired fifty years before Blakemore started his experiments.
Worth's brilliant investigations include six essential points, still
relevant, one of which is how amblyopia is acquired. He was aware of the
danger of accidentally causing amblyopia of the better eye by treating
children below the age of six.
Species differences
Research conducted on animals has been hampered by biological differences,
which are insurmountable. Animals used have mainly been cats and monkeys,
but chickens and tree shrews also have been used. Techniques have mainly
been to sew the eyelids closed, remove an eye, cause artificial strabismus
(either surgically or using prisms), or turn the material of the eye
opaque.
The human eye depends on the fovea and macula, which cats do not have.
These two areas are crucial in the study of amblyopia.[6] Researcher von
Noorden commented "Human amblyopia involves primarily foveal vision rather
than peripheral vision...".[7]
The neuroanatomy of the cat and human are different, highlighted by the
lack of references in clinical research literature to neuroanatomical
research in the cat.[8] The cat model has also proved to be unpredictive of
human conditions.
The primate eye has been found to be of different composition from the
human eye, as highlighted by Raviola and Wiesel. Their photographs have
revealed the poor correlation of experimental monkeys in short-sightedness
experiments with human myopia.[9] Animal experimenter Jampolsky has also
noted that common forms of strabismus in humans are rarely, if ever, found
naturally in monkeys. Aspects of the human condition include exotropia,
accommodative esotropia, A and V patterns, dissociated vertical deviation
and latent nystagmus. These are not features of induced and occurring money
strabismus. [10]The human visual system is unique when studied at the
detail necessary for knowledge to advance.
There's also differentiation between monkey species, as has been found by
the experiments. Monkeys eyelids were sewn closed, to find that one
species had eye elongation prevented by being given atropine, another did
not.[11]
Inducing the fake condition
Problems are also caused by the way amblyopia is induced. In humans born
with amblyopia, there are often complications caused by other
abnormalities, which doesn't apply to animals. The animal work revolves
around taking recordings from single cells, yet in humans vision has a high
psychological element - a problem animal experimenters have admitted.[12]
Cell recordings don't tell us what animals can see, or whether they see at
all.
Sewing the eyelid shut differs from human blindness such as that caused by
cataracts in the amount and quality of light reaching the retina. The
human condition, which is present from birth, differs from the experimental
condition, which is induced later. Primate experimenters have concluded
that this artificial way of inducing the condition is a cause of differing
results.[13] As all such methods are artificial, it is hard to see how
faith in the animal method can be maintained.
Misleading
Animal studies have yielded results which have been found to be incorrect
in application to humans. As 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."[14] Primate experiments have
misled us over the critical time at which amblyopia develops.[15] A
researcher expressed his hesitance to accept animal results, concluding
"the morphologic and functional organization of the visual system in cats
is substantially different from that in man." [16]
Boothe's team found two monkeys with congenital esotropia (eyes turned in),
and discovered they had absent or small accessory lateral rectus (ALR)
muscles.[17] Their conclusion that this was the cause of human esotropia
has proved incorrect: patients are been found to have normal ALR muscles.
Monkey experiments suggested that children wearing eye patches might be
harmful. Studies on children showed this was not the case. A researcher
involved described this as a "surprise" and suggested that we should ask
whether to believe animal results.[18]
A similar conclusion from cats prompted the response: "I...would hope that
their results, based on the experimental technique described, were not
interpreted to suggest that patching may do more harm than good, and would
not influence clinicians to be less vigorous with their patching therapy.
...I think work will be necessary to more closely simulate the human
clinical situation before further conclusions can be reached."[19]
Instead of vivisection
The animal method is not viable, but others are. Considering that all the
results taken from animal experiments have so far been wrong, or already
known, any future discoveries would have to be validated by the study of
human patients - the method by which all advances have so far been made.
Technology now enables us to gain information by using non-invasive imaging
technologies on patients. For example, modern magnetic resonance imaging
technologies can assess visual cortex function with a resolution of 1.4 mm.
[20] CAT scans, PET scans, and autopsy studies enable a more complete
picture to be built up. The findings will be based on human neurology, as
opposed to the very different neurology of an animal.
Resources available to study these proven and emerging, reliable techniques
will be increased once the unscientific pre-occupation with animal
experiments is abandoned.
References