However the academic world is divided, the twentieth century has achieved a terrible form of immortality. “It is in the very nature of things human,” Hannah Arendt observed, “that every act that has once made its appearance and has been recorded in the history of mankind stays with mankind as a potentiality long after its actuality has become a thing of the past.” No matter how remote, great crimes have a living power to influence the future. Tradition and taboo are unavailing. “No punishment,” Arendt wrote, “has ever possessed enough power of deterrence to prevent the commission of crimes.” On the contrary, “whatever the punishment, once a specific crime has appeared for the first time, its reappearance is more likely than its initial emergence could ever have been.”
It is in this sense that the twentieth century, having introduced into human history crimes never before imagined, or if imagined, never before undertaken, is immortal, and will, like the crucifixion, remain a permanent part of the human present.
It is simply there, an obelisk in human history: black, forbidding, irremovable, and inexpugnable.
David Berlinski, The Best of Times
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On Darwin’s bicentennial last year, his most prominent defender and ardent antitheist Richard Dawkins wrote a new book, The Greatest Show on Earth: The Evidence for Evolution. Ironically, he admits about all his previous pro-evolution books:
“Looking back on these books, I realized that the evidence for evolution is nowhere explicitly set out, and that it seemed like a good gap to close.”
One of his favourite examples, one he has been using for decades, is the alleged backwardly wired retina, a favourite example of supposed bad design. First, we republish a sample section from our refutation, The Greatest Hoax on Earth? showing that even with existing knowledge, Dawkins had no case. Then we report on a new discovery, conclusively showing that the allegedly inferior design is actually superior in producing sharper images and better colour distinctions.
From Greatest Hoax?:
Dawkins repeats a claim he has been making for over 20 years:
“But I haven’t mentioned the most glaring example of imperfection in the optics. The retina is back to front.
“Imagine a latter-day Helmholtz presented by an engineer with a digital camera, with its screen of tiny photocells, set up to capture images projected directly on to the surface of the screen. That makes good sense, and obviously each photocell has a wire connecting it to a computing device of some kind where images are collated. Makes sense again. Helmholtz wouldn’t send it back.
“But now, suppose I tell you that the eye’s ‘photocells’ are pointing backwards, away from the scene being looked at. The ‘wires’ connecting the photocells to the brain run over all the surface of the retina, so the light rays have to pass through a carpet of massed wires before they hit the photocells. That doesn’t make sense … ” (pp. 353–4)
Actually it does make sense, as ophthalmologists know, and have explained for years, so Dawkins has no excuse for repeating such discredited arguments. Dawkins’ analogy fails because photocells don’t have to be chemically regenerated, while the eye’s photoreceptors are chemically active, and need a rich blood supply for regeneration. As I wrote in By Design [see review], ch. 12:
Someone who does know about eye design is the ophthalmologist Dr George Marshall, who said:
“The idea that the eye is wired backward comes from a lack of knowledge of eye function and anatomy.”1
He explained that the nerves could not go behind the eye, because the choroid occupies that space. This provides the rich blood supply needed for the very metabolically active retinal pigment epithelium (RPE). This is necessary to regenerate the photoreceptors, and to absorb excess heat from the light. So the nerves must go in front rather than behind. But as will be shown below, the eye’s design overcomes even this slight drawback.
In fact, what limits the eye’s resolution is the diffraction of light waves at the pupil (proportional to the wavelength and inversely proportional to the pupil’s size); so alleged improvements of the retina would make no difference to the eye’s performance.
It’s important to note that the ‘superior’ design of Dawkins with the (virtually transparent) nerves behind the photoreceptors would require either:
- The choroid in front of the retina—but the choroid is opaque because of all the red blood cells, so this design would be as useless as an eye with a hemorrhage!
- Photoreceptors not in contact with the RPE and choroid at all—but without a rich blood supply to regenerate, then it would probably take months before we could see properly after we were photographed with a flashbulb or we glanced at some bright object.
Are squid eyes ‘properly’ wired?
Some evolutionists [including Dawkins in The Blind Watchmaker] claim that the cephalopod (e.g. squid and octopus) eye is somehow ‘right’, i.e. with nerves behind the receptor. They use this as a counter-argument to the points in the previous section about the need for the “backward” wiring. But no-one who has actually bothered to study cephalopod eyes could make such claims with integrity. In fact, cephalopods don’t see as well as humans, e.g. no colour vision, and the octopus eye structure is totally different and much simpler. It’s more like ‘a compound eye with a single lens’. And it is no accident that we say ‘eyes like a hawk/eagle’ rather than ‘eyes like a squid’, because the former really are sharper, despite their alleged ‘backward’ wiring.
Fibre Optic Plate
The above section explains why the vertebrate retina must be wired the way it is. But scientists at Leipzig University have recently shown that the vertebrate eye has an ingenious feature that overcomes even the slight disadvantage of the transparent nerves in front of the light receptors [the “carpet of massed wires” that Dawkins complains about].2
The light is collected and funneled through the nerve net to the receptors by the Müller glial cells, which act as optical fibres. Each cone cell has one Müller cell guiding the light to it, while several rods can share the same Müller cell.
The Müller cells work almost exactly like a fibre optic plate that optical engineers can use to transmit an image with low distortion without using a lens. The cells even have the right variation in refractive index for “image transfer through the vertebrate retina with minimal distortion and low loss.”2
Indeed, Müller cells are even better than optical fibres, because they are funnel-shaped, which collects more light for the receptors. The wide entrances to Müller cells cover the entire surface of the retina, so collect the maximum amount of light.
One of the research team, Andreas Reichenbach, commented:
“Nature is so clever. This means there is enough room in the eye for all the neurons and synapses and so on, but still the Müller cells can capture and transmit as much light as possible.”3
Dawkins complains further:
“…it gets even worse. One consequence of the photocells pointing backwards is that the wires that carry their data somehow have to pass through the retina and back to the brain. What they do, in the vertebrate eye, is all converge on a particular hole in the retina, where they dive through it. The hole filled with nerves is called the blind spot, because it is blind, but ‘spot’ is too flattering, for it is quite large, more like a blind patch, which again doesn’t inconvenience us much because of the ‘automatic Photoshop’ software in the brain. Once again, send it back, it’s not just bad design, it’s the design of a complete idiot.
“Or is it? If it were, the eye would be terrible at seeing, and it is not. It is actually very good. It is good because natural selection, working as a sweeper-up of countless little details, came along after the big original error of installing the retina backwards, and restored it to a high-quality precision instrument.” (pp. 354–5)
Once more, Dawkins shows no understanding of the need to regenerate the photocells, which necessitates this ‘backward wiring’. He also begs the question of how mutations and natural selection could create the sophisticated software, which rather speaks of intelligent programming (as does the real Photoshop). Some of this programming was explained in By Design, ch. 1:
Another amazing design feature of the retina is the signal processing that occurs even before the information is transmitted to the brain. This occurs in the retinal layers between the ganglion cells and the photoreceptors. For example, a process called edge extraction enhances the recognition of edges of objects. John Stevens, an associate professor of physiology and biomedical engineering, pointed out that it would take “a minimum of a hundred years of Cray [supercomputer] time to simulate what takes place in your eye many times each second.”4 And the retina’s analog computing needs far less power than the digital supercomputers and is elegant in its simplicity. Once again, the eye outstrips any human technology, this time in another area.
Indeed, research into the retina shows that the 12 different types of ganglion cells send 12 different ‘movies’, i.e. distinct representations of a visual scene, to the brain for final interpretation. One movie is mainly a line drawing of the edges of objects, and others deal only in motion in a specific direction, and still others transmit information about shadows and highlights. How the brain integrates these movies into the final picture is still a subject of intense investigation. Understanding this would help researchers trying to design artificial light sensors to help the blind to see.5
Ophthalmologist Peter Gurney, in his detailed response to the question, “Is the inverted retina really ‘bad design’?”6, also addresses the blind spot. He points out that the blind spot occupies only 0.25% of the visual field, so Dawkins is exaggerating to try to call it a patch rather than a spot. Furthermore, it is far (15°) from the visual axis, so that the normal visual acuity of the region is only about 15% of the foveola, the most sensitive area of the retina right on the visual axis. And having two eyes effectively means there is no blind spot. So the alleged defect is only theoretical, not practical. The blind spot is not considered handicap enough to stop a one-eyed person from driving a private motor vehicle. The main problem with only one eye is the lack of stereoscopic vision.
Problem for Dawkins’ own just-so story of eye evolution
In Dawkins’ earlier book Climbing Mt Improbable, he cited a computer simulation by Dan Nilsson and Susanne Pelger from a widely publicized paper.7 Taking their cue from Darwin, who started with a light-sensitive spot when ‘explaining’ the origin of the eye, their simulation starts with a light-sensitive layer, with a transparent coating in front and a light-absorbing layer behind. But the hypothetical ancestor starts with the nerve behind the light-sensitive spot, rather than from in front, as in the vertebrate eye. Yet the evolutionary just-so story can provide no transition from having the nerves behind to in front, with all the other complex coordinated changes that would have to occur as well.8
Indeed, Dawkins has no plausible explanation for the origin of the integrated components that work together to account for vision, such as that seen in vertebrates. Claiming that it is poorly designed because he has not carefully researched the matter does not explain how evolution created it.
New discovery: Müller cells enhance sharpness
At the time the book was written, it was thought that the Müller cells were mainly waveguides to transmit light without distortion, so mitigate the necessary disadvantage of needing the photoreceptors near the blood supply. But researchers Amichai Labin and Erez Ribak at the Technion-Israel Institute of Technology in Haifa found that the Müller cells are much more than that. They said:
“The retina is revealed as an optimal structure designed for improving the sharpness of images. … The fundamental features of the array of glial cells are revealed as an optimal structure designed for preserving the acuity of images in the human retina. It plays a crucial role in vision quality, in humans and in other species.”9
One reason is that images can be distorted by light “noise”, i.e. light that is reflected several times within the eye instead of coming directly through the pupil. But the Müller cells transmit the direct light strongly to the rods and cones, while the noise leaks out. This makes the images sharper.
Another problem with lenses is that they are basically prisms joined face-to-face, and have a tendency to separate the colours. This is called chromatic aberration. Expensive cameras have multiple lenses to try to avoid this problem. But “Müller cells’ wide tops allow them to ‘collect’ any separated colours and refocus them onto the same cone cell, ensuring that all the colours from an image are in focus.”10
Furthermore, the Müller cells are tuned to the visible region of the spectrum, and leak out other wavelengths, minimizing radiation and heat damage.
The researchers say:
“In this study, wave propagation methods allowed us to show that light guiding within the retinal volume is an effective and biologically convenient way to improve the resolution of the eye and reduce chromatic aberration. We also found that the retinal nuclear layers, until now considered a source of distortion, actually improve the decoupling of nearby photoreceptors and thus enhance vision acuity. Although this study was performed on data from human retinas and eyes, most of its consequences are valid for eyes with other retinal structure and different optics. They are also valid for the more common case of eyes without a central fovea.”
New Scientist reports:
“‘It suggests that light-coupling by Müller cells is a crucial event that contributes to vision as we know it,’ says Kristian Franze, a neurophysicist at the University of Cambridge and co-author of the 2007 study.2 “This work nicely complements our experimental data.’”10
Furthermore, this design may inspire scientists to copy it, just another example of biomimetics:
“The new understanding of the role of Müller cells might find applications in more successful eye transplants and better camera designs, says Ribak.”10
Evolutionists dogmatically hang on to dud argument
It’s notable that Kate McAlpine, writing in New Scientist, which is overtly anti-Christian, had to admit, “It looks wrong, but the strange, ‘backwards’ structure of the vertebrate retina actually improves vision,” after admitting that New Scientist had listed the backwardly wired eye as one of evolution’s biggest “mistakes””.
Yet not willing to junk a defunct evolutionary argument, she says:
“However, Kenneth Miller, a biologist at Brown University in Providence, Rhode Island cautions that this doesn’t mean that the backwards retina itself helps us to see. Rather, it emphasises the extent to which evolution has coped with the flawed layout. ‘The shape, orientation and structure of the Müller cells help the retina to overcome one of the principal shortcomings of its inside-out wiring,’ says Miller.”10
Miller is a professing Christian, but his worldview is indistinguishable for all practical purposes from the rabid atheists he loves to ally with against Bible-believers (see refutations of his books Finding Darwin’s God (2000), Only a Theory: Evolution and the Battle for America’s Soul (2008)). He, like Dawkins, has qualifications in neither ophthalmology (unlike Marshall and Gurney) nor physical optics (unlike me). First, he fails to address the important reasons for the backwardly-wired eye retina; second, he fails to show why it is a bad design anyway, especially given the newly discovered advantages of the wave guiding. Last, it is absurd given that the researchers think that this “flawed” layout might help to improve camera design!
This discovery thus nails one of Richard Dawkins’ favourite “proofs” of evolution in The Greatest Show on Earth. But judging by his record, he will not give up his fallacious arguments in the cause of his atheopathic faith.11
- Fibre optics in eye demolish atheistic ‘bad design’ argument
- Recurrent laryngeal nerve
- Sight and the centre of the universe
- Eye wiring clarified
- The left recurrent laryngeal nerve design in mammals is not poor design
- Evidence and evolutionary bias
- Fine tuning of ‘backward’ eye is vital for colour vision
- Richard Dawkins the ‘Apostle of Atheism’: how can he be answered?
- What about allegations of ‘badly designed’ features?
Original article: The Design of the Retina
There is no greater proof of the danger of over-specialization than the above argument. Dr. Richard Dawkins, an English ethologist and evolutionary biologist made an illegitimate claim concerning the design of the eye, a claim ophthalmologist Dr. George Marshall effortlessly refuted.
Apparently, the sciences have become so rigidly partitioned, an evolutionary biologist was incapable of merely asking an ophthalmologist about the true design of the eye before misrepresenting the implications of its structure.
Or, it could simply be Richard Dawkins believes something more than his own science.
The above article is from 2010 — that is 7 years ago. It was refuted long before that, but just yesterday the “poor design of the retina” was trotted out against by an atheist who wasn’t even aware of this article, or its destruction of his argument.
This has been going on now for well over 50 years.
If you still believe in evolution, I recommend you honestly investigate the scientific journals, as well as the tens of thousands of published dissents to evolutionary theory.
Understand the arguments.
Understand the terms.
Understand what the theory requires.
Understand what evidence there actually is and what evidence is missing.
Understand the probabilities.
If you are capable of honestly appraising premises and proofs, I suspect you will quickly see evolution in an entirely different light.
The subject of this sketch is, perhaps, the most original and variously gifted designer the world has ever known. At an age when most men have scarcely passed their novitiate in art, and are still under the direction and discipline of their masters and the schools, he had won a brilliant reputation, and readers and scholars everywhere were gazing on his work with ever-increasing wonder and delight at his fine fancy and multifarious gifts. He has raised illustrative art to a dignity and importance before unknown, and has developed capacities for the pencil before unsuspected. He has laid all subjects tribute to his genius, explored and embellished fields hitherto lying waste, and opened new and shining paths and vistas where none before had trod. To the works of the great he has added the lustre of his genius, bringing their beauties into clearer view and warming them to a fuller life.
His delineations of character, in the different phases of life, from the horrible to the grotesque, the grand to the comic, attest the versatility of his powers; and, whatever faults may be found by critics, the public will heartily render their quota of admiration to his magic touch, his rich and facile rendering of almost every thought that stirs, or lies yet dormant, in the human heart. It is useless to attempt a sketch of his various beauties; those who would know them best must seek them in the treasure—house that his genius is constantly augmenting with fresh gems and wealth. To one, however, of his most prominent traits we will refer—his wonderful rendering of the powers of Nature.
His early wanderings in the wild and romantic passes of the Vosges doubtless developed this inherent tendency of his mind. There he wandered, and there, mayhap, imbibed that deep delight of wood and valley, mountain—pass and rich ravine, whose variety of form and detail seems endless to the enchanted eye. He has caught the very spell of the wilderness; she has laid her hand upon him, and he has gone forth with her blessing. So bold and truthful and minute are his countless representations of forest scenery; so delicate the tracery of branch and stem; so patriarchal the giant boles of his woodland monarchs, that the’ gazer is at once satisfied and entranced. His vistas lie slumbering with repose either in shadowy glade or fell ravine, either with glint of lake or the glad, long course of some rejoicing stream, and above all, supreme in a beauty all its own, he spreads a canopy of peerless sky, or a wilderness, perhaps, of angry storm, or peaceful stretches of soft, fleecy cloud, or heavens serene and fair—another kingdom to his teeming art, after the earth has rendered all her gifts.
Paul Gustave Dore was born in the city of Strasburg, January 10, 1833. Of his boyhood we have no very particular account. At eleven years of age, however, he essayed his first artistic creation—a set’ of lithographs, published in his native city. The following year found him in Paris, entered as a 7. student at the Charlemagne Lyceum. His first actual work began in 1848, when his fine series of sketches, the “Labors of Hercules,” was given to the public through the medium of an illustrated, journal with which he was for a long time connected as designer. In 1856 were published the illustrations for Balzac’s “Contes Drolatiques” and those for “The Wandering Jew “—the first humorous and grotesque in the highest degree—indeed, showing a perfect abandonment to fancy; the other weird and supernatural, with fierce battles, shipwrecks, turbulent mobs, and nature in her most forbidding and terrible aspects. Every incident or suggestion that could possibly make the story more effective, or add to the horror of the scenes was seized upon and portrayed with wonderful power. These at once gave the young designer a great reputation, which was still more enhanced by his subsequent works.
With all his love for nature and his power of interpreting her in her varying moods, Dore was a dreamer, and many of his finest achievements were in the realm of the imagination. But he was at home in the actual world also, as witness his designs for “Atala,” “London—a Pilgrimage,” and many of the scenes in “Don Quixote.”
When account is taken of the variety of his designs, and the fact considered that in almost every task he attempted none had ventured before him, the amount of work he accomplished is fairly incredible. To enumerate the immense tasks he undertook—some single volumes alone containing hundreds of illustrations—will give some faint idea of his industry. Besides those already mentioned are Montaigne, Dante, the Bible, Milton, Rabelais, Tennyson’s “Idyls of the King,” “The Ancient Mariner,” Shakespeare, “Legende de Croquemitaine,” La Fontaine’s “Fables,” and others still.
Take one of these works—the Dante, La Fontaine, or “Don Quixote”—and glance at the pictures. The mere hand labor involved in their production is surprising; but when the quality of the work is properly estimated, what he accomplished seems prodigious. No particular mention need be made of him as painter or sculptor, for his reputation rests solely upon his work as an illustrator.
Dore’s nature was exuberant and buoyant, and he was youthful in appearance. He had a passion for music, possessed rare skill as a violinist, and it is assumed that, had he failed to succeed with his pencil, he could have won a brilliant reputation as a musician.
He was a bachelor, and lived a quiet, retired life with his mother—married, as he expressed it, to her and his art. His death occurred on January 23, 1883.
Knowest thou what a speck thou art in comparison with the Universe?—That is, with respect to the body; since with respect to Reason, thou art not inferior to the Gods, nor less than they. For the greatness of Reason is not measured by length or height, but by the resolves of the mind. Place then thy happiness in that wherein thou art equal to the Gods.
Epictetus, Golden Sayings of Epictetus, XXXIII, Epictetus (A.D. 50-A.D. 138).
Therapy that targets disease-causing mutations could become the first of its kind approved for use in the United States.
Advisers to the US Food and Drug Administration (FDA) have paved the way for the agency’s first approval of a gene therapy to treat a disease caused by a genetic mutation.
On 12 October, a panel of external experts unanimously voted that the benefits of the therapy, which treats a form of hereditary blindness, outweigh its risks. The FDA is not required to follow the guidance of its advisers, but it often does. A final decision on the treatment, called voretigene neparvovec (Luxturna), is expected by 12 January.
An approval in the lucrative US drug market would be a validation that gene-therapy researchers have awaited for decades. “It’s the first of its kind,” says geneticist Mark Kay of Stanford University in California, of the treatment. “Things are beginning to look more promising for gene therapy.”
Luxturna is made by Spark Therapeutics of Philadelphia, Pennsylvania, and is designed to treat individuals who have two mutated copies of a gene called RPE65. The mutations impair the eye’s ability to respond to light, and ultimately lead to the destruction of photoreceptors in the retina.
The treatment consists of a virus loaded with a normal copy of the RPE65 gene. The virus is injected into the eye, where the gene is expressed and supplies a normal copy of the RPE65 protein.
In a randomized controlled trial that enrolled 31 people, Spark showed that, on average, patients who received the treatment improved their ability to navigate a special obstacle course1. This improvement was sustained for the full year during which the company gathered data. The control group, however, showed no improvement overall. This was enough to convince the FDA advisory committee that the benefits of the therapy outweigh the risks.
That endorsement is an important vote of confidence for a field that has struggled over the past 20 years. In the early 1990s, gene therapy was red hot, says David Williams, chief scientific officer at Boston Children’s Hospital in Massachusetts. “You couldn’t keep young people out of the field,” he says. “Everyone wanted in.” Then came the death of a young patient enrolled in a gene-therapy clinical trial, and the realization that a gene therapy used to treat children with an immune disorder could cause leukaemia.
Investors backed away from gene therapy, and some academics grew scornful of it. Although European regulators approved one such therapy in 2012, for a condition that causes severe pancreatitis, many doubted that it worked. (The company that makes it has announced that it will not renew its licence to market the drug when it expires on 25 October.) “You’re too smart to work in this field,” a colleague told Kay. “It’s a pseudoscience.”
But some researchers kept plugging away at the problem, improving the vectors that shuttle genes into human cells. Over time, new clinical trials began to show promise, and pharmaceutical companies became more interested in developing treatments for rare genetic diseases. Gradually, investors returned.
Now, demand for gene-therapy vectors is so high that suppliers are oversubscribed, and researchers have to wait between 18 months and 2 years to get some of the reagents that they need for clinical studies, says Williams.
In the past few years, gene therapies have shown promise in clinical trials for a range of diseases — including haemophilia, sickle cell disease and an immune disorder called Wiskott–Aldrich syndrome. On 4 October, Williams and his colleagues published results of a gene-therapy trial to treat cerebral adrenoleukodystrophy (ALD), a devastating and sometimes fatal disorder that affects the nervous system and adrenal glands2. Disease progression was halted for the roughly 2-year duration of the study in 15 of 17 boys who were treated.
The FDA approved its first gene therapy, a treatment in which immune cells are engineered to combat cancer, on 30 August. Unlike Spark’s therapy, the cancer treatment does not target a specific disease-causing mutation, and is administered to immune cells that are removed from the body, engineered and then reinfused.
That is why researchers say that an FDA approval for voretigene neparvovec would be a landmark. “The general concept of gene therapy is replacing or compensating for a missing gene, and that’s what this does,” says Matthew Porteus, a paediatric haematologist also at Stanford. “People are so excited.”
But Spark’s treatment also highlights the limitations of this generation of gene therapies. Although the treatment seems to improve vision, it is still unclear how long the virus will continue to express the normal RPE65 gene — and thus how long its effects will last. “It isn’t a cure,” says Kay.
Similarly, the cerebral ALD therapy seemed to slow the effects of the disease in the brain, but is not expected to treat symptoms in other parts of the body, which can emerge later in life.
“I think we still need to have major improvements in the technology before we’re going to be able to cure these diseases,” says Kay. “But along the way there may be treatments that help make improvements.”
Original article: Gene Therapy for Blindness