Category Archives: Nature & Space

The Twelve Apostles


Witness the rugged splendour of the famous 12 Apostles, magnificent rock stacks that rise up majestically from the Southern Ocean on Victoria’s dramatic coastline.

Limestone cliffs

Created by constant erosion of the limestone cliffs of the mainland beginning 10–20 million years ago, the stormy Southern Ocean and blasting winds gradually eroded the softer limestone, forming caves in the cliffs.

The caves eventually became arches and when they collapsed rock stacks up to 45 metres high were left isolated from the shore. View the 12 Apostles at sunrise and sunset as they change colour from dark and foreboding in shadow to brilliant sandy yellow under a full sun.

How to get there

The 12 Apostles are located 275 kilometres west of Melbourne, approximately a four-hour drive along the Great Ocean Road.

Original article: The Twelve Apostles


Backwardly Wired Retina “An Optimal Structure”: New Eye Discovery Further Demolishes Dawkins



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?:

Backwardly-Wired Retina?

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:

Regenerating Photoreceptors

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

Blind Spot

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:

Signal Processing

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

 Update: see Refutation of critics of this article, including Dawkins’ fellow atheopath P.Z. Myers.

Related Articles

Further Reading

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.

Hugh Ross – The Science of Genesis and the Anthropic Principle

FDA Advisers Back Gene Therapy For Rare Form of Blindness

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.”

Gene Replacement

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.

Long Road

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 Williamschief 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.

Measured Expectations

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