Author: Truth & Hammer

Stephen C. Meyer is a geophysicist and author of New York Times bestseller, “Darwin’s Doubt.” Despite not being a Christian himself, after years of scientific study, Meyer came to the conclusion that there simply must be an intelligent designer behind our creation.

In addition, contrary to many within his discipline, Meyer believes that expert scientific study of the origins of the universe can conclude a number of assertions that are in common with the central tenets of theistic beliefs. In a wide-ranging interview on the Ben Shapiro Show, Meyer also criticized Darwin’s evolutionary theory as being unable to answer the biggest question of all — how did life actually begin?

Intelligent Design vs. Creationism

“Creationism is an interpretation from religious authority, whereas intelligent design is an inference from biological and physical, cosmological evidence,” Meyer noted of the differences between the two belief systems. “One starts from data of the natural world, one starts from Scripture.”

n addition, Meyer said, most creationists “hold to the view that the earth is very young — created maybe 10,000 years ago,” before qualifying that he himself is an “old earth” guy.

Interestingly, despite evolutionary biologist Charles Darwin often being heralded as the enemy of those who believes in a creator God, for Meyer, Darwin modeled what it meant to investigate the big questions of life with rigor and scientific integrity. Despite following Darwin’s scientific method, however, Meyer came to very different conclusions.

Darwin had a “principle of reasoning” that he used to help him understand cause and effect on some of the biggest questions of life.

“It is possible to formulate a case for intelligent design in a strictly scientific manner,” Meyer said. “When we think about the origin of information, it always arises from an intelligent source.”

Whether it is a “hieroglyphic inscription, a paragraph in a book, or information embedded in a radio signal, whenever you find information, you trace it back to its source, you always come to a mind not a process,” Meyer explained.

In studying the issue, Meyer, who wrote a Ph.D. on the “origin of life problem” at Cambridge University, said that by using the Darwinian method of reasoning, he “came to a different, non-Darwinian conclusion — that there is evidence of intelligent design.”

Can Intelligent Design Be Proven Wrong?

For many Christians, the creation question is a big one. Indeed, while there is a split over the mechanics of how our world came about, all believers would assert that God was, somehow, the creative force behind the world we now live in. With that in mind, is there any chance that a creator could actually be disproved?

“You would have to find an undirected process that was capable of producing information beyond a threshold that we have defined mathematically,” Meyer explained, adding that this would entail information arising “by chance, based on the probable resources of the universe.”

This, however, is unlikely to happen, because intelligent design posits that only “intelligence is capable of generating the amount of information needed for these big jumps in biological complexity in the history of life.” Indeed, for Christians, this intelligence or “mind,” would be equated to an infinite being — namely, God.

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Traditionally when we think of sound waves, we think of invisible vibrations moving weightless through the air – not carrying any mass.

That might be about to change. Physicists have just provided further evidence that particles of sound really can carry tiny amounts of mass. And that means they can produce their own gravitational fields – which could be a big deal for our understanding of space.

But let’s back up for a second and go back to the basics. Kick a ball, and you put energy into it. Einstein would tell you you’ve also contributed a tiny bit of mass by making it accelerate.

If that ball is a tiny particle, and the kick is a wave of sound, you might imagine the same thing. Yet for decades, physicists have argued over whether the momentum within a surge of jiggling particles adds up to a net amount of mass.

Last year, physicist Alberto Nicolis from Columbia University in New York worked with a colleague from the University of Pennsylvania in Philadelphia to investigate how different waves decay and scatter in a super cold fluid of helium.

Not only did they show that sounds can actually generate a non-zero value for mass, but they might also weirdly ‘float’ along gravitational fields in an anti-gravity sense.

This might not make much difference for relatively quiet booms and squeaks on Earth, but for the star-quaking roars that pulse through dense objects like neutron stars, interactions between massive sound waves and gravity could be important.

While the pair affirmed the possibility, it was limited to a specific set of conditions. So Nicolis has now used a different set of techniques to show that sounds have mass inside ordinary fluids and solids, and even create their own faint gravitational field.

Their new conclusion contradicts views that phonons are massless. Their movements don’t just respond to a gravitational field in strange ways, but are a source of a field in their own right.

In a Newtonian sense, this is the very definition of mass.  

So why is there so much confusion over this issue?

The core of the problem is in how waves move through a medium. Just as a wave of light is called a photon, a wave of vibration can be thought of as a unit called a phonon.

Imagine standing still at a rock concert, enjoying the show. Your body’s mass is the same it was in the morning when you stepped on the scales. Then, a killer track starts and your neighbour shoves you, accelerating your body.

Einstein’s law – the one that says energy equals mass times the speed of light squared – says the tiny bit of energy you gain from the push is also mass. Colliding with the next person, the energy transfers into them along with the imperceptibly small bit of mass. 

In this metaphor, the chain of body slams going back and forth through the crowd is the phonon, and since it’s a transfer of energy, you might be forgiven for immediately thinking it’s also a movement of mass.

Under such simple conditions, the perfect back-and-forth movement of the bodies and direct transfer of momentum can be described as a form of linear dispersion.

While energy levels might fluctuate during the back-and-forth jostle, your body resets to give the whole phonon cycle no mass overall. This linear dispersion gives each phonon a net mass of naught, just as with photons of light.

But reality isn’t always so straightforward. 

Light waves moving through a vacuum and phonons in a theoretically perfect material might well be linear, but solids and fluids jostling with one another obey a variety of other laws according to certain fields and influences.

Those are a little complicated, arising from the medium’s state and components.

So using approximations known as effective field theory, Nicolis and Columbia University colleagues Angelo Esposito and Rafael Krichevsk got a broad sense of how the phonon travels through such media and how to calculate their response to a gravitational field.

And what they showed was that even in these messy ‘real world’ conditions, the sound waves could carry mass.

To be clear, that mass isn’t exactly huge, as you’d expect. We’re talking roughly the same as the amount of energy in the phonon divided by the square of the speed of light. So … small.

It’s also important to keep in mind the mathematics behind the claim haven’t actually been put to the test. Sound foundations aside, somebody now needs to measure gravitational shifts in atoms chilled to near zero, something which just might be possible as we explore such condensates in space.

Alternatively, the researchers suggest it might be easier to weigh an earthquake. The sound generated by a large tremor could amount to billions of kilograms of mass.

Anybody up to that challenge?

This research was published in Physical Review Letters.

It was surprisingly simple. University of California, Berkeley, scientists inserted a gene for a green-light receptor into the eyes of blind mice and, a month later, they were navigating around obstacles as easily as mice with no vision problems. They were able to see motion, brightness changes over a thousandfold range and fine detail on an iPad sufficient to distinguish letters.

The researchers say that, within as little as three years, the gene therapy—delivered via an inactivated virus—could be tried in humans who’ve lost sight because of retinal degeneration, ideally giving them enough vision to move around and potentially restoring their ability to read or watch video.

“You would inject this virus into a person’s eye and, a couple months later, they’d be seeing something,” said Ehud Isacoff, a UC Berkeley professor of molecular and cell biology and director of the Helen Wills Neuroscience Institute. “With neurodegenerative diseases of the retina, often all people try to do is halt or slow further degeneration. But something that restores an image in a few months—it is an amazing thing to think about.”

About 170 million people worldwide live with age-related macular degeneration, which strikes one in 10 people over the age of 55, while 1.7 million people worldwide have the most common form of inherited blindness, retinitis pigmentosa, which typically leaves people blind by the age of 40.

“I have friends with no light perception, and their lifestyle is heart-wrenching,” said John Flannery, a UC Berkeley professor of molecular and cell biology who is on the School of Optometry faculty. “They have to consider what sighted people take for granted. For example, every time they go to a hotel, each room layout is a little different, and they need somebody to walk them around the room while they build a 3-D map in their head. Everyday objects, like a low coffee table, can be a falling hazard. The burden of disease is enormous among people with severe, disabling vision loss, and they may be the first candidates for this kind of therapy.”

Currently, options for such patients are limited to an electronic eye implant hooked to a video camera that sits on a pair of glasses—an awkward, invasive and expensive setup that produces an image on the retina that is equivalent, currently, to a few hundred pixels. Normal, sharp vision involves millions of pixels.

Correcting the genetic defect responsible for retinal degeneration is not straightforward, either, because there are more than 250 different genetic mutations responsible for retinitis pigmentosa alone. About 90 percent of these kill the retina’s photoreceptor cells—the rods, sensitive to dim light, and the cones, for daylight color perception. But retinal degeneration typically spares other layers of retinal cells, including the bipolar and the retinal ganglion cells, which can remain healthy, though insensitive to light, for decades after people become totally blind.

In their trials in mice, the UC Berkeley team succeeded in making 90 percent of ganglion cells light sensitive.

Isacoff, Flannery and their UC Berkeley colleagues will report their success in an article appearing online March 15 in Nature Communications.

To reverse blindness in these mice, the researchers designed a virus targeted to retinal ganglion cells and loaded it with the gene for a light-sensitive receptor, the green (medium-wavelength) cone opsin. Normally, this opsin is expressed only by cone photoreceptor cells and makes them sensitive to green-yellow light. When injected into the eye, the virus carried the gene into ganglion cells, which normally are insensitive to light, and made them light-sensitive and able to send signals to the brain that were interpreted as sight.

“To the limits that we can test the mice, you can’t tell the optogenetically-treated mice’s behavior from the normal mice without special equipment,” Flannery said. “It remains to be seen what that translates to in a patient.”

In mice, the researchers were able to deliver the opsins to most of the ganglion cells in the retina. To treat humans, they would need to inject many more virus particles because the human eye contains thousands of times more ganglion cells than the mouse eye. But the UC Berkeley team has developed the means to enhance viral delivery and hopes to insert the new light sensor into a similarly high percentage of ganglion cells, an amount equivalent to the very high pixel numbers in a camera.

Isacoff and Flannery came upon the simple fix after more than a decade of trying more complicated schemes, including inserting into surviving retinal cells combinations of genetically engineered neurotransmitter receptors and light-sensitive chemical switches. These worked, but did not achieve the sensitivity of normal vision. Opsins from microbes tested elsewhere also had lower sensitivity, requiring the use of light-amplifying goggles.

To capture the high sensitivity of natural vision, Isacoff and Flannery turned to the light receptor opsins of photoreceptor cells. Using an adeno-associated virus (AAV) that naturally infects ganglion cells, Flannery and Isacoff successfully delivered the gene for a retinal opsin into the genome of the ganglion cells. The previously blind mice acquired vision that lasted a lifetime.

“That this system works is really, really satisfying, in part because it’s also very simple,” Isacoff said. “Ironically, you could have done this 20 years ago.”

Isacoff and Flannery are raising funds to take the gene therapy into a human trial within three years. Similar AAV delivery systems have been approved by the FDA for eye diseases in people with degenerative retinal conditions and who have no medical alternative.

According to Flannery and Isacoff, most people in the vision field would question whether opsins could work outside their specialized rod and cone photoreceptor cells. The surface of a photoreceptor is decorated with opsins—rhodopsin in rods and red, green and blue opsins in cones—that are embedded in a complicated molecular machine. A molecular relay—the G-protein coupled receptor signaling cascade—amplifies the signal so effectively that we are able to detect single photons of light. An enzyme system recharges the opsin once it has detected the photon and becomes “bleached.” Feedback regulation adapts the system to very different background brightnesses. And a specialized ion channel generates a potent voltage signal. Without transplanting this entire system, it was reasonable to suspect that the opsin would not work.

But Isacoff, who specializes in G protein-coupled receptors in the nervous system, knew that many of these parts exist in all cells. He suspected that an opsin would automatically connect to the signaling system of the retinal ganglion cells. Together, he and Flannery initially tried rhodopsin, which is more sensitive to light than cone opsins.

To their delight, when rhodopsin was introduced into the ganglion cells of mice whose rods and cones had completely degenerated, and who were consequently blind, the animals regained the ability to tell dark from light—even faint room light. But rhodopsin turned out to be too slow and failed in image and object recognition.

They then tried the green cone opsin, which responded 10 times faster than rhodopsin. Remarkably, the mice were able to distinguish parallel from horizontal lines, lines closely spaced versus widely spaced (a standard human acuity task), moving lines versus stationary lines. The restored vision was so sensitive that iPads could be used for the visual displays instead of much brighter LEDs.

“This powerfully brought the message home,” Isacoff said. “After all, how wonderful it would be for blind people to regain the ability to read a standard computer monitor, communicate by video, watch a movie.”

These successes made Isacoff and Flannery want to go a step farther and find out whether animals could navigate in the world with restored vision. Strikingly, here, too, the green cone opsin was a success. Mice that had been blind regained their ability to perform one of their most natural behaviors: recognizing and exploring three-dimensional objects.

They then asked the question, “What would happen if a person with restored vision went outdoors into brighter light? Would they be blinded by the light?” Here, another striking feature of the system emerged, Isacoff said: The green cone opsin signaling pathway adapts. Animals that were previously blind adjusted to the brightness change and could perform the task just as well as sighted animals. This adaptation worked over a range of about a thousandfold—the difference, essentially, between average indoor and outdoor lighting.

“When everyone says it will never work and that you’re crazy, usually that means you are onto something,” Flannery said. Indeed, that something amounts to the first successful restoration of patterned vision using an LCD computer screen, the first to adapt to changes in ambient light and the first to restore natural object vision.

The UC Berkeley team is now at work testing variations on the theme that could restore color vision and further increase acuity and adaptation.