Where the slippery slope ends and the slippery cliff begins?

Why Does This Evolutionary Biologist Want to Euthanize Handicapped Babies?
Michael Egnor

Evolutionary biologist Jerry Coyne has written a controversial series of posts in which he advocates medical killing for severely handicapped babies. We have replied (here, here, here, here, here, here). Why would anyone advocate such a thing? What would justify deliberately killing a baby — actually using hospitals and doctors and nurses and medical science to kill children?

Coyne gives his rationale:

If you are allowed to abort a fetus that has a severe genetic defect, microcephaly, spina bifida, or so on, then why aren’t you able to euthanize that same fetus just after it’s born?

Of course, the ethics of aborting handicapped babies in the womb is a matter of considerable controversy, and there is by no means a consensus on it. Furthermore, one of the arguments used to support the pro-life position is that abortion, in addition to being intrinsically immoral, devalues all human life, and endangers handicapped children after birth as well. Coyne’s rationale for the medical killing of babies, which is that we allow abortion of these same children in the womb, gives credence to the pro-life argument. Coyne shows very clearly that there is a slippery slope.

Coyne offers another rationale:

After all, newborn babies aren’t aware of death, aren’t nearly as sentient as an older child or adult, and have no rational faculties to make judgments (and if there’s severe mental disability, would never develop such faculties).

Coyne argues, astonishingly, that the vulnerability of handicapped children justifies killing them. He isn’t (yet) advocating killing handicapped adults. His criterion (for now) for killing severely handicapped people is that they are unaware and can’t make decisions for themselves. In Coyne’s moral world, people who lack “rational faculties to make judgements” have less right to life than rational people do. You have a right to life, unless you are handicapped and don’t know what is happening to you. I have to respect Coyne’s candor, if nothing else.

It makes little sense to keep alive a suffering child who is doomed to die or suffer life in a vegetative or horribly painful state. After all, doctors and parents face no legal penalty for simply withdrawing care from such newborns, like turning off a respirator, but… we should be allowed, with the parents’ and doctors’ consent, to painlessly end their life with an injection.

Coyne doesn’t understand what “vegetative” means. Vegetative means that the child is unable to experience anything. A “vegetative” child can’t “suffer life in a vegetative or horribly painful state.” The child can’t “suffer” anything.

Furthermore, pain (for people who aren’t “vegetative”) is a common medical situation: the treatment for it is to treat the pain, not to kill the child. The fact is that handicapped children don’t ordinarily suffer intractable pain. Handicaps such as spina bifida, anencephaly, cerebral palsy, etc., are not intrinsically painful (such children often have an inability to feel pain in parts of their body). Coyne makes no mention whatsoever of medically treating the pain of the babies he proposes to kill. There are many highly effective methods of treating pain — thousands of different medications, devices, and operations that are used every day in hospitals and clinics and in homes around the world to alleviate pain. Much of medical practice is devoted to alleviating pain and suffering. Yet Coyne makes no mention of medically treating the (occasional) pain and suffering of handicapped children. His solution is to kill them.

Coyne sees the trend toward killing patients who suffer, rather than toward alleviating their pain, as a moral advance:

This change in views about euthanasia and assisted suicide are the result of a tide of increasing morality in our world…

Killing handicapped babies is not a moral advance. Devoting extra effort to their medical care, alleviating the (occasional) pain they do suffer, providing them and their families with medical and social and financial help to make their lives as happy and fulfilled as possible would be a moral advance. Respecting the lives of handicapped people is a moral advance. Killing them is moral regress, of a particularly horrendous sort.

Coyne explains the rationale of the euthanasia movement with shocking candor:

It’s time to add to the discussion the euthanasia of newborns, who have no ability or faculties to decide whether to end their lives. Although discussing the topic seems verboten now, I believe some day the practice will be widespread, and it will be for the better. After all, we euthanize our dogs and cats when to prolong their lives would be torture, so why not extend that to humans? Dogs and cats, like newborns, can’t make such a decision, and so their caregivers take the responsibility. (I have done this myself to a pet, as have many of you, and firmly believe it’s the right thing to do. Our pain at making such a decision is lessened knowing that dogs and cats, like newborns, don’t know about death and thus don’t fear it.)

The clarity is bracing. Coyne admits — he seems to celebrate it — that the slippery slope is real. Now that we have normalized abortion and assisted suicide, it’s time to normalize killing of newborns who don’t meet our definition of “fitness.” Let’s treat them, Coyne argues, like we treat our dogs. Love our babies when they’re healthy. Kill them when they are handicapped or a burden. And our babies’ vulnerability — the fact that they don’t understand — is, in the moral universe of euthanasia advocates, all the more reason to kill them. Life, it seems, is a right for the strong and the rational, but expendable for the weak and unaware.

What is particularly chilling about Coyne’s advocacy of infant euthanasia is not merely that he proposes killing handicapped babies. It is chilling that he makes no endorsement of the proper medical care of these children — where is his advocacy for the medical treatment of their (occasional) pain or of their handicap? Furthermore, it is chilling that he uses their vulnerability — the fact that as babies they are unaware and defenseless — as a reason, not to protect them, but to kill them.

So, why does Jerry Coyne want to kill handicapped babies? He has lots of reasons. But they all seem to boil down to one reason: He wants to kill them because they’re handicapped babies. Such honesty is rare from an advocate of euthanasia.

Euthanasia, fundamentally, is about killing vulnerable people. It should be resisted with every bit of our strength.

On the battle for academic freedom.

In Science Education, Academic Freedom Makes Progress Across America
David Klinghoffer | @d_klinghoffer

In a new ID the Future podcast, Sarah Chaffee surveys progress across the United States in enacting academic freedom (AF) legislation. Despite energetic disinformation campaigns by Darwin-only propagandists, the truth about the value of teaching critical thinking in science class is appreciated by more and more legislators, educators, and activists. Download the episode here, or listen to it here.

Miss Chaffee spoke to AF proponents in Alabama, Oklahoma, and Texas. Her interviewees stress the importance of “refraining from prohibiting teachers” from challenging their students with “more science not less,” of protecting educators from frivolous lawsuits and other career penalties, because “students have a right to know that there are a lot of deep questions here.”

Biologist Ray Bohlin, on the ground in Texas, makes a great point. Everyone always repeats the mantra about how “We need more scientists, We need more scientists, We need more scientists…” And that is true. But what about those students who can’t shake the intuition that life exceeds what Darwinian orthodoxy can explain – as, in fact, many professional scientists are coming to think?

Rather than make fools of those young people and tell them such doubts have no basis in objective science, why not admit the truth – that their insight is being borne out by research, including in mainstream evolutionary biology itself? Admit to them that the question of origins is complex: evolutionary theory has strengths, but also weaknesses.

Surely, in partly confirming what they already sense to be the case, that will have the effect of exciting their curiosity and encouraging them to consider science as a career in their adult lives. And that’s what we all want, says Dr. Bohlin, right?

On testing I.D

Yes, Intelligent Design Is Testable Science – A Resource Roundup
Evolution News | @DiscoveryCSC

After perusing a recent article here (“Desperately Seeking Evolutionary Innovation by Chance”), a reader offers a classic challenge:

You post lots of criticism of evolutionary biology. Have you made any advancement in formulation of your own theory? What predictive power has it shown, if any?

The query, which is really three ways of putting the same question, is a classic because it has been asked so many times in various forms – What predictions does ID make? Is it exclusively a negative case against Darwinian theory? Is it really science? etc. It just so happens that an excellent new ID the Future podcast features Center for Science & Culture Fellow Jonathan Witt discussing exactly this set of issues relating to design theory.

Dr. Witt explains, contrary to the objections of critics, how and why intelligent design is testable. He discusses predictions from biology and astrobiology, and points listeners to an extended list of testable ID predictions available online.  Listen to it here, or download it here.

As to the future of ID, without prematurely giving anything away, that is set to include research into aspects of the genetic code; investigations into genomic elements presumed non-functional based on evolutionary theory, but predicted to be functional based on ID, and much more.

That said, the reader asks valid questions. Intelligent design as a theory of design detection has made many scientific advances over the past few decades. In fact, while not always going explicitly by the name “intelligent design,” ID has made so many advances — often reported in peer-reviewed scientific papers — that it’s impossible to give a thorough answer to the reader’s questions in this brief format. But because we’ve discussed ID’s scientific status and predictive power many times over in the past, that’s not necessary.

The following links are of special interest and relevance:

• “How Do We Know Intelligent Design Is a Scientific ‘Theory’?”
• “Does Intelligent Design Help Science Generate New Knowledge?”
• “Straw Men Aside, What Is the Theory of Intelligent Design, Really?”
• “A Positive, Testable Case for Intelligent Design”
• “Intelligent design has scientific merit because it uses the scientific method to make its claims and infers design by testing its positive predictions”
• “How Can We Positively Test Intelligent Design?”
• “FAQ: Does intelligent design theory implement the scientific method?”
• “How Can We Know Intelligent Design is Science?”
• “No ID Research? Let’s Help Out This Iowa State Student”
• “Peer-Reviewed Articles Supporting Intelligent Design”
• “Bibliography and Annotated List of Peer-Reviewed Publications Supporting Intelligent Design”

And that’s just for starters. Dear reader, if you’ll study these links, you will find the answers to your questions and more. Enjoy.

Yet more primeval tech v. Darwin.

Ribosomes Optimized for Speed, Flexibility
Evolution News | @DiscoveryCSC

The DNA translation machines in the cell show unexpected complexity, forcing molecular biologists to revise what they thought they knew about ribosomes. In particular, they appear optimized for speed of self-duplication and modularized for flexibility.

Last September, we evaluated a fascinating paper about ribosomes that showed how this molecular machine that translates DNA “requires the orchestrated function of hundreds of proteins” — and that’s just to get to the “pre-ribosome” stage! Ribosomes are marvels of organization and function. Since then, more discoveries have shown additional design features of ribosomes.

A cell doesn’t have all day to build and operate these machines. In July, a paper in Science Advances revised the half-life of RNAs significantly downward. Instead of 5-20 minutes to float around and get translated, most messenger RNAs (mRNAs) last only about 2 minutes before being degraded by complex recycling pathways (see this from the University of Basel ). The production rate and decay rate are important factors in gene regulation. So if you think of “orchestrated function” again, the sheet music won’t do any good if the stage isn’t already set up and the players aren’t in their seats.

The ribosome is composed of large RNAs and proteins. The paper doesn’t state the half-life of the ribosomal RNAs, which make up the bulk of the ribosome, but it’s safe to assume the lifetime of each RNA is finite — probably a matter of minutes. An extra reason for assuming this is the rapid doubling of ribosomes during cell division. Before the cell can divide, all the proteins needed by the two daughter cells must be translated. This requirement effectively doubles the work for these machines.

How does the cell prepare for this increased workload? Rather than speed up translation, the ribosomes first duplicate themselves, effectively doubling the production capacity. This means that they have to prepare and assemble all their own RNAs and proteins first. Without efficient ways to accomplish this prerequisite, cell division could be seriously delayed.

An interesting model, published in Nature by Johan Paulsson’s team at Harvard, suggests that “Ribosomes are optimized for autocatalytic production.” They knew that ribosomes are already optimized in three ways. Now, they add a fourth:

Many fine-scale features of ribosomes have been explained in terms of function, revealing a molecular machine that is optimized for error-correction, speed and control. Here we demonstrate mathematically that many less well understood, larger-scale features of ribosomes — such as why a few ribosomal RNA molecules dominate the mass and why the ribosomal protein content is divided into 55–80 small, similarly sized segments — speed up their autocatalytic production. 

The authors, as evolutionists, will assume that Darwinian processes achieved this optimization. In their own words, however, we sense their astonishment at what these machines accomplish.

Ribosomes translate sequences of nucleic acids into sequences of amino acids. Their features are therefore typically explained in terms of how they affect translation. However, in recent years it has also become clear that ribosomes are exceptional as products of the ribosomal machinery. Not only do ribosomal proteins (r-proteins) make up a large fraction of the total protein content in many cells, but the autocatalytic nature of ribosome production introduces additional constraints. Specifically, the ribosome doubling time places a hard bound on the cell doubling time, because for every additional ribosome to share the translation burden there is also one more to make. Even for the smallest and fastest ribosomes, it takes at least 6 min, and typically much longer, for one ribosome to make a new set of r-proteins (Supplementary Information); and this estimate does not account for the substantial time that is invested in the synthesis of ternary complexes. This bound seems to explain the observed limits on bacterial growth, because ribosomes must also spend much of their time making other proteins, and shows that ribosomes are under very strong selective pressure to minimize the time they spend reproducing.

Whether “selective pressure” is the mother of invention is debatable to those of us who are Darwin skeptics, but the authors point out something important. The “orchestrated function of hundreds of proteins” has time limits. The conductor is pounding his foot and tapping his baton on the podium, rushing the orchestra to get in place. Imagine how much harder if each player, instrument, chair, and music stand has to make a copy of itself first for a show across town!

Based on observed facts about ribosomal RNAs and proteins, and how quickly they duplicate, the team created a mathematical model based on the assumption that “selective pressure” forces cells to optimize their ribosomes’ doubling time. Although the model worked for fast-reproducing bacteria, they presume the same time pressure constrains eukaryotic cells:

Similar principles might also apply to some eukaryotes, because the ribosomes of eukaryotes are larger and slower. In fact, even organisms in which cell doubling times are not limited by ribosome doubling times would benefit from faster ribosome production, allowing ribosomes to spend more of their time producing the rest of the proteome. This efficiency constraint was recently shown to have broad physiological consequences for cells, and here we demonstrate mathematically that it might also explain many broader features of the ribosome 

In the figure, they show that ribosomes are dominated by a few large RNAs and lots of small proteins, about 55 to 80 of them of similar size. The reason for this arrangement has long puzzled molecular biologists. According to the new model, ribosomes can reproduce their parts quicker when the proteins are relatively short, and there are lots of them. The existing ribosomes can crank out smaller building blocks faster, and the construction workers can assemble them faster, than if they had to wait for long, complex pieces to arrive.

It’s not necessary to get into the weeds to see the elegance of the solution. Ribosomes assemble faster with more, smaller proteins, reducing the time to duplicate themselves, so that they can get on with their main job of translating all the other proteins the cell needs before dividing. The faster you double the translating machinery, the faster you can double everything else in the cell.

The model also needs to explain why ribosomes include a few large RNAs. Evolutionists have typically invoked the “RNA World” story to suggest that ribosomal RNAs represent transitional forms or vestiges from the origin of life before cells happened upon ways to make proteins. Paulsson’s model suggests a different reason — a functional reason. RNAs only need to be transcribed, not translated. RNA enzymatic activity is not as efficient as protein, but RNA is quicker to make. The cell, therefore, is better off using it when time is of the essence.

The above analysis suggests a great efficiency advantage of using rRNA [ribosomal RNA] over protein, whenever chemically possible, and so could explain why ribosomes defy the general rule that enzymes are made mostly of protein (Fig. 1). This finding does not mean that the role of rRNA is merely to ensure appropriate overall dimensions of the ribosome; however, it does provide a fundamental reason for why proteins must be used sparingly in the ribosome, for example, to increase accuracy or speed up translation, whereas rRNA should be used wherever possible without compromising function. If even one-quarter of the rRNA mass were replaced with r-protein without increasing translation rates, many bacteria would not be able double as quickly as they do 

Do you see  optimization (a form of intelligent design) at work? The authors go into more detail about why rRNAs must be large. Their model shows that small rRNAs, unlike the small ribosomal proteins, would actually slow down duplication. Suffice it to say that the observed ratio of rRNA to ribosomal protein increases the efficiency by two orders of magnitude. Here’s a pithy analogy from a layman’s summary of the paper at Science Daily:

“An analogy for our findings would be to think of ribosomes not as a group of carpenters who merely build a lot of houses, but as carpenters who also build other carpenters,” Paulsson said. “There is then an incentive to divide the job into many small pieces that can be done in parallel to more quickly assemble another complete carpenter to help in the process.”

One other mystery about ribosomes might be solved by looking at it as an optimization problem: why do ribosomes vary? Mitochondrial ribosomes differ from those in the cytosol. Eukaryotic ribosomes differ from those of bacteria. If they perform the same function, why aren’t they all the same? Here’s a paper in  PLOS ONE from last November that opens a window on a possible reason: ribosome structure is modularized. In “The Modular Adaptive Ribosome,” a team from India says this:

The ribosome is an ancient machine, performing the same function across organisms. Although functionally unitary, recent experiments suggest specialized roles for some ribosomal proteins. Our central thesis is that ribosomal proteins function in a modular fashion to decode genetic information in a context dependent manner.

Interested readers can delve further into this open-access paper to see why ribosomes vary in different cell types or different environments. “A clear example is nervous tissue that uses a ribosomal protein module distinct from the rest of the tissues in both mice and humans,” they say. “Our results suggest a novel stratification of ribosomal proteins that could have played a role in adaptation, presumably to optimize translation for adaptation to diverse ecological niches and tissue microenvironments.”

When it comes to ribosomes, it appears to be a case of optimization all the way down.

Let’s give the last word to the Science Daily article.

Rather than being mere relics of an evolutionary past, the unusual features of ribosomes thus seem to reflect an additional layer of functional optimization acting on collective properties of its parts, the team writes.

“While this study is basic science, we are addressing something that is shared by all life,” Paulsson said. “It is important that we understand where the constraints on structure and function come from, because like much of basic science, it is unpredictable what the consequences of new knowledge can unlock in the future.”

Notice how that downplays evolution’s role, in spite of the authors’ Darwinian views. It also, even if not intending to do so, supports a design pespective, while showing how such a focus leads to productive science.

Now the middle ages redux?

Experts Decry Russia’s Threat to Ban the New World Translation of the Holy Scriptures.

ST. PETERSBURG, Russia—Russian authorities are attempting to ban the New World Translation of the Holy Scriptures published by Jehovah’s Witnesses, labeling it as “extremist.”

Ironically, if the court rules in favor of the prosecution, any ban placed on the New World Translation would “violate the amendment to Article 3 of the Federal Law on Extremism signed by Mr. Putin in the fall of 2015,” according to Dr. Ekaterina Elbakyan, professor of sociology and management of social processes at the Moscow Academy of Labor and Social Relations. The amendment to Article 3 clearly states: “The Bible, the Quran, the Tanakh, and the Kangyur, their contents, and quotations from them cannot be recognized as extremist materials.”  

“Who would have imagined that adopting a law giving immunity to certain holy texts would provoke the banning of other holy texts?” states Dr. Roman Lunkin, head of the Center for Religion and Society at the Institute of Europe, Russian Academy of Sciences in Moscow. “The first to suffer have been the Jehovah’s Witnesses, along with their translation of the Bible.” 

Additionally, “as an ICCPR [International Covenant on Civil and Political Rights] member state, Russia’s attempt to ban such a Bible would be contravening freedom of religion conventions,” notes Dr. Jeffrey Haynes, professor of politics and director of the Centre for the Study of Religion, Conflict and Cooperation at London Metropolitan University. 

The case against the New World Translation is being held at the Vyborg City Court, 138 kilometers (85 mi.) northwest of St. Petersburg. On April 26, 2016, the second day of preliminary hearings, the judge granted the prosecution’s request to suspend the case, pending a court-appointed analysis of the New World Translation. The Witnesses were not given a chance to present their defense, and the court assigned the analysis to be done by the Center for Sociocultural Expert Studies, whose negative conclusions about the New World Translation served as the basis for the prosecutor’s original claim. Assigning the center to analyze the New World Translation again violates the precedent set by Russia’s Supreme Court to disqualify an expert if he has previously expressed his opinion about a subject being considered in court.

While the court-appointed analysis is pending, scholars have expressed their regard for the Witnesses’ translation. One such scholar, Dr. Gerhard Besier, director of the Sigmund Neumann Institute for the Research on Freedom and Democracy, comments: “The New World Translation has received high praise worldwide from Bible scholars representing diverse religious communities.”

Likewise, the Moscow-based SOVA Center for Information and Analysis stated in the February 2016 edition of their monthly news release Misuse of Anti-Extremism: “We don’t find any signs of extremism in the New World Translation.” Since then, in almost every monthly news release, SOVA Center has repeated its definitive position against Russia’s actions, such as was published in June 2016: “We would like to reiterate that we view persecution against Jehovah’s Witnesses in Russia and bans against their literature and communities as religious discrimination.”

Facts About the New World Translation

For over a century, Jehovah’s Witnesses in Russia worshipped using a variety of Bible translations, including the Russian synodal and Makarios translations. In 1994, the Witnesses embarked on what would be a 12-year project to translate the Bible into contemporary Russian. In 2007, the complete New World Translation in Russian was released. Since then, over 4.8 million copies in Russian have been produced. The New World Translation is available, in whole or in part, in 137 languages, with over 217 million copies printed. The nearly 175,000 Witnesses in Russia use a variety of peaceful and societally responsible methods to offer Bibles to interested ones free of charge.

Media Contacts:

International: David A. Semonian, Office of Public Information, 1-718-560-5000

Russia: Yaroslav Sivulskiy, 7-812-702-2691

Thanks to the modern cosmogony OOL science is not the only circus in town.

Cosmic Inflation Theory Loses Hangups About Scientific Method
Denyse O'Leary

Two features of our universe puzzle cosmologists: One is the horizon problem: The universe looks the same in all directions and the cosmic microwave background radiation is about the same temperature everywhere. As String Theory for Dummies puts it, “This really shouldn’t be the case, if you think about it more carefully.” Assuming that current measurements are correct, the radiation must have exceeded the speed of light if it really communicated in this way, but that is forbidden by the standard Big Bang model of the universe.

Then there is the the “flatness problem”: “The matter density and expansion rate of the universe appear to be nearly perfectly balanced, even 14 billion years later when minor variations should have grown drastically” (Dummies). Inconveniently, the apparent 1:10^66 fine-tuning  of the Big Bang, of which horizon and flatness are features, is frequently used as an argument for the  the existence of God.

Cosmic inflation theory, first proposed by Alan Guth  in 1981, modified the Big Bang theory (the Standard Model) by proposing that the universe, instead of unfolding at a steady pace, expanded rapidly shortly after it was created, which could account for apparent fine-tuning.

Inflation is not the only naturalist theory on offer. Perhaps the speed of sound was faster than the speed of light back then or else there were existence of extra dimensions of space-time, as postulated by string theory. But, as cosmologist Will Kinney admits, “The takeaway result here is that this idea of inflation turns out to be the only way to do it within the context of standard physics” (Phys.org).

It could have worked if the wheels hadn’t fallen off earlier this year. In “Pop Goes the Universe” (Scientific American, February 2017), Anna Ijjas, Paul J. Steinhardt, and Abraham Loeb (IS&L) advocated a different scenario: “[O]ur universe began not with a bang but with a bounce from a previously contracting cosmos.” The “bouncing cosmology” was initially proposed by Steinhardt and others in 2001, and fleshed out in 2014. When BICEPS II failed to find evidence of inflation in 2014, Michael Slezak  crowed at New Scientist “Inflation is dead, long live inflation! The very results hailed this year as demonstrating a consequence of inflationary models of the universe — and therefore pointing to the existence of multiverses – now seem to do the exact opposite. If the results can be trusted at all, they now suggest inflation is wrong, raising the possibility of cyclic universes that existed before the big bang.” Some were willing to trade the shadowy multiverse for (at least) one other (past) universe, however modest.

An exchange of letters followed, between the three authors (IS&L) and 33 cosmologists who defended early rapid inflation, among whom readers may recall Alan H. Guth, Sean Carroll, Andrei D. Linde, Stephen Hawking, Lawrence Krauss, Martin Rees, George F. Smoot III, Leonard Susskind, Alexander Vilenkin, and Steven Weinberg.

The 33 signatories pointed to the fact that 14,000 papers that use the word “inflation” or “inflationary” in their titles or abstracts have been written by 9,000 scientists. They were stung by the accusation that inflationary cosmology “cannot be evaluated using the scientific method” and that some proponents have proposed discarding a defining property of science: “empirical testability.” They retort that “it has been subjected to a significant number of tests and so far has passed every one.” That would settle the matter except that, as they admit, “Inflation is not a unique theory but rather a class of models based on similar principles.” Empirical science, they concluded with a flourish, “is alive and well!”

The trouble is, thousands of papers can indeed be wrong. One wonders how many papers were written on the formation of the continents before plate tectonics was proposed. And if cosmic inflation has passed so many tests, why do so many variant models survive? Planck data showed in 2015 that the simplest models are no longer tenable and need to be supplemented by exotic physics.

IS&L replied that “The claim that inflation has been confirmed refers to the outdated theory before we understood its fundamental problems,” including the fact that generic inflation leads to eternal inflation and, in consequence, a multiverse: “And if inflation produces a multiverse in which, to quote a previous statement from one of the responding authors (Guth), ‘anything that can happen will happen’—it makes no sense whatsoever to talk about predictions. Unlike the Standard Model, even after fixing all the parameters, any inflationary model gives an infinite diversity of outcomes with none preferred over any other. This makes inflation immune from any observational test.”

Science writer Dennis Overbye calls the inflation controversy a crisis in cosmology. But maybe it is more of a crossroads.

All parties to the dispute assume, as a metaphysical stance, that science cannot address the possibility that the universe shows evidence of design. Even if design turns out to be the best explanation and the most fruitful for progress, it cannot be accepted, as a matter of first principles.

So what options remain? One can earn a living in cosmology enforcing one problematic theory against its rivals. But the charges and countercharges between the three and the 33 raise a more promising possibility: Change the rules for evidence. For example, the 33 defend the multiverse: “If the multiverse picture is valid, then the Standard Model would be properly understood as a description of the physics in our visible universe, and similarly the models of inflation that are being refined by current observations would describe the ways inflation can happen in our particular part of the universe.”

But multiverse cosmology flourishes entirely without evidence. So, by its nature, it would be consistent with any finding whatever.

In 2014, not a good year for inflationary theory (gravitational waves were just dust), Steinhardt told Nature that the multiverse bubble had burst. But in the same piece, he warned that “the inflationary paradigm is so flexible that it is immune to experimental and observational tests.” In May 2017, for example, we were told by one team that dark energy is pushing the universe to expand but we have not established the existence of dark energy; it is itself a theoretical concept.

Experimental physicist Rob Sheldon offers some observations on the “firestorm” ignited by IL&S: Paul Steinhardt was an inflationary cosmologist himself in the early 1980s but he concluded in 2002 that it would not work.

The whole purpose of the inflationary theory is negated by its development. It was invented to explain the 1:10^66 fine-tuning of the Big Bang, but in the end, it required 1:10^10^100 fine-tuning. (The first number has 66 zeroes after it, the second number has a hundred, trillion, trillion, trillion, trillion, trillion, trillion, trillion, trillion zeroes after it.)

Steinhardt pleads ignorance as to why he advocated the theory in the first place. At the time it looked like it had just one or two zeroes after the probability, but research added a few more until the theory just wasn’t justified anymore. So the real question becomes, why do 33 famous physicists included Nobel prize-winners, still like the theory and think Steinhardt has lost his marbles?

Applying one of science philosopher Imre Lakatos’s concepts, Sheldon labels cosmic inflation a “seriously” degenerating science program. It illuminates only itself, not nature.

But is degeneration still a failure? What if naturalism changes the role of a science program? Perhaps stubbornly contrary evidence merely shows the need for more drive and zeal in generating new naturalist theories, not more reflection and evaluation of that direction. With enough such theories tried and discarded, more convincing ones will surely appear. Especially now because, the multiverse (“anything that can happen will happen”) is becoming so much a fixture of popular science culture that careers will thrive simply on formulating clever arguments for its existence, not on demonstrating it. Metaphysics again.

Lamarck redux v. Darwin?

Evolution’s Third Rail — Transgenerational Epigenetics Can Have a Profound Impact
Cornelius Hunter

In the spring of 2006 I gave a talk on the campus of Cornell University and afterwards was joined by then Cornell professors Richard Harrison and Kern Reeve for a sort of panel discussion or debate about biological evidences and origins. I presented a dozen or so interesting and important evidences that I felt needed to be recognized in any discussion of origins. The evidences falsified key predictions of evolution and so needed to be acknowledged and reckoned with, one way or another.

One of the items on my list was the so-called directed adaptation mechanisms which, broadly construed, can include everything from non-random, directed, mutations to transgenerational epigenetic inheritance. But I was in for a big surprise when Harrison and Reeve gave their response.

Directed adaptation is reminiscent of Lamarckism. Rather than natural selection acting over long time periods on biological variation which is random with respect to need, directed adaptation mechanisms provide rapid biological change in response to environmental challenges. Like physiological responses, directed adaptation can help an organism adjust to shifts in the environment. But those adaptations can then be inherited by later generations. Stresses which your grandparents were subjected to may be playing out in your own cells.

In the 20th century, evolutionists had strongly rejected any such capability. Lamarckism was the third rail in evolutionary circles. And for good reason, for it would falsify evolutionary theory. But empirical evidence had long since pointed toward the unthinkable, and by the 21st century the evidence was rapidly mounting.

While there was of course still much to learn in 2006 about directed adaptation (as there still is today for that matter), it could no longer be denied, and needed to be addressed. At least, that is what I thought.

I was shocked when Harrison and Reeve flatly denied the whole story. Rick waved it off as nothing more than some overblown and essentially discredited work done by Barry Hall and John Cairns, back in the 1970s and 80s (for example here ).

But there was a body of work that had gone far beyond the work of Hall and Cairns. Incredulously I responded that entire books had been written on the subject. Rick was quick to respond that “entire books are written about all kinds of discredited things.”

True enough. It was me versus two professors on their home turf with a sympathetic audience, and there was no way that I was going to disabuse them of what they were convinced of.

Confirmation testing and theory-laden evidence are not merely philosophical notions. They are very real problems. I’m reminded of all this every time a new study adds yet more confirmation to the directed adaptation story, such as the recent paper out of Nicola Iovino’s lab on transgenerational epigenetic inheritance in house flies, which states:

Gametes carry parental genetic material to the next generation. Stress-induced epigenetic changes in the germ line can be inherited and can have a profound impact on offspring development.

The press release gives little indication of the controversy as it admits that these findings were once considered impossible:

It has long been thought that these epigenetic modifications never cross the border of generations. Scientists assumed that epigenetic memory accumulated throughout life is entirely cleared during the development of sperms and egg cells.

It is hard enough to see how organisms can respond intra-lifetime to environmental challenges, but how can it be inherited as well? For epigenetic changes that occur in somatic cells, that information must enter into the germ line as well. Somehow it must be incorporated into the sperm and/or egg cells.

It is an enormous problem to explain how such capabilities evolved. Not only are a large number of mutations required to make this capability work, it would not be selected for until the particular environmental condition occurred. That means that, under evolution, it would be not preserved, even if it could somehow arise by chance.

Redundant no more?

Paper Finds Functional Reasons For "Redundant" Codons, Fulfilling a Prediction from Intelligent Design

Casey Luskin 

A new peer-reviewed paper in the journal Frontiers in Genetics, "Redundancy of the genetic code enables translational pausing," finds that so-called "redundant" codons may actually serve important functions in the genome. Redundant (also called "degenerate") codons are those triplets of nucleotides that encode the same amino acid. For example, in the genetic code, the codons GGU, GGC, GGA, and GGG all encode the amino acid glycine. While it has been shown (see here) that such redundancy is actually optimized to minimize the impact of mutations resulting in amino acid changes, it is generally assumed that synonymous codons are functionally equivalent. They just encode the same amino acid, and that's it.

Well, think again. The theory of intelligent design predicts that living organisms will be rich in information, and thus it encourages us to seek out new sources of functionally important information in the genome. This new paper fulfills an ID prediction by finding that synonymous codons can lead to different rates of translation that can ultimately impact protein folding and function.

This means that DNA contains multiple languages or encoded commands occupying the same string of contiguous bases. On the one hand, a string of nucleotide bases encodes amino acids. On the other hand, that same string contains information about the rate at which the ribosome should translate the protein so that it can properly fold into the right shape. The paper calls this "translational pausing." The ribosome is capable of reading both sets of commands -- as they put it, "[t]he ribosome can be thought of as an autonomous functional processor of data that it sees at its input." To put it another way, the genetic code is "multidimensional," a code within a code. This multidimensional nature exceeds the complexity of computer codes generated by humans, which lack the kind of redundancy of the genetic code. As the abstract states:

The codon redundancy ("degeneracy") found in protein-coding regions of mRNA also prescribes Translational Pausing (TP). When coupled with the appropriate interpreters, multiple meanings and functions are programmed into the same sequence of configurable switch-settings. This additional layer of Ontological Prescriptive Information (PI_o) purposely slows or speeds up the translation decoding process within the ribosome. Variable translation rates help prescribe functional folding of the nascent protein. Redundancy of the codon to amino acid mapping, therefore, is anything but superfluous or degenerate. Redundancy programming allows for simultaneous dual prescriptions of TP and amino acid assignments without cross-talk. This allows both functions to be coincident and realizable. We will demonstrate that the TP schema is a bona fide rule-based code, conforming to logical code-like properties. Second, we will demonstrate that this TP code is programmed into the supposedly degenerate redundancy of the codon table. We will show that algorithmic processes play a dominant role in the realization of this multi-dimensional code.

They write that the ribosome's ability to undergo translational pausing "reveal[s] the ribosome, among other things, to be not only a machine, but an independent computer-mediated manufacturing system." The paper even suggests, "Cause-and-effect physical determinism...cannot account for the programming of sequence-dependent biofunction."

Apart from ID's expectation of finding new layers of information in the genome, the paper implicitly challenges some common evolutionary assumptions. The notion that shared synonymous codons are functionally irrelevant has been used to buttress arguments for Darwinian evolution.

For one thing, some evolutionists claim that phylogenetic signals can be carried by the distribution of synonymous codons since they're functionally equivalent. This paper suggests otherwise.

For another, seeking to infer the activity of natural selection, evolutionary biologists statistically analyze the frequency of synonymous (thought to be functionally unimportant) and nonsynonymous (thought to be functionally important) codons in a gene. (We've discussed this previously here andhere.) As the thinking goes, if synonymous codons are functionally unimportant, then three conclusions may follow: a bias toward synonymous codons implies purifying selection in the gene, a bias towards nonsynonymous codons implies positive selection, and an equal balance implies neutral evolution (no selection). But if synonymous codons can have important functional meaning, then the whole methodology goes out the window, and hundreds of studies that used these methods to infer "selection" during the supposed "evolution of genes" could be wrong.

The evidence supports the view that synonymous codons have divergent effects upon translation, as the paper finds: "Data shows that with fixed levels of tRNA's, synonymously encoded mRNA's translate with different speeds" and "Recent work has built on the above observations showing a strong relationship between specific arrangements of codons in mRNA to the rate of translation." Genetic modifications in the lab can even induce translational pausing:

"Pausingfunction" is caused by specific mRNA codon sequences rather than by tunnel-protein interactions to amino acid sequences. This contention is supported by data involving the substitution of rare codons with synonymous codons in E. coli. If the pausing effect was solely related to the amino acid chain sequence, then replacing codons with synonymous codons should still produce the same folded amino acid chain with the same translation speed. However, substitution of rare codons with synonymous codons did produce a change in speed and conformation changes.

These changes in translational speed can have phenotypic effects:

For example, a silent mutation in the human gene ABCB1 caused a conformational change to occur in the P-glycoprotein. This protein folded differently caused by a temporal change in translation affecting the timing of the folding process. ... Thus, the protein folding pathways are affected by changes in the coding regions of DNA" (internal citations removed).

In short, "redundant" codons are not necessarily redundant at all. As the paper puts it: "we show why the term "degeneracy" is completely inappropriate. The dual coding functionality of redundancy is anything but 'degenerate.' It represents, instead, far more sophistication, layers, and dimensions of formal prescription." In fact, this paper "defines new universal linguistic-like rules needed to identify and characterize codon mappings of TP events." The authors write:

The TP code exhibits distinct meaning in relation to mappings between codons and pausing units. The TP code also exhibits a syntax or grammar that obeys strict codon relationships that demonstrate language properties. Because of the redundancy of the genetic code, it could be argued that the TP language is a subset of the genetic language. The subspace of the TP language resides, and thus appears to have a dependency on, the primary genetic code. Within this subspace, however, we argue that the TP language is decoupled from and remains independent of the protein-coding language.

Their conclusion about the high-information capacity of the genetic code is striking:

Redundancy in the primary genetic code allows for additional independent codes. Coupled with the appropriate interpreters and algorithmic processors, multiple dimensions of meaning, and function can be instantiated into the same codon string. We have shown a secondary code superimposed upon the primary codonic prescription of amino acid sequence in proteins. Dual interpretations enable the assembly of the protein's primary structure while enabling additional folding controls via pausing of the translation process. TP provides for temporal control of the translation process allowing the nascent protein to fold appropriately as per its defined function. This duality in the coding function acts to reduce the redundancy in the genetic code when viewed holistically. The functionality of condonic redundancy denies the ill-advised label of "degeneracy." When simultaneously combined with other coding schemas such as intron/exon boundary conditions, and overlapping and oppositely oriented promoters, multiple dimensions of independent coding by the same codon string has become apparent.

In his 2001 book No Free Lunch, William Dembski explained the primary prediction of intelligent design:

[W]hat about the predictive power of intelligent design? Intelligent design offers one obvious prediction, namely, that nature should be chock-full of specified complexity and therefore should contain numerous pointers to design ... This prediction is increasingly being confirmed. (p. 362)

Multidimensional codes and new levels of specified complexity are exactly what ID predicts, and they're exactly what this paper is reporting. It's this sort of sophisticated, information-rich control that is expected by intelligent design, in contrast to Darwinian biology which fails to anticipate it. On the contrary, Darwinian advocates publish mountains of papers banking upon the unquestioned assumption that there is no important, functional reason for the existence of "redundant" or "degenerate" features. Slowly but surely, the data are turning the tide in the evolution debate.