Search This Blog

Thursday, 27 August 2015

Yet more on the ancient roots of Darwinism

The Ancient Philosophical Roots of Darwinism

Six centuries before the Christian era (B.C.E.), the Greek philosopher Anaximander asserted that the first living things emerged from formless matter and then underwent transmutations to produce a wide variety of forms. In what some commentators regard as a primitive form of evolutionary theory, Anaximander apparently held that humans descended from some other species of animal -- probably a fish.48 In the fifth century B.C.E., the Greek philosopher Empedocles taught that the chance interplay of earth, air, fire and water produced disconnected organs and limbs that wandered aimlessly about until they combined spontaneously to make whole creatures. Most of the resulting combinations were monstrosities -- with faces and breasts on the back as well as front, or half ox and half human -- that were so maladapted that they perished. Among the few that survived were creatures that eventually developed into modern humans.49

Leucippus and Democritus in the fifth century B.C.E. and Epicurus in the fourth century B.C.E. advocated a materialistic philosophy in which no gods exist -- only atoms and the void.50 In the first century B.C.E., the Roman philosopher Lucretius immortalized this view in his long poem “On the Nature of Things.” Book Five begins with an attack on religion and teleology, then it lays out a theory of survival of the fittest that is remarkably similar to Darwin’s. Although Lucretius did not suggest that all living things are descended from a common ancestor, he believed that all things -- including living organisms and human beings -- are products of aimless interactions among atoms. If they are well adapted to their environment, they survive and leave descendants; if not, they perish.51

Some modern followers of Charles Darwin regard these ancient thinkers as their intellectual forebears. According to a 1996 statement on a pro-evolution web site maintained by the University of California at Berkeley, “evolutionary theory begins” with Anaximander. Although his ideas “drew on the religious and mythical ideas of his time, he was still one of the first to attempt an explanation of the origin and evolution of the cosmos based on natural laws.” Thus Anaximander’s theory “bears some resemblance to evolutionary theory.” According to the same web site Empedocles proposed a theory that “seems a bit bizarre today” but was nevertheless “a sort of evolutionary theory: Past natural selection is responsible for the forms we see today. Empedocles also ascribed the origin of the life of today to the interplay of impersonal forces, in which chance, not the gods, played the major role.” Thus the Greeks “led the way in developing a general scientific worldview -- one in which natural, non-miraculous explanations for the causes of phenomena were sought.”52

Of course, there were differences between the ideas of the ancient Greeks and modern evolutionary theory, but they were similar in one fundamental respect: They attributed cosmic and biological origins to unguided natural processes rather than divine design. As modern evolutionary biologist Ernst Mayr put it, the ancient Greek theories “constitute the first scientific revolution, so to speak, a rejection of supernatural in favor of materialistic explanations.”53

For Mayr and the author of the Berkeley evolution web site, and for other followers of Charles Darwin, “science” is synonymous with “materialistic explanation.” In this respect, they are following in the footsteps of ancient materialistic philosophers.

This is why modern controversies over evolution are not really about empirical science. Although many of Darwin’s followers believe that he presented overwhelming evidence for his theory, nothing could be further from the truth. The Origin of Species is just warmed-over materialistic philosophy, decorated with illustrations borrowed from nineteenth-century science.

On why Darwinism loses on every sale.

A Leaky Faucet: Why Darwinian Evolution Leads to Loss of Information
Ann Gauger August 26, 2015 11:03 AM

In 2010 biochemist Michael Behe published a paper in the Quarterly Review of Biology in which he concisely stated the first rule of adaptive evolution: "Break or blunt any functional coded element whose loss would yield a net fitness gain." By this he meant several things. First, there are indeed adaptive mutations -- that is, mutations that yield a benefit to the cell under a particular set of circumstances. Second, the primary way such adaptation occurs is by breaking or inactivating some non-essential pre-existing function, in order to make the cell more fit, more competitive than its neighbors.

Behe was talking about microbes -- viruses and bacteria -- but his rule also applies at the cellular level in higher organisms. The best example where this rule is played out is in cancer. Cancers develop when one or more normal functions in a cell are disrupted or broken. The ironic thing is that for the cancer cells, this breaking increases their fitness, their rate of growth and cell division, and thus is beneficial -- to them. Normal constraints have been removed, allowing uncontrolled growth. For the cancer cell that's good, but bad for us, of course. So one can say that cancer is a prime example of what adaptive evolution can accomplish on the multicellular level, by breaking or disrupting some normal function.

What does Behe's first rule of adaptive evolution say about evolution in general? If most "beneficial" mutations are due to the loss of something rather than a gain of something, we are losing information when most adaptations occur, sometimes irreversibly. Let me give an example.

Microbiologist Ralph Seelke and I published a paper in 2010 where we demonstrated that cells always, or nearly always, take the easiest road to success. Given a choice between a simple two-step path leading to repair of two genes needed to make tryptophan, versus a one-step path that eliminated expression of the those genes, only one out of a trillion cells went down the path toward making tryptophan, even though that path would ultimately be much more beneficial. Why did this happen?

The genes to be repaired were overexpressed -- too much of their products were made. Because one of the genes was broken in two places, no tryptophan could be made. Thus both genes were expensive to keep around. It was easier for the cell to break the useless genes than to repair them -- one step instead of two -- and the cells, having no foresight, took that path. Some of those cells deleted the genes, thus losing the information needed to make tryptophan for good.

Let me explain in everyday terms. A faucet leaking badly but with no way to hook it up to a hose is entirely useless. While it is relatively easy to repair the faucet, requiring only two parts, the owner of the faucet doesn't know that. Since he can do without the faucet, he is likely to cap it to stop the expense of the wasted water. But he has lost the ability to water his backyard using that faucet.

Like the clueless homeowner, evolution has no foresight and does not know there is a big payoff just two mutations away. If the cells can prevent the overexpression of the tryptophan genes or remove them in a single step, that's what they will do, especially since there are many more ways to inactivate a gene than to repair it. Any cell that does this instantly becomes more fit than its neighbors, because it is spending less energy making useless stuff.

In fact, that is what we observed. Nearly all the cells inactivated the genes (only one out of a trillion didn't). Some of the cells even deleted the genes, thus losing the capacity to make tryptophan for good. Darwinian evolution travels by the shortest road, without regard for where it's headed. And if the shortest road is to break an existing function -- to lose information -- that's the path it chooses.

I'm sure you can think of parallels in the business world, when only the bottom line, corporate fitness, is what matters, and executives have no long-term vision. They don't see how some things, if adjusted, may yield big payoffs. As a result, whole technologies can be decimated or lost in a push for efficiency, technologies that if maintained could prove vital in the future. But fortunately, unlike Darwinian evolution, we do have foresight and can plan ahead. We do have the capacity for innovation, and can make wise choices or correct our mistakes.


The process of innovation is the opposite of the first rule of adaptive evolution. In the biological world, the quickest road to adaptation may be to delete or inactivate genes that are not necessary. But you don't get new features by deleting information. Building something new, which is what is required to explain the diversity around us, requires more than the happenstance and selection of Darwinian evolution. It requires foresight, planning, and a clear picture of the goal. It requires intelligent design.

Wednesday, 26 August 2015

On the advance of Jehovah's Word in the British isles

Bedell’s Bible—One Small Step to Better Bible Understanding
WHEN English cleric William Bedell went to Ireland in 1627, he found a very puzzling situation. Ireland, a predominantly Catholic country, was ruled by Protestant Britain. Protestant Reformers had already translated the Bible into local languages all over Europe. Yet no one seemed interested in translating it into Irish.

Bedell felt strongly that the Irish people “ought not to be neglected till they can learn English.” He set out to produce a Bible in the Irish language. But he met with bitter opposition, particularly from Protestant sources. Why was that?

OPPOSITION TO THE USE OF IRISH

William Bedell
Bedell made it his business to learn Irish himself. He encouraged students to use Irish when he became provost, or head, of Trinity College in Dublin and when he later became the bishop of Kilmore. As a matter of fact, when Queen Elizabeth I of England founded Trinity College, she did so to produce ministers who could teach her subjects the Bible’s message in their mother tongue. Bedell tried to make that happen.

In the Kilmore diocese, by far the majority of people spoke Irish. So Bedell insisted on having ministers who could speak Irish. He made his appeal in the spirit of the apostle Paul’s words at 1 Corinthians 14:19, which says: “In a congregation I would rather speak five words with my mind, that I might also instruct others, than ten thousand words in a tongue,” that is, in a language little understood.

But influential authority figures made every effort to stop him. According to historians, some asserted that the use of Irish was “dangerous to the State” and others suggested that it was “against the interests of the Government.” Some felt that it was in the interests of England to keep the Irish in ignorance. In fact, laws were enacted that required the Irish to abandon their own language and customs and to learn English and follow English ways and manners.

BEDELL’S BIBLE PROJECT

Bedell was not deterred by such dictatorial views. Early in the 1630’s, he started translating the recently published English-language Bible (the King James Version of 1611) into Irish. He wanted to produce a Bible that was understandable to as many people as possible. He felt strongly that the poor people could not search the Scriptures to find the way to everlasting life as long as the Bible remained a sealed book to them.—John 17:3.

Bedell was not the first to see this. Some 30 years earlier, another bishop, William Daniel, had seen how difficult it was for anyone to learn what the Bible taught when it came, as he put it, “in the cloud of an unknown tongue.” Daniel had translated the Christian Greek Scriptures into Irish. Bedell now took on the task of translating the Hebrew Scriptures. What is known as Bedell’s Bible includes both his work and William Daniel’s earlier work. As things turned out, Bedell’s Bible—the first complete Bible in Irish—was the only translation of the Bible into Irish for the next 300 years.

Bedell, a qualified Hebrew scholar, enlisted two native speakers of Irish to help with the translation from English into Irish. As they progressed with their work, Bedell, along with one or two trusted helpers, painstakingly checked and revised each verse. For reference, they consulted an Italian translation made by Swiss theologian Giovanni Diodati, as well as the Greek Septuagint and a precious old Hebrew Bible manuscript.

The team followed the lead of the translators of the King James Version (many of whom Bedell would have known personally) and included God’s personal name in a number of places in their Bible. For example, at Exodus 6:3, they rendered God’s name “Iehovah.” Bedell’s original manuscript is preserved in Marsh’s Library, Dublin, Ireland.—See the box “Bedell Remembered and Recognized.”

FINALLY PUBLISHED

Bedell completed his project about 1640. But he could not immediately publish it. Why? For one thing, he still faced unrelenting opposition. Detractors vilified Bedell’s chief translator, hoping thus to discredit his work. They even maliciously had him arrested and imprisoned. As if that were not enough, Bedell found himself in the middle of a bloody and bitter anti-English rebellion, which broke out in 1641. Local Irish people protected Bedell for a time despite his English origins because they recognized his genuine concern for them. Eventually, however, rebel soldiers imprisoned him in very poor conditions. No doubt this hastened his death in 1642. He never saw his work published.


Bedell’s work almost perished completely when his home was ransacked and destroyed. Thankfully a close friend managed to rescue all his translated documents. In time, Narcissus Marsh, who later became the archbishop of Armagh and the primate of the Church of Ireland, got hold of them. He received financial support from scientist Robert Boyle and courageously published Bedell’s Bible in 1685.

A SMALL YET SIGNIFICANT FORWARD STEP

Bedell’s Bible did not receive worldwide acclaim. Still, it was one small yet significant step toward better Bible understanding, especially for people who spoke Irish—not only in Ireland but also in Scotland and many other places. They could now satisfy their spiritual need as they read God’s Word in their mother tongue.—Matthew 5:3, 6.

“When we read Bedell’s Bible, we heard the words of the Bible in our mother tongue. This was a crucial key that opened the way for me and my family to learn the wonderful truths found in the Scriptures”
Bedell’s Bible has continued to help lovers of truth to do that right up to modern times. One speaker of Irish, who in relatively recent times learned what the Bible really teaches, says: “When we read Bedell’s Bible, we heard the words of the Bible in our mother tongue. This was a crucial key that opened the way for me and my family to learn the wonderful truths found in the Scriptures.”

Bedell Remembered and Recognized

For nearly 300 years after the publication of Bedell’s Bible in 1685, no other complete Bible in Irish was published. Then, in 1981, Catholic scholars produced the Maynooth Bible, a translation in modern Irish. In its foreword, the Maynooth Bible recognizes the “great achievement on the part of The Church of Ireland when they published their version of the Bible in the 17th century.” That, of course, was Bedell’s translation, although, in fact, until very recently the Catholic Church prohibited Catholics from reading the Bedell Bible.

The scholars who produced the Maynooth Bible published some of their preparatory work in 1971. One part of this was the Pentatúc (Pentateuch), the first five books of the Bible. In recognition of the pioneering work that Bedell had done, those Catholic scholars included the note “In memory of William Bedell” inside its cover page.
The translators of the Pentatúc used the Irish term “Iávé” for God’s name in many of the places where it appears in the Hebrew Scriptures, represented by the Tetragrammaton or YHWH. Examples can be found at Exodus 6:2-13. Sadly, when the complete Maynooth Bible was eventually published, the editors—unlike Bedell—decided to remove the divine name completely from their translation and substitute “an Tiarna” (the Lord) in its place.

A critique of reductionism

Rumors of Wars

Pentagon: China's man-made islands growing, now thousands of acres
Published August 22, 2015FoxNews.com



China has built up and reclaimed even more land in the South China Sea than previously thought -- with an archipelago of man-made islands now spanning 2,900 acres, according to a new Pentagon report released Friday.

The size of China's artificial island territory in the disputed waters represents a 50 percent jump over the most recent estimate of 2,000 acres. 

Since Chinese land reclamation efforts began in December 2013, the country has reclaimed land at seven of its eight Spratly Island outposts and, as of June 2015, had reclaimed more than 2,900 acres of land, according to the Asia-Pacific Maritime Security Strategy report released Friday.

Although land reclamation – the dredging of the sea floor material for use as land – is not new or even unique in the South China Sea, “China’s recent land reclamation campaign significantly outweighs other efforts in size, pace and nature,” the report states. By comparison, Vietnam has reclaimed a total of 80 acres and Taiwan has eight acres near the airstrip on its sole outpost on Aba Island. 

Before this year, defense officials thought Beijing had only reclaimed about 500 acres of landmass to build the artificial islands. However, the lands are now big enough for buildings and equipment. The Pentagon report warned the infrastructure would allow China to have a "more robust power projection" in the South China Sea. Citing China's own statements the outposts "will have a military component," the report also said China is completing the construction of an airstrip. 

The report said China may, then, be able to use the outposts as an alternative airstrip for "carrier-based aircraft," allowing China "to conduct sustained operations with aircraft carriers in the area."

The runway, though, is just part of China's unusual and alarming "land reclamation" project. Earlier this year, the U.S. military called the project "extensive," involving China "pumping sand on to live coral reefs" and then paving over them with concrete. 

The Defense Department warns the outposts can be used for surveillance systems, harbors and logistical support. A report earlier this year described how China has "excavated deep channels and built new berthing areas to allow access for larger ships to the outposts." 

U.S. officials fear the islands could be used for military purposes and may pose a threat to one of the world’s biggest commercial shipping routes as China claims land in what other countries see as international waters, according to The Wall Street Journal.

Defense officials also believe China’s assertiveness poses a risk of possible confrontation down the line with the U.S.

Friday’s report comes about a month before Chinese President Xi Jinping is scheduled to make a visit to Washington, where the South China Sea will be among the issues at hand. 

The U.S. has repeatedly questioned whether Beijing had ceased the land reclamation projects, as it claimed earlier this month. Chinese embassy spokesman Zhu Haiquan told The Wall Street Journal on Thursday the projects stopped in June and the facilities being built on the islands include those for public good.

“China stands ready to open these facilities to other countries upon completion,” Zhu said. “We hope the U.S. side will view this in an objective and balanced way and respect regional countries’ efforts to maintain the peace and stability of the South China Sea.”

China has also increased patrols on the disputed areas to “increase its effective control” over the islands, according to the report. 

The latest moves from China have some U.S. military officials pushing the Pentagon to be more aggressive in countering China in the region. They’ve wanted more assertive maritime and air patrols to fly within the 12 nautical mile territorial limit of some of the disputed lands China claims, according to The Wall Street Journal.

On Thursday, Secretary of Defense Ash Carter said the military would go where and when it wanted, but it remained unclear whether they’ve flown within the 12 nautical mile zone of the islands.

Tuesday, 25 August 2015

File under "Well said" V

"Then said I, Wisdom is better than strength: nevertheless the poor man's wisdom is despised, and his words are not heard."
Ecclesiastes 9:16KJV

On the Challenge of protecting our children.

The pedophile next door
CNN Staff
Updated 2232 GMT (0532 HKT) August 21, 2015 

(CNN)As a child of divorce, Katie Griffin seemed to be adjusting well to weekdays with her mom and weekends with her dad.

When Katie stopped wanting to visit her dad a few years later, her parents attributed it to early adolescence, and to Katie wanting to do her own thing.

Then, one evening, Katie's mother, Janet Griffin, received an upsetting phone call from her daughter.

Bruce Sawhill, 63
Wanted for sodomy
Last seen in 2001 in Missouri
Previously served three years in prison in 1988 for statutory sodomy
May have found work in Oregon or Washington in 2004 or 2005

"I don't know why, but I just knew," Janet told CNN's "The Hunt with John Walsh." "...And she said it was Bruce. She said, 'He's been touching me and making me touch him and I just can't go there anymore.'"

"Bruce" was Bruce Sawhill. Sawhill had been close friends with Katie's father, Ken Griffin, since high school. When Sawhill got married to his wife, Keni Jo, the new couple decided to move in a mile down the road from Ken. On occasion, Ken had allowed Bruce and Keni Jo to babysit Katie. Now, Ken raced over to his "friend's" home in a blind fury.

"I just decked him," Ken Griffin said.

How could Sawhill do the unthinkable to his good friend's daughter?

'It's always the most charming guy'
The Griffins contacted the sheriff's office and filed a report. When investigators ran a record check on Sawhill, they made a shocking discovery: Sawhill was a registered sex offender.

"It's hard to describe that kind of betrayal," Ken Griffin said.

The Griffins had always known that Sawhill had a record, but he had claimed he was busted for growing marijuana. Now they discovered that was a cover story; he had actually been convicted in St. Louis County for the sexual abuse of a 13-year-old. The official charge was sodomy.

"It's always the most charming guy," Walsh said of Sawhill, who was released on parole in 1992. "...It's always the guy that everybody loves that hides that one big dangerous, dark secret."

Sawhill was arrested again on September 25, 2001, for the abuse of Katie Griffin, and charged with two counts of sodomy in the first degree. He was released one month later on a $50,000 bond. A trial date was eventually set for October 29, 2002.

Katie overcame her fears, and decided she wanted to testify against Sawhill in court. She wanted to let everyone know what Sawhill had done to her.

"She was so worried that he may do it to another child," Janet Griffin said.

But when trial day arrived, there was no sign of Sawhill -- or his wife. They've been on the run ever since.

Numbing the pain of trauma
Katie was so distraught when Sawhill fled that her parents decided a change in scenery might help.

She agreed to go to stay with her older half-sister, Pam Hansen, who lived in Colorado. There she began seemingly adjusting to a new life, going to school and making friends right away, according to her family.



But, a year later, she was dead. Her sister found her in the basement; she had apparently suffocated while inhaling spraypaint fumes -- a cheap high known as "huffing." She was just 12 years old.

"I think [Sawhill] set into motion [the] events that led up to Katie's death. I have no doubt in my mind about that," Ken Griffin said.

"I blame Bruce for taking her innocence away, for making her grow up faster than she had to -- just not letting her be a little girl," Hansen said.

Have you seen Bruce Sawhill?
Bruce Sawhill wears a set of upper dentures. He has a distinctive loud laugh, and likes to laugh at his own jokes. He enjoys casual drinking and is known to be very sociable in bars. He has grown marijuana in the past and could be working on a marijuana farm. He's also a skilled drywall installer, plasterer and painter. It is believed he's still with Keni Jo.


If you've seen Bruce Sawhill or have any information as to his whereabouts please make the call. 1-866-THE-HUNT or go online to CNN.com/TheHunt. We'll pass your tip on to the proper authorities and if requested will not reveal your name.

A hostile takeover? II:Lamarck's revenge.

Epigenetic Change: Lamarck, Wake Up, You're Wanted in the Conference Room!
Denyse O'Leary August 25, 2015 3:58 AM


If we wish to hear what the fossils are telling us, we must find out how they came to be what they were (and how their descendants came to be what they are today). For generations, scientists have looked to Darwinian evolution (natural selection acting on random mutations) almost exclusively to account for all that. Questions were considered settled if a Darwinian account could be provided.

Talk to the Fossils.jpgThat was not because any law of nature shows that Darwinism must be the correct explanation. Rather because, as Richard Dawkins put it, "Darwinism is the only known theory that is in principle capable of explaining certain aspects of life" (p. 287, Blind Watchmaker, 1986).

But when we looked at horizontal gene transfer (HGT), we found that Dawkins' claim is incorrect.

To recap, Darwinism entails vertical transfer of genes from a common ancestor to descendants. Horizontal gene transfer means transfer of genes from one organism to another on contact, irrespective of the ancestry of either life form. HGT is a form of evolution, yes. But it drastically weakens the status of Darwinism as the "only known theory." Any Darwinian claim about evolution must first rule out HGT as a possible explanation. And, as we shall shortly see, it must rule out epigenetics as well.

Why does this historic shift in the burden of proof receive comparatively little attention? Probably it's due to the overwhelming acceptance of Darwinism as a cultural metaphor and philosophy of life. One thinks, for example, of Amazon citing "purposeful Darwinism" and taking Darwinian Theory to the max as a defense against a recent exposé of the firm's labor conditions. The concepts Amazon advances are scientifically meaningless but culturally meaningful. And culture drowns out science.

Thus, when talking to fossils (or current living forms), our challenge is to listen to what they have to say, not what the Darwinian interpreters of the fossils (and of almost everything else) have to say.

Which brings us to epigenetics. Jean-Baptiste Lamarck (1744-1829) was an early evolutionist who proposed that life forms could acquire information from their environment and pass it on in their genes. He was dismissed, when not ridiculed, by Darwinists for many decades (though not, as it happens, by Darwin). But the basic thrust of his idea has recently resurfaced in epigenetics.

There is an irony in the way the resurgence came about. A key science achievement of the 1990s was the mapping of the human genome. Those were the days when Nobelist Walter Gilbert, extolling the Human Genome Project, would hold up a data CD and inform his audience, "Here is a human being; it's me!"

But what if it isn't? What if it is just a CD containing important information about Gilbert but by no means the whole story? What if the rest of the story is created in the continuous stream of life? Scientists are just now beginning to learn about the hitherto unrecognized "second genetic code," the epigenome, which greatly increases both the complexity and the uniqueness of the information in living systems.

Epigenetics is the study of the systems and processes by which genes' expression can be altered, not randomly as in Darwinism, but by specific, predictable, repeatable, and researchable events -- and then inherited in the altered state. Research has shown methylation to be a key mechanism. It is described thus:

Not all genes are active at all times. DNA methylation is one of several epigenetic mechanisms that cells use to control gene expression.... a common epigenetic signaling tool that cells use to lock genes in the "off" position. In recent decades, researchers have learned a great deal about DNA methylation, including how it occurs and where it occurs, and they have also discovered that methylation is an important component in numerous cellular processes, including embryonic development, genomic imprinting, X-chromosome inactivation, and preservation of chromosome stability.
Epigenetic changes like methylation do not change a cell's DNA, but they do change how the DNA functions. In rodent studies, for example, stress can trigger a series of chemical reactions that dictate how active some genes will be in passing on the effects of parental stress.

Such inheritance of acquired traits is gradually gaining acceptance in academic science, but we are still in an early stage of understanding the mechanisms. Or, as one researcher put it, "... we're all having a hell of a time figuring out how they work." And another: "Although many are scratching their heads over the holes in the proposed mechanism, few are suggesting that the underlying phenomenon is a fairy tale."

Most genes, it turns out, are not so much selfish as willing to hang out with the wrong crowd and learn bad habits. You'd think so, to read this in a special issue of Science:

The molecular legacy extends beyond gene transfer to include mitochondria and epigenetics (Lane et al., p. 756). Finally, the gestation and birthing processes also shape offspring, and preterm birth is now a focus of research (Romero et al., p. 760).
Here are some other findings that give some sense of the scope of the changes epigenetics brings to our understanding of the history of life:

-- Bacteria rewrite their DNA epigenetically. Carl Zimmer notes in Quanta:

For students of the history of biology, this kind of heredity echoes a largely discredited theory promoted by the naturalist Jean-Baptiste Lamarck in the early 19th century. Lamarck argued for the inheritance of acquired traits. ... The advent of genetics seemed to crush this idea. There didn't appear to be any way for experiences to alter the genes that organisms passed down to their offspring. But CRISPR revealed that microbes rewrite their DNA with information about their enemies -- information that Barrangou showed could make the difference between life and death for their descendants.
New analysis techniques will help define the role that bacterial epigenetics plays in creating antibiotic resistance.

-- Lab research show how it works in animals. It's not just the womb environment because the male parent's contribution, via alterations in sperm, is substantial. From Nature:

Male rats fed a high-fat diet, for example, beget daughters with abnormal DNA methylation in the pancreas. Male mice fed a low-protein diet have offspring with altered liver expression of cholesterol genes. And male mice with pre-diabetes have abnormal sperm methylation, and pass on an increased risk of diabetes to the next two generations.
Epigenetic stress effects found in rats can last for generations. Similarly, in a recent mouse study, reported in Nature, sperm RNA showed heritable signs of trauma for two more generations. And starved mice produced pups whose offspring risked diabetes. In another mouse study, it was found that "Without any change to DNA at all, methyl groups could be added or subtracted, and the changes were inherited much like a mutation in a gene."

-- Epigenetics can influence animal behavior in later generations as well. "Transgenerational epigenetic inheritance is not a solved field -- it's very much in flux," one researcher admits, but it seems that epigenetic memory of experienced stress can cross generations and travel from cell to cell during early development: "It does not change the sequence of genes but rather how the DNA is packaged and how genes are expressed." Recent rodent studies suggest that "an animal parent's exposure to drugs, alcohol, and stress can alter brain development and behavior in their offspring."

For example, from one study on how mice can inherit fear of a smell from their male parent, we learn:

Somehow, the information about the frightening smell gets into a mouse's testes and results in lower methylation of the Olfr151 gene in sperm DNA. The researchers even ran experiments using in vitro fertilization to make sure that the father was not in some way passing on a fear of acetophenone through interactions with the mother. The epigenetic tweak in the sperm is perpetuated in the offspring's DNA, leading to increased expression of the receptor in the animals' noses and, ultimately, enhanced sensitivity to the smell.
Much more work remains, of course, and this finding was questioned, as "too good to be true." But the authors pointed out that they had not cherry picked the data; they had included in the supplemental materials experiments that did not yield statistically significant results.

If The Scientist isn't hanging the epigenetics study authors out to dry, it's most likely because the editors think there is something to be said for their model. It may help resolve longstanding questions, for example, about how animals appear to "know" things they did not learn by experience. To say that their knowledge is an "instinct" just means we don't know how they know. Epigenetic studies, by contrast, may identify a specific mechanism by which the information is transmitted.

-- Epigenetics may influence human health too. It's fine to inherit "good genes" (we heard plenty about that from the eugenicists for over a century!). But what if a package of "good genes" gets damaged in transit and arrives that way? Genes can be inherited in an awakened state, and may influence metabolism, behavior, and proneness to disease, including heart disease and diabetes. From one researcher:

According to Ishii, the take-home message is this: "I hope that people understand that various stresses can change gene expression without DNA sequence change." He says the youngest among us -- developing embryos and infants -- may be especially sensitive to that kind of stress-induced epigenetic change and "we should be more careful about stresses on them."
In another study, traumatized pregnant women who had been near 9-11 not only had significantly lower cortisol levels in their saliva but so did their children, measured after birth. Researchers noted that the effect was most obvious when the exposed children were in the third trimester. Subsequent studies on stressed rats identified differences in DNA methylation, the way that DNA is chemically modified.

Similarly, Project Ice Storm found "a distinctive 'signature' in the DNA of children born in the aftermath of the massive Quebec ice storm" (1998):

Thirteen years later, the researchers found that DNA within the T cells -- a type of immune system cell -- of 36 children showed distinctive patterns in DNA methylation. The researchers concluded for the first time that maternal hardship, predicted the degree of methylation of DNA in the T cells. The "epigenetic" signature plays a role in the way the genes express themselves. This study is also the first to show that it is the objective stress exposure (such as days without electricity) and not the degree of emotional distress in pregnant women that causes long lasting changes in the epigenome of their babies.
It's early days yet, but there is also some evidence that parents' poverty can promote children's obesity. Privation may reprogram DNA in the womb to turn certain genes involving appetite up or down. "Whenever you find food, eat all you can," perhaps? This may continue into adulthood, when no shortage actually exists. As one researcher explains, "If genetics is the alphabet, epigenetics is the spelling that guides the activity of our cells."

So the role epigenetics may play in obesity generally, some immunities, chronic diseases, and even cancer is now actively studied. With respect to cancer, some researchers have found that epigenetic regulation is required to ensure the correct number of chromosomes in daughter cells after division, and "tumor cells frequently have either too few or too many chromosomes, leading to the incorrect expression of a number of genes."

Many of these findings may need modification or replacement, but we can no longer rule out the possibility that modifications in great-grandparents' diet or environment affect later generations' health or life span. These changes are not Darwinian genetic inheritance; the parent did not have a randomly mutated "gene" for, say, obesity, but rather an experience (chronic hunger, perhaps) that altered the way genes controlling appetite are expressed. The alterations are passed on, at least for a generation or so. Thus, epigenetics is not to be confused with genetic or any other kind of determinism; it is not a prophecy, merely a tool for assessing sources of risk.

-- Can epigenetics influence human behavior as well as human health? Possibly; for example, early abuse can change gene expression in children:

The researchers found an association between the kind of parenting children had and a particular gene (called the glucocorticoid receptor gene) that's responsible for crucial aspects of social functioning and health.
If such findings hold up, they may shed light on "broken adoptions," where rescued children continue to behave as if they were living in a low trust/high threat environment. In any event, "born bad" just doesn't cut it any more, by way of explanation. If epigenetics provides valid insights, we can at least hope for more realistic rehabilitation strategies.

As epigenetics slowly achieves acceptance in science culture, medical genomicist Stephan Beck thinks that epigenomic epidemiology is "at the same stage genomic epidemiology was at eight years ago, when most studies were small and rarely identified the same genetic variants for any one disease." The workshop material for a conference in Sweden in March 2015, "Epigenetics as the Meeting Point Between Nature and Nurture," offers a challenge, "There are obstacles in terms of a suspicion of biological explanations among some scholars and simplifications of social and philosophical problems among some scientists. The two cultures must be bridged and the bridge, we suggest, is epigenetics."

Yes indeed. Consider the controversial revisit of Darwinian race theory in science writer Nicholas Wade's recent book, Troublesome Inheritance. Epigenetics makes such theories irrelevant as well as divisive. The question isn't whether certain characteristics show up more often in one group than another, but what is the mechanism? As Michael Behe would say, how exactly?

Epigenetics should lead to revisions in textbooks, some European researchers say, perhaps unaware of the Darwin followers camped outside the offices of education authorities, protecting their tax-funded domain. That said, epigenetics coverage did increase in the most recent edition of Darwinian evolutionist Ken Miller's popular university text. The book now features a definition of epigenetics, cross-referenced to a paragraph on the subject.

Some, nonetheless, stand athwart epigenetics and yell STOP!! It is, after all, very new and is not settling in with ease. A "key concept" quote from The Scientist reads: "The concept of cellular memory passed onto offspring may not be as crazy as it appears." There is nothing crazy about epigenetics, unless one is committed to genetic fatalism, featuring the "fat gene," the "gay gene," the "infidelity gene," the "violence gene," etc., that supposedly "make" people do things.

"End the Hype over Epigenetics & Lamarckian Evolution," Real Clear Science demands, noting that "mammals are completely different beasts" from worms and plants, where epigenetic inheritance has been demonstrated:

Therefore, be very skeptical of studies which claim to have detected health effects due to epigenetic inheritance. The hype may soon fade, and the concept of Lamarckian evolution may once again return to the grave.
A philosophy may underlie this outburst, if we go by the article in Cell referenced at RCS: "Since the human genome was sequenced, the term 'epigenetics' is increasingly being associated with the hope that we are more than just the sum of our genes."

It's not a "hope," it's a fact. And the accusation of "hype" sounds odd, considering the widespread Darwinian hype about all things gene, attributing to "genes" every phenomenon from bad driving to wonder at the universe.

Real Clear Science goes on to worry that the epigenome oppresses women:

Epigenetics is the next big field that the media, fearmongers, and political hacks will attempt to exploit. ... The authors worry, perhaps rightly so, that the media hype surrounding epigenetics will once again turn its focus on mothers. Will the government once again regulate what pregnant women can eat, drink, and do? And if so, why not regulate the behavior of men, as well? Epigenetics, after all, can affect sperm quality.
The authors referred to had published an op-ed in Nature which advises, "Society: Don't blame the mothers - Careless discussion of epigenetic research on how early life affects health across generations could harm women." That's an odd concern, as most mothers would gladly avoid passing on a chronic disorder, if they had the correct information. And epigenetics is principally about establishing the correct information.

Meanwhile, the onetime chief lobbyist for Darwin in American schools has been heard to say:

It was almost a relief when an antievolutionist contended that the books should be rejected because they don't include epigenetics. At least the epigenetics argument is relatively recent (perhaps only 5-8 years old). In creation-think, including epigenetics in biology textbooks will weaken evolution because epigenetics is evidence against evolution.
Note the curious term "the epigenetics argument," as if everyone agrees that epigenetics' only potential is as a political strategy.

But life goes on... Some quibble over whether epigenetics is truly "Lamarckian." Quibbles aside, ours is not the world of the "This Is You" CD.1 Some acknowledged experts even say, "Epigenetics can drive genetics" and that it "appears to be one of the main drivers of intergenerational changes, not simply a passive component." Meanwhile, epigenomics is making its debut, courtesy a decade's worth of data analysis program development.

So, far from heading to the grave, epigenetics has invested in bigger equipment.

Many epigenetics findings, like many findings in horizontal gene transfer may be revised or replaced, but the direction is not likely to change. So how does epigenetics feature in evolution? There are two opinions about that. The epigenome is said to evolve faster than the genome, but most of its changes don't last for more than a few generations. Perhaps that is because they are overridden by further changes due to new conditions: In a pioneer study, researchers concluded that "epigenetic changes are many orders of magnitude more frequent than conventional DNA mutations, but also often short lived."

Yet epigenomic diversity, according to other research, allows plants to adapt to adapt to a variety of environments worldwide. Changes in plant habitats may massively impact animal evolution. So it may come down to a question of what kind of change we are looking for. What counts as a change?

To the extent that epigenetics casts doubt on simplistic Darwinian or other schemes of evolution, its main role may be that of "spoiler." For example, recently, Swedish researchers found that epigenetics, not Darwinian evolution, is the cause of wide variation in domestic chicken types. They say their findings explicitly disagree with "[t]he traditional Darwinian explanation," which is interesting in view of the fact that Darwin's own pigeon breeding is often used as a way of introducing his theory to the public.

So what can we now say about evolution, the history of life?: Provided we are not looking for miraculous transformations, we have indeed seen some evolution. We have seen that life forms can progress toward the same target without common ancestry (convergent evolution). Sharing genes (horizontal gene transfer) can result in new features in a life form. Epigenetics can result in offspring inheriting features from their parents that were created in their parents' own lifetime, rather than inherited from a previous common ancestor.

But another possibility arises as well: Can a life form evolve by losing instead of gaining features (devolution)? We shall see.

Notes:

(1) Quoted in Dorothy Nelkin, "Less Selfish than Sacred? Genes and the Religious Impulse in Evolutionary Psychology," in Hilary Rose and Steven Rose, eds., Alas, Poor Darwin: Arguments Against Evolutionary Psychology (London: Random House, Vintage, 2001), p. 18.


See the rest of the series to date at "Talk to the Fossils: Let's See What They Say Back."

The book of Haggai Young's Literal Translation

Haggai 1Young's Literal Translation (YLT)

In the second year of Darius the king, in the sixth month, in the first day of the month, hath a word of Jehovah been by the hand of Haggai the prophet, unto Zerubbabel son of Shealtiel, governor of Judah, and unto Joshua son of Josedech, the high priest, saying:
2 Thus spake Jehovah of Hosts, saying: This people! -- they have said, `The time hath not come, The time the house of Jehovah [is] to be built.'
3 And there is a word of Jehovah by the hand of Haggai the prophet, saying:
4 Is it time for you -- you! To dwell in your covered houses, And this house to lie waste?
5 And now, thus said Jehovah of Hosts, Set your heart to your ways.
6 Ye have sown much, and brought in little, To eat, and not to satiety, To drink, and not to drunkenness, To clothe, and none hath heat, And he who is hiring himself out, Is hiring himself for a bag pierced through.
7 Thus said Jehovah of Hosts: Set your heart to your ways.
8 Go up the mountain, and ye have brought in wood, And build the house, and I am pleased with it. And I am honoured, said Jehovah.
9 Looking for much, and lo, little, And ye brought [it] home, and I blew on it, Wherefore? -- an affirmation of Jehovah of Hosts, Because of My house that is waste, And ye are running -- each to his house,
10 Therefore, over you refrained have the heavens from dew, And the land hath refrained its increase.
11 And I proclaim draught on the land, And on the mountains, and on the corn, And on the new wine, and on the oil, And on what the ground doth bring forth, And on man, and on beast, And on all labour of the hands.'
12 And Zerubbabel son of Shealtiel, and Joshua son of Josedech, the high priest, and all the remnant of the people, do hearken to the voice of Jehovah their God, and unto the words of Haggai the prophet, as Jehovah their God had sent him, and the people are afraid of the face of Jehovah.
13 And Haggai, messenger of Jehovah, in messages of Jehovah, speaketh to the people, saying: `I [am] with you, an affirmation of Jehovah.'
14 And Jehovah doth stir up the spirit of Zerubbabel son of Shealtiel, governor of Judah, and the spirit of Joshua son of Josedech, the high priest, and the spirit of all the remnant of the people, and they come in, and do work in the house of Jehovah of Hosts their God,
15 in the twenty and fourth day of the sixth month, in the second year of Darius the king.

Young's Literal Translation (YLT)

Haggai 2Young's Literal Translation (YLT)

In the seventh [month], in the twenty and first of the month, hath a word of Jehovah been by the hand of Haggai the prophet, saying:
2 `Speak, I pray thee, unto Zerubbabel son of Shealtiel, governor of Judah, and unto Joshua, son of Josedech, the high priest, and unto the remnant of the people, saying:
3 Who among you hath been left that saw this house in its former honour? And what are ye seeing it now? Is it not, compared with it, as nothing in your eyes?
4 And now, be strong, O Zerubbabel, An affirmation of Jehovah, And be strong, O Joshua, son of Josedech, the high priest, And be strong, all ye people of the land, An affirmation of Jehovah, And do ye -- (for I [am] with you, An affirmation of Jehovah of Hosts) --
5 The thing that I covenanted with you, In your coming forth from Egypt, And My Spirit is remaining in your midst, fear not.
6 For thus said Jehovah of Hosts: Yet once more -- it [is] a little, And I am shaking the heavens and the earth, And the sea, and the dry land,
7 And I have shaken all the nations, And they have come [to] the desire of all the nations, And I have filled this house [with] honour, Said Jehovah of Hosts.
8 Mine [is] the silver, and Mine the gold, An affirmation of Jehovah of Hosts.
9 Greater is the honour of this latter house, Than of the former, said Jehovah of Hosts, And in this place do I give peace, An affirmation of Jehovah of Hosts.'
10 On the twenty and fourth of the ninth [month], in the second year of Darius, hath a word of Jehovah been by the hand of Haggai the prophet, saying:
11 Thus said Jehovah of Hosts: `Ask, I pray thee, the priests [of] the law, saying:
12 Lo, one doth carry holy flesh in the skirt of his garment, and he hath come with his skirt against the bread, or against the pottage, or against the wine, or against the oil, or against any food -- is it holy?' And the priests answer and say, `No.'
13 And Haggai saith, `If the unclean of body doth come against any of these, is it unclean?' And the priests answer and say, `It is unclean.'
14 And Haggai answereth and saith, `So [is] this people, and so [is] this nation before Me -- an affirmation of Jehovah -- and so [is] every work of their hands, and that which they bring near there -- it is unclean.
15 And now, lay [it], I pray you, to your heart, From this day, and onwards, Before the laying of stone to stone in the temple of Jehovah.
16 From that time [one] hath come to a heap of twenty, And it hath been ten, He hath come unto the wine-fat to draw out fifty purahs, And it hath been twenty.
17 I have smitten you with blasting, And with mildew, and with hail -- All the work of your hands, And there is none of you with Me, An affirmation of Jehovah.
18 Set [it], I pray you, to your heart, from this day and onwards, from the twenty and fourth day of the ninth [month], even from the day that the temple of Jehovah hath been founded, set [it] to your heart.
19 Is the seed yet in the barn? And hitherto the vine and the fig, And the pomegranate, and the olive-tree, Have not borne -- from this day I bless.'
20 And there is a word of Jehovah a second time unto Haggai, on the twenty and fourth of the month, saying:
21 `Speak unto Zerubbabel governor of Judah, saying: I am shaking the heavens and the earth,
22 And have overturned the throne of kingdoms, And I have destroyed the strength of kingdoms of the nations, And overturned chariot and its charioteers, And come down have horses and their riders, Each by the sword of his brother.
23 In that day -- an affirmation of Jehovah of Hosts, I take thee, Zerubbabel, son of Shealtiel, My servant -- an affirmation of Jehovah, And have set thee as a signet, for on thee I have fixed, An affirmation of Jehovah of Hosts!

Young's Literal Translation (YLT)

Monday, 24 August 2015

Darwinism vs the real world VII

Understanding Cardiovascular Function: Real Numbers and Valvular Heart Disease
Howard Glicksman August 23, 2015 5:54 AM


Editor's note: Physicians have a special place among the thinkers who have elaborated the argument for intelligent design. Perhaps that's because, more than evolutionary biologists, they are familiar with the challenges of maintaining a functioning complex system, the human body. With that in mind, Evolution News & Views is delighted to present this series, "The Designed Body." Dr. Glicksman practices palliative medicine for a hospice organization.


Unlike the brain, the liver, and the kidneys, the heart has only one job to do. But oh, what a job! It is responsible for pumping the blood, which contains everything the cells need to live, to organs like the brain, the liver, and the kidneys.

the-designed-body4.jpgBut as with any job, there are certain parameters that define how well it is being done. A car's job is to overcome the laws of nature to transport its driver from point A to point B in a certain amount of time. If it can't do its job properly, it is likely due to problems like inadequate gas flow into the engine or poor cylinder compression. So too, there are certain parameters that must be met for the heart to do its job -- otherwise, due to the laws of nature, the body won't be able to function properly or may even die.

My last article in this series showed that since the heart is a muscle, it needs its own blood supply, which is provided by the coronary arteries. However, the laws of nature demand that the coronary arteries be wide enough to accommodate enough blood flow. A person with coronary artery disease has narrowing of the blood vessels and reduced blood flow to one or more regions of the myocardium.

Clinical experience tells us that people with this condition are not able to be as active as our earliest ancestors would have to have been to survive. When evolutionary biologists expound on how human life came into being, they must not only talk about how the heart looks, but also how it must work within the laws of nature to do its job properly. For, as important as having adequate and properly controlled coronary blood flow is for survival, so too is having proper valve function.

The heart is a muscular pump that is divided into a right and left side by a wall called the septum. The right side pumps blood to the lungs and the left side pumps blood to the rest of the body. Each side of the heart consists of a thin-walled upper chamber, called the atrium, and a more muscular lower chamber, called the ventricle.

There are "V" shaped, one-way valves that point in the direction of blood flow between the atria and the ventricles, and the ventricles and their outflow tracts. When the valves open, they direct blood forward to where it is supposed to go and when they close, they prevent blood from going backward to where it is not supposed to go. The triscuspid valve is located between the right atrium and ventricle and the pulmonary valve is located between the right ventricle and the main pulmonary artery. The mitral valve is located between the left atrium and ventricle and the aortic valve is located between the left ventricle and the aorta.

But how do the valves know when to open and close? Just as blood, because it is matter and has mass, must follow the laws of nature by being pumped throughout the body by the heart, so too, whether the heart valves stay open or closed is also a function of those same laws.

Imagine you are trying to get into a saloon through its swinging door. A heavily muscled bouncer is blocking you from the other side. What must you do to get inside? Pressure is defined as "the force per unit area applied in a direction perpendicular to the surface of an object". To get into the saloon, you must apply more pressure to your side of the swinging door than the bouncer can apply to his.

When it comes to the heart and how its valves work within the laws of nature, it is important to remember that those laws state that the pressure inside a chamber with a given amount of fluid is inversely related to the size of the chamber. This means that with a given amount of blood inside an atrium or a ventricle, if its volume decreases, the pressure within it increases, and if its volume increases, the pressure within it decreases. Also, just like in meteorology, where air always moves from an area of higher to lower pressure, so too, when a pathway is available, blood always moves from an area of higher to lower pressure.

In the left side of the heart, at the beginning of systole, when the ventricle begins to contract, the pressure within it quickly rises above that of the left atrium, causing the mitral valve to close. This prevents blood from flowing back into the atrium. As systole continues, and contraction of the left ventricle peaks, the pressure within it rises above that of the aorta and forces the aortic valve to open. This allows blood from the left ventricle to flow out of the heart into the systemic circulation.

Then, as blood leaves the left ventricle and it begins to relax, the pressure within it quickly drops below that of the aorta, making the aortic valve snap shut to prevent blood from going back into the heart. Early in diastole, as the left ventricle relaxes further and venous blood from the lungs returns to the left atrium, the mitral valve opens because the pressure within the left atrium rises above that of the left ventricle.

Throughout diastole, the blood returning to the left side of the heart through the pulmonary veins enters the left ventricle through the left atrium by way of the open mitral valve. The same process takes place in the right side of the heart for the tricuspid and pulmonary valves as well. With diastole ending and systole beginning, the cardiac cycle starts over again and the heart valves open and close as dictated by the laws of nature.

Just as a clogged fuel line can reduce the flow of gas and compromise engine function, resulting in loss of power to a car, so too, diminished blood flow through any of the heart valves can compromise cardiac output resulting in loss of power to the body. In addition, just as leaky valves in one or more cylinders of a car engine can cause poor compression and loss of power, so too, leaky heart valves that allow blood to go back in the wrong direction, can reduce the efficiency of cardiac function and result in loss of power to the body.

If our earliest ancestors had any of these heart valve defects they never could have survived to reproduce. How do we know this? Valvular Heart Disease.

Just like the guy-wires used to stabilize a tent, or the mast of a ship, the mitral valve is attached to muscles anchored in the ventricle to strengthen it. However, degeneration of the valve or ischemic injury to its supporting muscles can weaken it and when the left ventricle contracts, instead of all of the blood going through the aortic valve into the aorta, some of it goes through the mitral valve back into the left atrium. This is called mitral regurgitation, and it reduces cardiac efficiency and output, particularly during exercise, because only some of the blood goes where it is supposed to go. Most people with this condition have fatigue, lack of energy and shortness of breath with limited exertion.

Anyone who has tried to blow up a balloon can appreciate the effect of obstruction to flow and the kind of force needed to overcome it. The aortic valve area is normally 3-4 cm2. When degeneration, thickening, and hardening of the valve occurs, this causes its opening to narrow resulting in aortic stenosis.

The smaller the opening, the harder the left ventricle has to work to pump blood into the systemic circulation. An area of 1-1.5 cm2 is considered moderate, and less than 1 cm2, severe, aortic stenosis. Since blood flow to the systemic circulation is compromised, people who have this condition are prone to angina, dizziness and syncope (passing out), weakness, and shortness of breath, often with very limited activity.

It is important to keep in mind that in addition to mitral regurgitation and aortic stenosis, other less common valve problems, like mitral stenosis and aortic and tricuspid regurgitation, can occur. In fact, it is not unusual for one or more of these valve disorders to be present together.

In my last two articles we looked at how, when it comes to coronary blood flow and heart valve function, real numbers can lead to debility. But there are two more components of cardiac function that still need to be considered when trying to explain how our ancient ancestors had the ability to survive within the laws of nature: heart muscle contractility and the heart's electrical system.


Keep in mind that in real life, it is not unusual for the heart to suffer from a defect involving all four of these factors, which together would have made survival impossible for our earliest ancestors.

Yet more on life's antidarwinian bias I

The Octopus Genome: Not "Alien" but Still a Big Problem for Darwinism
Casey Luskin August 24, 2015 3:39 AM

These days, new genomes of different types of organisms are being sequenced and published on a regular basis. When some new genome is sequenced, evolutionary biologists expect that it will be highly similar to the genomes of other organisms that are assumed to be closely related.

As ENV already noted, the latest organism to have its genome sequenced has confounded that expectation: the octopus, whose genome was recently reported in Nature. It turns out to be so unlike other mollusks and other invertebrates that it's being called "alien" by the scientists who worked on that project.

One article on the subject was titled "Don't freak out, but scientists think octopuses 'might be aliens' after DNA study":

Not to send you into a meltdown or anything but octopuses are basically 'aliens' -- according to scientists.
Researchers have found a new map of the octopus genetic code that is so strange that it could be actually be an "alien".

[...]

"The octopus appears to be utterly different from all other animals, even other molluscs, with its eight prehensile arms, its large brain and its clever problem-solving abilities," said US researcher Dr Clifton Ragsdale, from the University of Chicago.

[...]

Analysis of 12 different tissues revealed hundreds of octopus-specific genes found in no other animal, many of them highly active in structures such as the brain, skin and suckers.

Obviously no one thinks the octopus is an "alien" from another planet. (Nature News quotes one co-author of the paper on the genome noting that the alien quip is a "joke.") But it certainly is alien to standard evolutionary expectations that genomes of related species ought to be highly similar. Thus, Nature points out the large number of unique genes found in the octopus genome:
Surprisingly, the octopus genome turned out to be almost as large as a human's and to contain a greater number of protein-coding genes -- some 33,000, compared with fewer than 25,000 in Homo sapiens.
This excess results mostly from the expansion of a few specific gene families, Ragsdale says. One of the most remarkable gene groups is the protocadherins, which regulate the development of neurons and the short-range interactions between them. The octopus has 168 of these genes -- more than twice as many as mammals. This resonates with the creature's unusually large brain and the organ's even-stranger anatomy. ...

A gene family that is involved in development, the zinc-finger transcription factors, is also highly expanded in octopuses. At around 1,800 genes, it is the second-largest gene family to be discovered in an animal, after the elephant's 2,000 olfactory-receptor genes.

The analysis also turned up hundreds of other genes that are specific to the octopus and highly expressed in particular tissues. The suckers, for example, express a curious set of genes that are similar to those that encode receptors for the neurotransmitter acetylcholine. The genes seem to enable the octopus's remarkable ability to taste with its suckers.

Scientists identified six genes for proteins called reflectins, which are expressed in an octopus's skin. These alter the way light reflects from the octopus, giving the appearance of a different colour -- one of several ways that an octopus can disguise itself, along with changing its texture, pattern or brightness.

The technical paper explains that the octopus genome reveals "massive expansions in two gene families previously thought to be uniquely enlarged in vertebrates: the protocadherins, which regulate neuronal development, and the C2H2 superfamily of zinc-finger transcription factors." Moreover:
We identified hundreds of cephalopod-specific genes, many of which showed elevated expression levels in such specialized structures as the skin, the suckers and the nervous system.
They conclude: "Our analysis suggests that substantial expansion of a handful of gene families, along with extensive remodelling of genome linkage and repetitive content, played a critical role in the evolution of cephalopod morphological innovations, including their large and complex nervous systems." In other words, the cephalopod genome is unusual in many major respects, unlike other organisms we've sequenced.
Actually, that's not completely correct. There are some peculiar similarities between the cephalopod genome and something else they've seen -- but they aren't the kind of similarities that were predicted by common descent. The technical papers notes that the cephalopod genome bears unexpected resemblance in certain respects to vertebrate genomes -- and since these similarities aren't predicted by common descent, they predictably attribute it to convergent evolution:

the independent expansions and nervous system enrichment of protocadherins in coleoid cephalopods and vertebrates offers a striking example of convergent evolution between these clades at the molecular level.
Indeed, even within cephalopods they found evidence of convergent evolution (i.e., genetic similarity that didn't fit the expectations of common descent): "Surprisingly, our phylogenetic analyses suggest that the squid and octopus protocadherin arrays arose independently. Unlinked octopus protocadherins appear to have expanded ~135 Mya, after octopuses diverged from squid."
But the big story here is the large number of unique genes found in the octopus genome. The technical paper elaborates on one of these major gene groups:

The octopus genome encodes 168 multi-exonic protocadherin genes, nearly three-quarters of which are found in tandem clusters on the genome (Fig. 2b), a striking expansion relative to the 17-25 genes found in Lottia [a limpet], Crassostrea gigas (oyster) and Capitella [polychaete worm, and annelid] genomes.
The paper doesn't even try to speculate about how these unique cephalopod genes might have arisen. The standard view -- that new genes originate via gene duplication -- is hardly mentioned. But invoking gene duplication requires one to find another gene elsewhere that's similar. Given that cephalopods apparently have many unique genes not similar to genes found in other organisms, gene duplication might not be a candidate explanation in many of these cases. One wonders if future investigators will resort to "de novo" gene origin.
What's that? Stephen Meyer explains in Darwin's Doubt:

Remember: ORFans, by definition, have no homologs. These genes are unique -- one of a kind -- a fact tacitly acknowledged by the increasing number of evolutionary biologists who attempt to "explain" the origin of such genes through de novo ("out of nowhere") origination.
[...]

Many other papers invoke de novo origination of genes. Long mentions, for example, a study seeking to explain the origin of an antifreeze protein in an Antarctic fish that cites "de novo amplification of a short DNA sequence to spawn a novel protein with a new function." Likewise, Long cites an article in Science to explain the origin of two human genes involved in neurodevelopment that appealed to "de novo generation of building blocks -- single genes or gene segments coding for protein domains," where an exon spontaneously "originated from a unique noncoding sequence." Other papers make similar appeals. A paper in 2009 reported "the de novo origin of at least three human protein- coding genes since the divergence with chimp[s]," where each of them "has no proteincoding homologs in any other genome." An even more recent paper in PLoS Genetics reported "60 new protein- coding genes that originated de novo on the human lineage since divergence from the chimpanzee," a finding that was called "a lot higher than a previous, admittedly conservative, estimate."

Another 2009 paper in the journal Genome Research was appropriately titled "Darwinian Alchemy: Human Genes from Noncoding RNA." It investigated the de novo origin of genes and acknowledged, "The emergence of complete, functional genes -- with promoters, open reading frames (ORFs), and functional proteins -- from 'junk' DNA would seem highly improbable, almost like the elusive transmutation of lead into gold that was sought by medieval alchemists." Nonetheless, the article asserted without saying how that: "evolution by natural selection can forge completely new functional elements from apparently nonfunctional DNA -- the process by which molecular evolution turns lead into gold."

The presence of unique gene sequences forces researchers to invoke de novo origin of genes more often than they would like. After one study of fruit flies reported that "as many as ~12% of newly emerged genes in the Drosophila melanogaster subgroup may have arisen de novo from noncoding DNA," the author went on to acknowledge that invoking this "mechanism" poses a severe problem for evolutionary theory, since it doesn't really explain the origin of any of its "nontrivial requirements for functionality." The author proposes that "preadaptation" might have played some role. But that adds nothing by way of explanation, since it only specifies when (before selection played a role) and where (in noncoding DNA), not how the genes in question first arose. Details about how the gene became "preadapted" for some future function is never explained. Indeed, evolutionary biologists typically use the term "de novo origination" to describe unexplained increases in genetic information; it does not refer to any known mutational process. (Darwin's Doubt, pp. 216, 220-221.)

In other words, de novo isn't an explanation at all. It's more like a magic wand to be invoked when evolutionary biologists encounter some unique gene and they have no way to explain its origin via duplication from a similar pre-existing gene. (As an evolutionary mechanism, gene duplication has its own issues.)
Nonetheless, a recent article in Quanta Magazine points out just how many recent scientific studies have resorted to calling upon de novo origin of genes:

For most of the last 40 years, scientists thought that this was the primary way new genes were born -- they simply arose from copies of existing genes. The old version went on doing its job, and the new copy became free to evolve novel functions.
Certain genes, however, seem to defy that origin story. They have no known relatives, and they bear no resemblance to any other gene. They're the molecular equivalent of a mysterious beast discovered in the depths of a remote rainforest, a biological enigma seemingly unrelated to anything else on earth.

The mystery of where these orphan genes came from has puzzled scientists for decades. But in the past few years, a once-heretical explanation has quickly gained momentum -- that many of these orphans arose out of so-called junk DNA, or non-coding DNA, the mysterious stretches of DNA between genes. "Genetic function somehow springs into existence," said David Begun, a biologist at the University of California, Davis.

If the idea that "Genetic function somehow springs into existence" doesn't sound compelling to you, join the club. But that's about as much detail as you're likely to get from proponents of de novo gene origination. One proponent of this idea in the article is even quoted saying: "It's hard to see how to get a new protein out of random sequence when you expect random sequences to cause so much trouble." Unfortunately for evolutionists, this problem seems to be common among animals, as the Quanta article continues:
This metamorphosis was once considered to be impossible, but a growing number of examples in organisms ranging from yeast and flies to mice and humans has convinced most of the field that these de novo genes exist. Some scientists say they may even be common. Just last month, research presented at the Society for Molecular Biology and Evolution in Vienna identified 600 potentially new human genes. "The existence of de novo genes was supposed to be a rare thing," said Mar Albà, an evolutionary biologist at the Hospital del Mar Research Institute in Barcelona, who presented the research. "But people have started seeing it more and more."

Whenever you see "de novo" origin of a gene invoked, you know that evolutionary biologists lack any explanation for how that gene arose. Scientists haven't had much time yet to analyze the cephalopod genome, but given early reports of many unique genes, it will be interesting to learn to what extent they are forced to invoke these mysterious processes -- what amounts to evolution ex nihilo -- to explain how this "alien" genome arose.