Debunking the junk DNA myth.

More Secret Codes in “Junk DNA”
Evolution News | @DiscoveryCSC

Scientists find the most interesting things when they suspect function in poorly understood parts of the genome, rather than relegating them to the junk pile as useless. Here are two recent examples.

Silent Code in Action in Actin

“Actin is an essential and abundant intracellular protein that plays a major role in developmental morphogenesis, muscle contraction, cell migration, and cellular homeostasis,” say Vedula et al. in a paper in the journal eLife. A protein this vital commands our attention. How does it perform so many different functions? What governs the destination and activity of the different forms of actin?

The paper reads like a scientific detective story. A team of researchers from the University of Pennsylvania and the National Institutes of Health wanted to know why two forms of actin (isoforms) are nearly indistinguishable in terms of their sequence (except for four amino acids at one end), but perform very different functions in the cell. They also found it intriguing that these isoforms, β-actin and γ-actin, are coded by different genes, but end up looking very similar.

Let’s divulge the conclusion in the title of the paper: “Diverse functions of homologous actin isoforms are defined by their nucleotide, rather than their amino acid sequence.” Do you hear the word “code” coming? How about “silent code”?

Here we tested the hypothesis that β- and γ-actin functions are defined by their nucleotide, rather than their amino acid sequence, using targeted editing of the mouse genome. Although previous studies have shown that disruption of β-actin gene critically impacts cell migration and mouse embryogenesis, we demonstrate here that generation of a mouse lacking β-actin protein by editing β-actin gene to encode γ-actin protein, and vice versa, does not affect cell migration and/or organism survival. Our data suggest that the essential in vivo function of β-actin is provided by the gene sequence independent of the encoded protein isoform. We propose that this regulation constitutes a global ‘silent code’ mechanism that controls the functional diversity of protein isoforms. 

Good old controlled experimentation, using the CRISPR editing tool, showed that editing the gene for one form produced working copies of the other form. Mice that had defective genes for γ-actin could be rescued by editing the β-actin gene to produce γ-actin. All they had to do was edit five nucleotides to produce healthy mice with no β-actin at all, even though previous knockout experiments showed that mice without the β-actin gene die early in development. How could this be?

Further experiments suggested that it’s not the resulting amino acid sequence that determines the function, but “silent” substitutions in the gene. Something in the β-actin gene was regulating the outcome in a different way, even though it generated only γ-actin. The γ-actin isoform went to where β-actin normally went, and performed its function as if it were β-actin.

The researchers note that different isoforms of actin can have vastly different ribosome densities, differing up to a thousand-fold. In the cytoplasm, some isoforms can compensate for other ones. This arrangement provides flexibility to the cell in most cases:

These results suggest the actin isoform with similar ribosome density can plausibly compensate for the loss of one of the isoforms. In agreement, given the orders of magnitude difference in ribosome density between β-actin and other actin isoforms, none of the other actin isoforms can compensate for the loss of β-actin. We propose that changes in ribosome density arising from silent substitutions in nucleotide sequence, affect translation dynamics and protein accumulation rates, which in turn regulate functional diversity of actins.

The authors feel this kind of “silent code” may be at work in other protein families as well. The word “code” is ubiquitous throughout this paper. In another case, they describe the targeting of one actin isoform to the cell periphery by what they call “zipcode-mediated transport.” They have more to say about coding than evolution, in fact, except in one paragraph where they invoke the common Darwinian excuse that an essential gene tends to be conserved against alteration:

Despite the fact that non-muscle actin isoform genes have evolutionarily diverged > 100  million years ago, they have retained remarkable sequence conservation, far higher than what  would be expected if the synonymous substitutions in their coding sequence were completely randomized. (Erba et al., 1986). This is consistent with our idea that actin isoform coding  sequence exists under additional evolutionary pressure, over and above the conservation of  amino acid sequence. We propose that at least some of this pressure is aimed to maintain the divergent translation dynamics within the actin family, in order to drive their divergent functions.

It appears, however, that intelligent design research could be more productive in follow-up studies. They conclude, “Further systematic analysis of knockouts of homologous isoforms would enable establishing the universality of the ‘silent code.’”

Dark Matter in Your Brain

A more appropriate term for “junk DNA” might be “dark matter” — sequences that are not yet understood. Nature News illustrates a good use of this metaphor in an article, “‘Dark matter’ DNA influences brain development.” Amy Maxmen writes, “Researchers are finally figuring out the purpose behind some genome sequences that are nearly identical across vertebrates.”

A puzzle posed by segments of ‘dark matter’ in genomes — long, winding strands of DNA with no obvious functions — has teased scientists for more than a decade. Now, a team has finally solved the riddle.

The conundrum has centred on DNA sequences that do not encode proteins, and yet remain identical across a broad range of animals. By deleting some of these ‘ultraconserved elements’, researchers have found that these sequences guide brain development by fine-tuning the expression of protein-coding genes.

There’s no reason to suspect that any of the heroes of this article doubt evolutionary theory. But one lead researcher of a new paper did what a good design scientist would do: keep looking for function until you find it.

The results, published on 18 January in Cell, validate the hypotheses of scientists who have speculated that all ultraconserved elements are vital to life — despite the fact that researchers knew very little about their functions.

“People told us we should have waited to publish until we knew what they did. Now I’m like, dude, it took 14 years to figure this out,” says Gill Bejerano, a genomicist at Stanford University in California, who described ultraconserved elements in 2004.

What they found is the opposite of evolutionary expectations, even though the article assumes evolution:

Bejerano and his colleagues originally noticed ultraconserved elements when they compared the human genome to those of mice, rats and chickens, and found 481 stretches of DNA that were incredibly similar across the species. That was surprising, because DNA mutates from generation to generation — and these animal lineages have been evolving independently for up to 200 million years.

Genes that encode proteins tend to have relatively few mutations because if those changes disrupt the corresponding protein and the animal dies before reproducing, the mutated gene isn’t passed down to offspring. On the basis of this logic, some genomicists suspected that natural selection had similarly weeded out mutations in ultraconserved regions. Even though the sequences do not encode proteins, they thought, their functions must be so vital that they cannot tolerate imperfection.

You have to wonder what function Darwinian evolution had in this research. The expectations were wrong, the results were surprising, and the team found more design than was previously known — to the point of implying perfection. The only evolution-talk sounds like an after-the-fact gloss to keep the preferred narrative from being falsified.

For more on the tortured subject of supposed trash in the genome, see The Myth of Junk DNA, by Jonathan Wells.

On ancient Babylon:The Watchtower Society's commentary.

BABYLON



Babʹy·lon) [Confusion].

1. The later name given to Babel. This city of renown was located along the Euphrates River on the Plains of Shinar approximately 870 km (540 mi) E of Jerusalem and some 80 km (50 mi) S of Baghdad. The ruins of Babylon extend over a vast area in the form of a triangle. Several mounds are scattered over the area. Tell Babil (Mujelibe), in the northern part of the triangle, preserves the ancient name and is located about 10 km (6 mi) N of Hilla, Iraq.​—See BABYLON No. 2; SHINAR.

The city lay on both sides of the Euphrates River. A double system of walls surrounded Babylon, making it seemingly impregnable.

The inner rampart, constructed of crude bricks, consisted of two walls. The inner wall was 6.5 m (21.5 ft) thick. The outer wall, situated 7 m (23 ft) away, was about 3.5 m (11.5 ft) thick. These walls were buttressed by defense towers, which also served to reinforce the walls structurally. About 20 m (66 ft) outside the outer wall was a quay made of burnt brick set in bitumen. Outside this wall was a moat connected with the Euphrates to the N and S of the city. It provided both water supply and protection against enemy armies. Babylonian documents indicate that eight gates gave access to the interior of the city. So far, four of Babylon’s gates have been discovered and excavated.

The outer rampart E of the Euphrates was added by Nebuchadnezzar II (who destroyed Solomon’s temple), thus enclosing a large area of the plain to the N, E, and S for the people living nearby to flee to in case of war. This outer rampart also consisted of two walls. The inner wall, made of unbaked bricks, was about 7 m (23 ft) thick and was buttressed with defense towers. Beyond this, about 12 m (40 ft) away, was the outer wall of baked bricks, made in two parts that were interlocked by their towers: one was almost 8 m (26 ft) thick, and the adjoining part was about 3.5 m (11.5 ft) thick.

Nabonidus joined the ends of the outer rampart by constructing a wall along the eastern bank of the river. This wall was about 8.5 m (28 ft) wide and also had towers as well as a quay 3.5 m (11.5 ft) wide.

Herodotus, Greek historian of the fifth century B.C.E., says that the Euphrates River was flanked on either side with a continuous quay, which was separated from the city proper by walls having gateways. According to him, the city walls were about 90 m (295 ft) high, 26.5 m (87 ft) thick, and about 95 km (59 mi) long. However, it appears that Herodotus exaggerated the facts regarding Babylon. Archaeological evidence shows that Babylon was much smaller in size, with the outer rampart much shorter in length and height. No evidence has been found to verify the existence of a quay lining the immediate western bank of the river.

Streets ran through the city from the gates in the massive walls. The Processional Way, the main boulevard, was paved and the walls alongside it were decorated with lions. (PICTURE, Vol. 2, p. 323) Nebuchadnezzar II repaired and enlarged the old palace and built a summer palace some 2 km (1.5 mi) to the north. He also built a great structure of vaulted archways, tier upon tier, known as the Hanging Gardens of Babylon and famed as a “wonder of the ancient world.”

This sprawling metropolis astride the watercourse of the Euphrates was a commercial and industrial center of world trade. More than an important manufacturing center, it was a commercial depot for trade between the peoples of the East and the West, both by land and by sea. Thus her fleet had access to the Persian Gulf and the seas far beyond.

History. Nimrod, who lived in the latter part of the third millennium B.C.E., founded Babylon as the capital of man’s first political empire. Construction of this city, however, suddenly came to a halt when confusion in communication occurred. (Ge 11:9) Later generations of rebuilders came and went. Hammurabi enlarged the city, strengthened it, and made it the capital of the Babylonian Empire under Semitic rule.

Under the control of the Assyrian World Power, Babylon figured in various struggles and revolts. Then with the decline of the second world empire, the Chaldean Nabopolassar founded a new dynasty in Babylon about 645 B.C.E. His son Nebuchadnezzar II, who completed the restoration and brought the city to its greatest glory, boasted, “Is not this Babylon the Great, that I myself have built?” (Da 4:30) In such glory it continued as the capital of the third world power until the night of October 5, 539 B.C.E. (Gregorian calendar), when Babylon fell before the invading Medo-Persian armies under the command of Cyrus the Great.

That fateful night in the city of Babylon, Belshazzar held a banquet with a thousand of his grandees. Nabonidus was not there to see the ominous writing on the plaster wall: “MENE, MENE, TEKEL and PARSIN.” (Da 5:5-28) After suffering defeat at the hands of the Persians, Nabonidus had taken refuge in the city of Borsippa to the SW. But Jehovah’s prophet Daniel was on hand in Babylon on that night of October 5, 539 B.C.E., and he made known the significance of what was written on the wall. The men of Cyrus’ army were not sleeping in their encampment around Babylon’s seemingly impregnable walls. For them it was a night of great activity. In brilliant strategy Cyrus’ army engineers diverted the mighty Euphrates River from its course through the city of Babylon. Then down the riverbed the Persians moved, up over the riverbanks, to take the city by surprise through the gates along the quay. Quickly passing through the streets, killing all who resisted, they captured the palace and put Belshazzar to death. It was all over. In one night Babylon had fallen, ending centuries of Semitic supremacy; control of Babylon became Aryan, and Jehovah’s word of prophecy was fulfilled.​—Isa 44:27; 45:1, 2; Jer 50:38; 51:30-32; see PICTURE, Vol. 2, p. 325; CYRUS.

From that memorable date, 539 B.C.E., Babylon’s glory began to fade as the city declined. Twice it revolted against the Persian emperor Darius I (Hystaspis), and on the second occasion it was dismantled. A partially restored city rebelled against Xerxes I and was plundered. Alexander the Great intended to make Babylon his capital, but he suddenly died in 323 B.C.E. Nicator conquered the city in 312 B.C.E. and transported much of its material to the banks of the Tigris for use in building his new capital of Seleucia. However, the city and a settlement of Jews remained in early Christian times, giving the apostle Peter reason to visit Babylon, as noted in his letter. (1Pe 5:13) Inscriptions found there show that Babylon’s temple of Bel existed as late as 75 C.E. By the fourth century C.E. the city was in ruins, and eventually passed out of existence. It became nothing more than “piles of stones.”​—Jer 51:37.

Today nothing remains of Babylon but mounds and ruins, a veritable wasteland. (PICTURE, Vol. 2, p. 324) The book Archaeology and Old Testament Study states: “These extensive ruins, of which, despite Koldewey’s work, only a small proportion has been excavated, have during past centuries been extensively plundered for building materials. Partly in consequence of this, much of the surface now presents an appearance of such chaotic disorder that it is strongly evocative of the prophecies of Isa. xiii. 19–22 and Jer. l. 39 f., the impression of desolation being further heightened by the aridity which marks a large part of the area of the ruins.”​—Edited by D. W. Thomas, Oxford, 1967, p. 41.

Religion. Babylon was a most religious place. Evidence from excavations and from ancient texts points to the existence of more than 50 temples. The principal god of the imperial city was Marduk, called Merodach in the Bible. It has been suggested that Nimrod was deified as Marduk, but the opinions of scholars as to identifications of gods with specific humans vary. Triads of deities were also prominent in the Babylonian religion. One of these, made up of two gods and a goddess, was Sin (the moon-god), Shamash (the sun-god), and Ishtar; these were said to be the rulers of the zodiac. And still another triad was composed of the devils Labartu, Labasu, and Akhkhazu. Idolatry was everywhere in evidence. Babylon was indeed “a land of graven images,” filthy “dungy idols.”​—Jer 50:1, 2, 38.

The Babylonians believed in the immortality of the human soul.​—The Religion of Babylonia and Assyria, by M. Jastrow, Jr., 1898, p. 556.

The Babylonians developed astrology in an effort to discover man’s future in the stars. (See ASTROLOGERS.) Magic, sorcery, and astrology played a prominent part in their religion. (Isa 47:12, 13; Da 2:27; 4:7) Many heavenly bodies, for example, planets, were named after Babylonian gods. Divination continued to be a basic component of Babylonian religion in the days of Nebuchadnezzar, who used it to reach decisions.​—Eze 21:20-22.

Israel’s Age-Old Enemy. The Bible makes many references to Babylon, beginning with the Genesis account of the original city of Babel. (Ge 10:10; 11:1-9) Included in the spoil taken by Achan from Jericho was “an official garment from Shinar.” (Jos 7:21) After the fall of the northern kingdom of Israel in 740 B.C.E., people from Babylon and other areas were brought in to replace the captive Israelites. (2Ki 17:24, 30) Hezekiah made the mistake of showing messengers from Babylon the treasures of his house; these same treasures as well as some of Hezekiah’s “sons” were later taken to Babylon. (2Ki 20:12-18; 24:12; 25:6, 7) King Manasseh (716-662 B.C.E.) was also taken captive to Babylon, but because he humbled himself, Jehovah restored him to his throne. (2Ch 33:11) King Nebuchadnezzar took the precious utensils of Jehovah’s house to Babylon, along with thousands of captives.​—2Ki 24:1–25:30; 2Ch 36:6-20.

The Christian Greek Scriptures tell how Jeconiah (Jehoiachin), taken prisoner to Babylon, was a link in the lineage to Jesus. (Mt 1:11, 12, 17) The apostle Peter’s first canonical letter was written from Babylon. (1Pe 5:13; see PETER, LETTERS OF.) That “Babylon” was the city on the Euphrates, and not Rome as claimed by some.

See BABYLON THE GREAT.

2. The Babylonian Empire was also referred to by the name of its capital city, Babylon, and was centered in the lower Mesopotamian valley.​—MAP, Vol. 2, p. 321.

Sometimes historians subdivide Babylonia, calling the northern part Akkad (Accad) and the southern part Sumer or Chaldea. Originally this territory was designated in the Scriptures as “the land of Shinar.” (Ge 10:10; 11:2; see SHINAR.) Later, when dominating rulers made Babylon their capital, this area was known as Babylonia. Because Chaldean dynasties sometimes held sway, it was also called “the land of the Chaldeans.” (Jer 24:5; 25:12; Eze 12:13) Some of the ancient cities in Babylonia were Adab, Akkad, Babylon, Borsippa, Erech, Kish, Lagash, Nippur, and Ur. The Babylonian Empire, of course, extended beyond Babylonia, taking in Syria and Palestine down to the border of Egypt.

About the first half of the eighth century B.C.E., an Assyrian king by the name of Tiglath-pileser III (Pul) ruled Babylonia. (2Ki 15:29; 16:7; 1Ch 5:26) Later a Chaldean called Merodach-baladan became the king of Babylon, but after 12 years he was ousted by Sargon II. Sennacherib, in succeeding Sargon II, faced another Babylonian revolt led by Merodach-baladan. After Sennacherib’s unsuccessful attempt to capture Jerusalem in 732 B.C.E., Merodach-baladan sent envoys to Hezekiah of Judah possibly to seek support against Assyria. (Isa 39:1, 2; 2Ki 20:12-18) Later Sennacherib drove out Merodach-baladan and crowned himself ruler of Babylon, a position he held until death. His son Esar-haddon rebuilt Babylon. The Babylonians rallied around Nabopolassar and bestowed the kingship on him. With him began the Neo-Babylonian dynasty that was to continue until Belshazzar. That dynasty from Nabopolassar’s son Nebuchadnezzar on to Belshazzar is represented in Bible prophecy by the head of gold of Nebuchadnezzar’s dream image (Da 2:37-45) and, in a dream-vision of Daniel, by a lion that had the wings of an eagle and the heart of a man.​—Da 7:4.

In 632 B.C.E. Assyria was subdued by this new Chaldean dynasty, with the assistance of Median and Scythian allies. In 625 B.C.E., Nabopolassar’s eldest son, Nebuchadnezzar (II), defeated Pharaoh Necho of Egypt at the battle of Carchemish, and in the same year he assumed the helm of government. (Jer 46:1, 2) Under Nebuchadnezzar, Babylon was “a golden cup” in the hand of Jehovah to pour out indignation against unfaithful Judah and Jerusalem. (Jer 25:15, 17, 18; 51:7) In 620 B.C.E. he compelled Jehoiakim to pay tribute, but after about three years Jehoiakim revolted. In 618 B.C.E., or during Jehoiakim’s third year as tributary ruler, Nebuchadnezzar came against Jerusalem. (2Ki 24:1; 2Ch 36:6) However, before he could be taken by the Babylonians, Jehoiakim died. Jehoiachin, having succeeded his father, quickly surrendered and was taken captive along with other nobility to Babylon in 617 B.C.E. (2Ki 24:12) Zedekiah was next appointed to the throne of Judah, but he too rebelled; and in 609 B.C.E. the Babylonians again laid siege to Jerusalem and finally breached its walls in 607 B.C.E. (2Ki 25:1-10; Jer 52:3-12) That year, 607 B.C.E., when Jerusalem was laid desolate, was a significant one in the counting of time until Jehovah, the Universal Sovereign, would set up the world ruler of his choice in Kingdom power.​—See APPOINTED TIMES OF THE NATIONS (Beginning of ‘trampling’).

One cuneiform tablet has been found referring to a campaign against Egypt in Nebuchadnezzar’s 37th year (588 B.C.E.). This may be the occasion when mighty Egypt was brought under Babylonian control, as foretold by the prophet Ezekiel evidently in the year 591 B.C.E. (Eze 29:17-19) Finally, after a 43-year reign, which included both conquest of many nations and a grand building program in Babylonia itself, Nebuchadnezzar II died in October of 582 B.C.E. and was succeeded by Awil-Marduk (Evil-merodach). This new ruler showed kindness to captive King Jehoiachin. (2Ki 25:27-30) Little is known about the reigns of Neriglissar, evidently the successor of Evil-merodach, and of Labashi-Marduk.

More complete historical information is available for Nabonidus and his son Belshazzar, who were evidently ruling as coregents at the time of Babylon’s fall.

By now the Medes and Persians under command of Cyrus the Great were on the march to take over control of Babylonia and become the fourth world power. During the night of October 5, 539 B.C.E. (Gregorian calendar), Babylon was seized, and Belshazzar was slain. In the first year of Cyrus, following the conquest of Babylon, he issued his famous decree permitting a group that included 42,360 males, besides many slaves and professional singers, to return to Jerusalem. Some 200 years later, Persian domination of Babylonia came to an end when Alexander the Great captured Babylon in 331 B.C.E. By the middle of the second century B.C.E. the Parthians, under their king Mithradates I, were in control of Babylonia.

Since Jewish communities had been flourishing in this land, Peter the apostle to the Jews went to Babylon, and it was from there that he wrote at least one of his inspired letters. (Ga 2:7-9; 1Pe 5:13) Jewish leaders in these Eastern communities also developed the Babylonian Targum, otherwise known as the Targum of Onkelos, and produced a number of manuscripts of the Hebrew Scriptures. The Petersburg Codex of the Latter Prophets, dated 916 C.E., is noteworthy because it embodies a mixture of both Eastern (Babylonian) and Western (Tiberian) readings.

The fix was in?

Hummingbird Study Illustrates Problem with Darwinian Explanations

Evolution News | @DiscoveryCSC

Many people keep hummingbird feeders in their back yards, to enjoy the aerobatics of these colorful, quicker-than-the-eye, miniature marvels. Paul Nelson says, “There’s a kind of jewel-like quality that they have” that makes them so admirable. In  Flight: The Genius of Birds, after seeing details about hummingbird science set to dazzling video, it’s no wonder Nelson speaks of the “exquisite workmanship” evident in their construction.

The big question facing science should be, “How did such exquisite workmanship come about?” How can a creature weighing only a few ounces perform maneuvers that flight engineers cannot begin to imitate? And yet evolutionists often seem fixated on much smaller questions, such as “How did one hummer evolve to be larger than another hummer?” A good example of this comes from the University of British Columbia, which announces, “Evolution — and skill — help hefty hummingbirds stay spry.” Looking right past the magnificent photo of a hummingbird’s iridescent feathers and beautiful head and eyes, the authors rush to give credit to blind processes of nature, right from the first word.

Evolved differences in muscle power and wing size — along with a touch of skill — govern hummingbirds’ inflight agility, according to new research in Science.

The findings by University of British Columbia biologists show that larger species of hummingbirds, despite their increased mass, are able to adapt to outmaneuver smaller species.

“Studies of bats, birds and other animals show that increases in body mass can have a detrimental effect on many aspects of flight,” says Roslyn Dakin, co-lead author on the study.

“But with hummingbirds, the correlated evolution of increased wing size and muscle mass helps larger species compensate for their greater body masses.”

You can summarize all the lessons of this study published in Science in just one sentence: “Bigger hummingbirds evolved bigger muscles, and smaller hummingbirds evolved smaller muscles, but all of them can maneuver equally well.” Fascinating. Science marches on.

It’s not that the scientists were lazy. Dakin et al. “recorded over 330,000 maneuvers, including many repeated maneuvers for each bird.”

How does agility evolve? This question is challenging because natural movement has many degrees of freedom and can be influenced by multiple traits. We used computer vision to record thousands of translations, rotations, and turns from more than 200 hummingbirds from 25 species, revealing that distinct performance metrics are correlated and that species diverge in their maneuvering style. Our analysis demonstrates that the enhanced maneuverability of larger species is explained by their proportionately greater muscle capacity and lower wing loading. Fast acceleration maneuvers evolve by recruiting changes in muscle capacity, whereas fast rotations and sharp turns evolve by recruiting changes in wing morphology. Both species and individuals use turns that play to their strengths. These results demonstrate how both skill and biomechanical traits shape maneuvering behavior.

Evolve, evolve, evolve. Everything is explainable by Darwin’s blind process of mistakes that survived the trash heap. That includes “both skill and biomechanical traits” because they are results of evolution, too. Is science advanced by work that ends up saying, “big hummingbirds evolved to be bigger, and small hummingbirds evolved to be smaller”? It wouldn’t matter if they recorded 500,000 maneuvers, or a million maneuvers. The fix was in: evolution would take all the credit.

This result explains why hummingbird maneuverability scales positively with species mass, even though mass has the opposite effect on individual performance: Larger species can achieve maneuverability through the evolution of disproportionate increases in muscle capacity and wing size.

It’s hard to even call natural selection a “process.” It’s more like a statement after the fact, a filter that allows one conclusion but omits all others. Natural selection is not an active agent; it doesn’t cause anything. The bird doesn’t choose to evolve, and the environment doesn’t make it evolve. The Darwinian just looks at the finished product, and says, “it evolved.” The reader is left looking at this masterpiece of flying jewelry, wondering if anything has been explained at all.

Thus, species-level evolutionary changes in muscle capacity and wing morphology affect different, correlated suites of behaviors.

No doubt this study took a lot of work, but the evolution statements do not logically emerge from the data. The scientists learned things about feathers, wing shapes, glycolysis in the muscles, and other measurable factors between different hummingbird species. But what’s evolution got to do with it?

Given that muscle capacity is the primary species-level trait associated with accelerations this result suggests that evolved changes in muscle capacity can compensate for relatively small wings.

The uselessness of evolutionary explanations can be seen by substituting the word “happenstance” for “evolve” in one of their concluding paragraphs:

A key result of our comparative analysis is that evolved [happenstance] changes in the wings primarily determine turns and rotations, whereas evolved [happenstance] changes in muscle capacity primarily determine translations. This indicates that different flight maneuvers evolve by [happenstance] recruiting different traits.

Lest any evolutionist complain that we’re leaving out the ‘selection’ part of the equation, it must be noted that selection is by happenstance, too. No mind is governing the outcome in the Darwinian view of the world. ‘But if selection didn’t operate, the bird would not survive!’ is the comeback. OK then, how satisfying is it to explain anything with the statement, “If it didn’t evolve, it wouldn’t exist”? It’s like the anthropic principle in cosmology, which (in one version) states, “If the universe were not finely tuned to an astonishingly intricate degree, we wouldn’t be here arguing about it, so it must have just happened to work out that way.” There’s something deeply unsatisfying in that kind of explanation.

The paper by Dakin et al., notice, is trying to explain hummingbird differences by evolution. Peter C. Wainright, in a companion piece in Science, points to the paper with the “how” word: “How hummingbirds stay nimble on the wing.” He says the authors “probe the evolution of flight maneuverability in hummingbirds”; he speaks of “the evolution” of hummingbirds; he mentions “the role of flight ability evolution in hummingbird diversification.” Our contention is, what’s the e-word got to do with it? For anything learned about hummingbird maneuverability due to wing shape, tail rotation, or muscle mass, does it help to say that evolution (happenstance) did it? Does this improve scientific understanding of a wonder of nature? Thinking people want to know how this wonder came about. Happenstance is not an answer. It is not an explanation.

You’ll learn more about hummingbirds in nine minutes of the Illustra film than in this paper with its 64 references and 18 mentions of evolution. You’ll learn that:

Engineers are light-years behind the bird that inspired robotic flyers.

Their wings can beat more than 100 times a second.

Hummingbirds are built for speed and maneuverability.

No other bird can fly backward and hover in mid-air while feeding on flowers.

The highly-maneuverable tail is a balancing organ the bird uses to guide direction.

The flight muscle represents about 43% of the bird’s mass.

Hummingbirds employ 3 specialized types of wing beats for forward, backward, and hovering motion.

Hummers have a unique shoulder joint that enables these flight strategies.

Unlike on any other bird, hummingbird wings generate lift on the backstroke.

The shoulder joint can rotate the wing 140 degrees by twisting the upper arm bone, making the entire wing invert on the backstroke.

To supply the muscles with oxygen, the bird’s heart beats as much as 1,250 beats per minute.

The nerve synapses fire at an incredible rate to make this muscular contraction possible.

The hummingbird consumes twice its body weight in nutrients each day.

During waking hours, the bird eats every 10 to 15 minutes.

A comparable diet for a human would be 150 pounds of food a day.

The hummingbird tongue is about twice as long as its beak.

The tongue acts as an automatic nectar trap (see video clip for demonstration).

The tongue traps nectar in less than 1/20th of a second, thousands of times a day.

Surely these observational facts cry out for an explanation more elegant than, “they evolved.” We respond to these observations, Paul Nelson concludes, like responding to the work of an artist. We doubt that any artist would appreciate having elegant craftsmanship attributed to happenstance.

Yet more on rethinking hell

Time to decanonise higher ed?:Pros and cons.

Yet more on the historical Jesus IV

Yet more on the historical Jesus III

Yet more on the historical Jesus II

Yet more on the historical Jesus.

Why the case for design remains undeniable.

Losing the Forest by Fixating on the Trees — A Response to Venema’s Critique of Undeniable

Douglas Axe | @DougAxe

I was asked recently to take part in an online  symposium.  The journal Sapientia, published by the Carl F.H. Henry Center, invited four theistic evolutionists to review my book,  Undeniable: How Biology Confirms Our Intuition That Life Is Designed,  after which I was to provide a single response. Anticipating that the reviews would all be negative, I saw this not as an opportunity to convert my critics but rather as an opportunity to demonstrate to open-minded people the power of common-sense reasoning. This is, after all, the main theme of Undeniable: that ordinary curious people are well equipped to see through all the technical huff and bluff used by people with PhDs to defend the evolutionary explanation of life.

I agreed to participate, even though the deck was stacked against me in several respects. First, considering the critical view I take not just of Darwinism but also of the academic echo chamber that, with iron-lung-like artificiality, allows this otherwise dead theory to persist, it should be clear that I wrote primarily for people outside the echo chamber. The exclusion of anyone who fits that description from providing even one of the reviews of my book therefore raises questions about the true intent of the exercise. Second, although I was offered the advantage of having the last word, my response was restricted to about a third the total length of the four critiques (though I did get this adjusted upward a bit). And third, I only realized after my response was submitted that it would be published a full month after the first of the critiques became public.

I hereby unstack the deck.

My official symposium response, to be published March 5, doesn’t give much space to my first critic, Dennis Venema This is mostly because, not knowing the order in which the critiques would be published, I had already dealt with the problems that Venema’s piece shares with the others — his complete lack of engagement with the actual argument of Undeniable, his misconstrual of this as an argument from intuition, and his accompanying charge of anti-intellectualism. The second reason I chose not to spend many words on Venema is that he relied heavily on technical criticisms, whereas the whole point of Undeniable is to give people a better option than trying to follow the technical toing and froing. My claim is that you don’t need to be able to follow technical arguments about genes and proteins and mutations in order to understand why Darwin’s explanation of life can’t possibly be correct.

That said, I don’t want to give the impression that Venema’s technical criticisms can’t be answered. They can. My point is that people can have a perfectly solid basis for knowing that Venema’s position is wrong even if they can’t fully follow his technical points or my responses to those points (below). If I’m right about this, then Venema’s “Trust me — I’m a scientist” approach isn’t going to work. He’s going to have to enable intelligent non-scientists to make sense in their own minds of the claim that things like humming birds and cheetahs and humans just happen in a universe like ours.

I’m pretty sure he can’t do so (though I would welcome an attempt). Perhaps he has his own doubts about this, which would explain why he chose to ignore the main argument of Undeniable.

My forthcoming official response makes that point. Here I’d like to show why you should be cautious about trusting Venema’s take on this simply because he’s a scientist.

First, the fact that Venema looks to a non-scientist — Vincent Torley, an English teacher with a PhD in the philosophy of mind — as though he were an authority on my protein work serves as a strong indicator that Venema isn’t an authority either in this area. With that in mind, let’s consider Venema’s dual claims in order: 1) “we now know that proteins do not need to be stably folded in order to function,” and 2) “we also know that functional proteins are not rare within sequence space.”

Conditional Folding Is Still Folding

On the first point, Venema surely knows he’s misleading his readers. With respect to proteins, folding refers to the process by which initially floppy protein chains lock into well-defined three-dimensional structures that perform specific functions within cells. Venema cites a good review paper on so-called “intrinsically disordered proteins,” claiming the existence of this class of proteins shows that protein function doesn’t actually require folding. However, if Venema read the paper, he knows it has a section titled “Coupled folding and binding,” referring to the “mechanism by which disordered interaction motifs associate with and fold upon binding to their targets” (emphasis added). In other words, the term “intrinsically disordered proteins” is a misnomer (whoever coined the term evidently didn’t know what the word intrinsic means). A better term would be conditionally folded proteins.

Moreover, anyone who reads this review paper with open eyes will see that conditional folding is in fact a remarkable design feature. As the authors say, “An exciting recent finding is that many proteins containing low-complexity or prion-like sequences can promote phase separation to form membrane-less organelles within the cytoplasm or nucleoplasm, thus contributing to their compartmentalization in a regulated manner.” Speaking of conditionally folded proteins in general, the authors note that the levels of these proteins within cells are “tightly regulated to ensure precise signaling in time and space, and mutations in [them] or changes in their cellular abundance are associated with disease.”

So, if Venema pictures these conditional folders as being easy evolutionary onramps for mutation and selection to make unconditionally folded proteins, he’s badly mistaken. Both kinds of proteins are at work in cells in a highly orchestrated way, both requiring just the right amino-acid sequences to perform their component functions, each of which serves the high-level function of the whole organism. The point of Undeniable is that we don’t need to know the exact improbabilities of each of these component functions to know that the whole thing can’t happen by chance. We merely need to see that a great many things have to come together in the right way for systems like this to be made. The obvious fact that every one of these things is improbable if left to chance makes getting the whole thing utterly impossible.

Storytelling Isn’t Science

On the second point (the rarity of functional sequences) Venema appeals to two lines of evidence. First, he sees “strong evidence” that “new genes that code for novel, functional proteins can pop into existence from sequences that did not previously encode a protein.” The authors of the paper he cites in support of this are more cautious. Like all authors, they want to think the evidence they provide is strong, but considering the number of assumption involved, they are compelled to be more tentative: “These results suggest that BSC4 may be a newly evolved gene” (emphasis added).

The observable facts are what they are: brewers’ yeast has a gene that isn’t found intact in similar yeast species and appears to play a back-up role of some kind. The question is how to interpret these facts. And this is where Venema and I take different approaches. Like most biologists, Venema starts with the assumption that evolution works as claimed (or maybe he would say openness to the possibility that it does) and then he looks at genomes as if they were the record of evolutionary accomplishments — evolution’s CV, as it were. But once you go down this road of thinking you can divine the past by “reading” it from genomes, you tend to get sucked in. The distinction between stories and facts becomes blurred to the point where every new story is seen as confirmation of that initial assumption that evolution works. Then, having become hooked on this way of thinking, you have no inclination to step back and take a critical view of the whole thing.

A more critical approach is necessary for getting the science right. Stories about how things happened can’t become scientifically compelling until we show: 1) that things could have happened that way, and 2) that no other way they could have happened is comparably likely. Having taken this critical approach for decades, I’ve become convinced that all naturalistic explanations of life fail at step 1. That’s the point of Undeniable, and while Venema may dislike this point, his aversion to it is not an answer to it.

To ignore is not to refute.

If we retain an appropriate degree of skepticism about the grand evolutionary story, other interpretations of the facts surrounding BSC4 present themselves, one being that similar yeast species used to carry a similar gene which has now been lost. The fact that the version of this gene in brewers’ yeast is interrupted by a stop codon that reduces full-length expression to about 9 percent of what it would otherwise be seems to fit better with a gene on its way out than a gene on its way in. I admit that’s just another story, the point being that there’s usually more than one possible story.

The motives for telling these stories can be as interesting as the stories themselves, as  this paper in Nature Reviews Genetics reveals. The abstract starts by presenting a problem:

Gene evolution has long been thought to be primarily driven by duplication and rearrangement mechanisms. However, every evolutionary lineage harbours orphan genes that lack homologues in other lineages and whose evolutionary origin is only poorly understood.

Translation: Genomic sequencing has revealed something that contradicted evolutionary thinking — namely, an abundance of genes that don’t appear to have any evolutionary history (hence the name orphan genes).

Now, if biologists were as cautious about stories as they ought to be, this discovery would have been a huge wakeup call. Instead it was merely an occasion to recraft the story, keeping it true to the grand theme of life being the product of natural causes. By this constrained way of thinking, orphan genes must be able to pop into existence naturally because, well — here they are! Accordingly, the authors of the above paper “solve” the problem they posed by positing that “de novo evolution out of non-coding genomic regions is emerging as an important additional mechanism” for the origin of existing genes.

Don’t Forget: The Point in Dispute Is the Sufficiency of Chance

The focus should indeed be on mechanisms — detailed, self-critical, scientifically tested accounts of just how new functional genes would “pop into existence.” More specifically, with respect to the present debate, the key question is not what happened when and where. As interesting as that question is, the crucial question for our purposes is this: Could these things have happened by chance?

Venema and I both believe the universe popped (banged) into existence long ago, and we both recognize the implausibility of the claim that this just happened. Likewise, we both understand the profound significance of this distinction between an intended universe and an accidental one. Given all this agreement, Venema should be equally concerned to make the same distinction for life, all the way down to individual genes. The crucial question isn’t whether genes popped into existence but whether they popped into existence by chance. If he recognized this, he would be less distracted by the stories and more genuinely interested in the probabilities. After all, the only adjudicator on questions of chance is probability.

Rhetoric Isn’t Science

To his credit, Venema at least gives a nod in this direction by citing a piece of experimental work by Neme and coworkers that claims to show functional DNA sequences are highly probable — abundant within the space of possibilities. These scientists inserted synthetic pieces of DNA with random sequences into an existing genetic element that, when placed in bacterial cells, forces these cells to churn out loads of RNA from the inserts and also to churn out any protein chain they might happen to encode (by chance). After experimenting with these encumbered bacterial strains, they claim that “the majority of randomly generated sequences have reproducible biochemical activity.”

Though the shortcomings of this study wouldn’t be evident to every reader, they were evident to me when I read the paper last spring, just after it appeared. I was therefore pleased to see a polite explanation of some of the problems published in Current Biology last July. The authors of this critique left no doubt as to the magnitude of the flaws: “we have reservations about the correctness of the conclusion of Neme et al. that 25% of their random sequences have beneficial effects…”

Indeed, it’s hard to escape the conclusion that Neme and coworkers deliberately overstated their case. They concluded that most randomly generated sequences have “biochemical activity,” but what they showed is far less impressive. They merely showed that if you burden bacteria by forcing them to churn out RNA and protein from random inserts, it’s fairly easy to find sequence-dependent effects on growth — not because anything clever has been invented, but because the burden of making so much junk varies slightly with the kind of junk. That means any junk that slows the process of making more junk by gumming up the works a bit would provide a selective benefit. Such sequences are “good” only in this highly artificial context, much as shoving a stick into an electric fan is “good” if you need to stop the blades in a hurry.

Yes, junk sequences can have a measurable effect in situations like this, but the word function implies something considerably more than mere effect, and the term “biochemical activity” used by Neme et al. is so clearly incorrect that it’s hard to believe the reasons for choosing it weren’t more rhetorical than scientific.

In the end, then, Venema’s technical complaints come to nothing. In his position, I would probably be inclined to respond with more technical complaints. He is, of course, free to do so, but he would do himself a favor to hit pause and consider whether there really may be a clear logical reason that the natural causes he wants to credit with inventing life can’t actually deserve that credit.

Yet more in defense of Adam and Eve.

Adam and the Genome and “Predetermined Conclusions”
Evolution News | @DiscoveryCSC

In two previous posts (here and here), we saw that evolutionary genomicist Richard Buggs and biologist Dennis Venema have been debating online about Venema’s argument in Adam and the Genome that human genetic diversity refutes a traditional view of Adam and Eve. (Find the rest of our series of posts on the book here.)  Buggs explained that Venema’s allusion to human leukocyte antigen (HLA) genes (also called major histocompatibility complex, or MHC, genes) do not refute an original human couple. In his  Nature Ecology & Evolution blog post, Buggs writes, “Hyper-variable loci like MHC genes or microsatellites have so many alleles that they seem to defy the idea of a single couple bottleneck until we consider that they have very rapid rates of evolution, and could have evolved very many alleles since a bottleneck.” Buggs also explained in a  comment at The Skeptical Zone  that the ability of MHC genes to evolve rapidly isn’t a good argument for a large ancestral population size:

MHC loci are pretty exotic. Several studies show that they evolve fast and may be under sexual selection, pathogen-mediated selection, and frequency-dependent selection; they may also have heterozygote advantage (see e.g. [link]). The maintenance of MHC polymorphism is still “an evolutionary puzzle” ([link]). There is some evidence for convergent evolution of HLA genes ([link, link, link, link]). If the whole case for large human ancestral population sizes rests on MHC loci, I think this is inadequate to prove the point, given our current state of knowledge on MHC evolution.

Buggs isn’t the only qualified biologist who has looked at arguments from MHC genes against Adam and Eve and found them lacking. In the book Science and Human Origins, Ann Gauger considered the evidence, and found it compatible with an initial couple. She recounts her investigation of this topic:

When I began this study, I was prepared to accept that there was too much genetic diversity among these genes to have passed through just two first parents. To my surprise, I found that even this most polymorphic (most varied) region of our genome does not rule out the possibility of a first couple.

(Science and Human Origins, p. 106)

As Gauger points out, the evolutionary biologist Francisco Ayala had calculated that there were 32 different HLA alleles in existence when the human lineage diverged from chimps, requiring “that the minimum size of the ancestral population was no fewer than 4,000, with a long-term average effective population size of 100,000.” She explains why this supposedly refuted Adam and Eve:

Because of this minimal estimate of 4,000, Ayala claimed that at no time was it possible for the human population to have passed through a bottleneck of two. In his view, there is just too much ancestral diversity in HLA-DRB1.

(Science and Human Origins, p. 111)

After reviewing Ayala’s arguments, however, she found that his model had both explicit and implicit assumptions that were dubious:

These explicit assumptions include a constant background mutation rate over time, lack of selection for genetic change on the DNA sequences being studied, random breeding among individuals, no migrations in or out of the breeding population, and a constant population size. If any of these assumptions turn out to be unrealistic, the results of a model may be seriously flawed.

There are also hidden assumptions buried in population genetics models, assumptions that rely upon the very thing they are meant to demonstrate. For example, tree-drawing algorithms assume that a tree of common descent exists. The population genetics equations also assume that random processes are the only causes of genetic change over time, an assumption drawn from naturalism. What if non-natural causes, or even unknown natural causes that do not act randomly, have intervened to produce genetic change?

(Science and Human Origins, p. 112)

Gauger realized that in this case, Ayala had wrongly assumed a lack of selection on these genes, and wrongly assumed a constant background mutation rate. Another study that corrected for these problems found that only seven copies of HLA need have existed, which Gauger calls a “dramatically lower estimate for the number of HLA-DRB1 alleles in the ancestral population than the number Ayala found in his study (i.e. seven alleles versus thirty-two).” (p. 113) A later paper reported that HLA-DRB1 alleles numbered only four or five at the time of our supposed split from chimps. This number is low enough to have passed through a single couple.

Now of course Venema cites papers that looked at many other genes and their various alleles in the human genome. So there’s a lot more data that remains to be evaluated. But note why Gauger chose to study HLA genes:

I chose to look at the HLA-DRB1 story because it seemed to provide the strongest case from population genetics against two first parents. If it were true that we share thirty-two separate lineages of HLA-DRB1 with chimps, it would indeed cause difficulties for an original couple. But as we have seen, the data indicate that it is possible for us to have come from just two first parents.

(Science and Human Origins, p. 120)

For a short online summary of Gauger’s argument, see here.

A Prescient Warning

If perhaps the strongest argument against Adam and Eve — from population genetics — has fallen apart, what will happen when other genes are similarly scrutinized? Of course we should wait and see what the evidence says, but Gauger’s warning is prescient:

[O]ne thing is clear right now: Adam and Eve have not been disproven by science, and those who claim otherwise are misrepresenting the scientific evidence.

(Science and Human Origins, p. 121)

Indeed, much data remains to be examined. And Gauger and some of her colleagues, such as Ola Hössjer, have been addressing that data. They have published two peer-reviewed papers that present models for potentially testing population genetics arguments against a first couple at our origin: 

• Ola Hössjer, Ann Gauger, and Colin Reeves, “Genetic Modeling of Human History Part 1: Comparison of Common Descent and Unique Origin Approaches,” BIO-Complexity, Vol. 2016 (3).
• Ola Hössjer, Ann Gauger, and Colin Reeves, “Genetic Modeling of Human History Part 2: A Unique Origin Algorithm,” BIO-Complexity, Vol. 2016 (4).

Their papers evaluate the assumptions underlying the standard evolutionary model of human origins and find “it is full of gaps and weaknesses.” The authors maintain that “a unique origin model where humanity arose from one single couple with created diversity seems to explain data at least as well, if not better.”

Created Founder Diversity

After reviewing five main mechanisms invoked by standard evolutionary models of population genetics to explain human genetic diversity (mutation, genetic drift, natural selection, recombination, and colonization and migration), the first paper observes:

Neo-Darwinism accounts for the above-mentioned mechanisms I-V, and among them germline mutations are essentially the only way by which novel DNA can arise. The theory does not allow for large amounts of new and suddenly appearing diversity. The reason is that neo-Darwinism is framed within methodological naturalism. This prevailing approach to science only allows for natural hypotheses. But if an intelligent designer is invoked as a possible explanation, and if humanity originates from one single couple, it is possible that their chromosomes were created with considerable diversity from the beginning.

Thus, the authors propose a sixth mechanism of genetic change, called created founder diversity. Created founder diversity is biologically plausible for DNA of non-sex chromosomes, and would allow for initial genetic diversity among all four sets of autosomes in the first couple.

The authors note that the “main argument against a unique origin is that the nucleotide diversity of human DNA data seems too high in order make a single founding couple possible.” But they argue it is possible that humans are descended from an initial couple if “they were created with genetic diversity in their autosomal and X-chromosome DNA.” They conclude: “Any common descent model faces a challenge to explain the genetic differences rather than the similarities with other species, the consequences of inbreeding depression and increased genetic entropy, human DNA mixture with archaic populations, and that our DNA resembles a mosaic of about four founder genomes.” Thus, they find, “The provisional conclusion is that a unique origin model seems more plausible.”

 Their second paper presents mathematical algorithms “for testing different historical scenarios of the human population,” including common ancestry models, and models where humans “all descend from one single couple.” Their mathematical approach can simulate human history by varying different parameters, including population expansion, bottlenecks, colonization and migration patterns, mating and reproduction schemes, and various types of mutations in autosomal chromosomes, sex chromosomes, and mitochondrial DNA. Additionally, “An important parameter of the model is the created diversity of the founder generation, since it facilitates a higher degree of genetic diversity for a relatively young population within autosomal and X chromosomal regions, and possibly also for mitochondrial DNA.”

Their algorithms incorporate what they identify as the six major mechanisms of genetic change: (i) genetic drift, (ii) genetic recombination, (iii) colonization and migration, (iv) mutations, (v) natural selection, and (vi) initial created founder diversity. They note that “common descent models only include the first five mechanisms, but (vi) is important in order to generate enough diversity for a population with only one founding couple.” Indeed, they observe that a “particularly important parameter is the created diversity, which makes it possible to obtain a substantial amount of genetic diversity for nuclear autosomal and X-chromosome DNA, during a relatively short period of time.”

After going through a detailed mathematical analysis of the model, they conclude, “In subsequent papers, we plan to simulate human DNA data from our proposed model in order to assess how well it fits real data,” with the ultimate goal of finding “the best fitting population history within a unique origin framework, and then to compare it with a best fitting common ancestry model.”

The Best Treatment of This Issue

Probably the best treatment of this issue found anywhere is the chapter “An Alternative Population Genetics Model,” by Ann Gauger, Ola Hössjer, and Colin Reeves in the book  Theistic Evolution: A Scientific, Philosophical, and Theological Critique. There, they find key human genomic diversity evidence is highly compatible with Adam and Eve:

Block Structure of DNA. A large part of our autosomal and X-chromosomes have apparently been recombined into blocks of varying length. Many of them are of the order 10,000 nucleotides long, but the variation in length is large. But even though the blocks are long, there is still very little variation within them. Each block comes in just a few variants, four for many parts of the genome. Our chromosomes are different mosaics of these block variants.

This DNA block structure is remarkably consistent with a unique origin hypothesis. If Adam and Eve were created with DNA diversity, there would have been four different copies of each autosomal chromosome — two in Adam and two in Eve. Their four chromosomes have since been scrambled by ancestral recombinations, and today each of us has one mosaic of the four founder chromosomes inherited from our father, and another one from our mother.

After reviewing various aspects of the genetic evidence, they conclude:

We have argued that a unique origin model (with a young or old age of humanity) with created diversity should have at least the same explanatory power for human genetic data as the most popular common descent scenario of today. Any model must be able to explain the big genetic differences between humans and other species, solve the problem of inbreeding depression, support the viability of human and archaic population admixtures, and give reasons why our DNA resembles a mosaic of about four founder genomes. The conclusion is that the unique origin model seems more plausible.

They end their chapter by discussing the models they are currently in the process of testing (the aforementioned technical papers).

We are currently working on implementing a model based on backward simulation. The intent is to validate it with real data. This is a long-term project, whose outcome we hope to publish elsewhere. Using this approach, it may be possible to demonstrate that a unique origin model is able to replicate current human diversity as well or better than the common descent model. That is the purpose of the model—to test this possibility. Therefore, if more than one plausible account of human origins can explain the data, the common descent model of our origin from ape-like ancestors can no longer be claimed as conclusive proof that there could not have been a single first pair. Thus, it would be premature to discard traditional interpretations of the reality and historicity of Adam and Eve.

Obviously  more work remains to be done. But if Venema wants to maintain that Adam and Eve are truly refuted, he’s going to have to contend with this modelling research, which isn’t complete, but already points in a promising direction.

In fact, Venema did respond — though only very briefly, and very dismissively — to this work.  As we explained here,  on the BioLogos website Venema called the papers “a (poor) attempt to argue for a predetermined conclusion that humans were specially created as a pair in the Middle East. It does not offer a mechanism to deal with the obvious problems of such an approach other than an appeal to ‘created diversity.’” University of Stockholm mathematician Ola Hössjer, who co-authored the papers, responded:

Venema basically criticizes the Middle East version of the unique origin model, saying the African DNA looks older than non-European DNA, both from single locus allele frequency statistics and from two locus linkage disequilibrium patterns. But we also point out that this is a drawback of the Middle East unique origin model (on the other hand we argue that a ME origin has other advantages, for instance less inbreeding depression). We offer some tentative explanations (reference 50, for instance) of why African DNA could look older even if humanity originated in the Middle East. Venema rules out these explanations as inadequate. This may very well be true, but it remains to be seen when the model is implemented.

It’s worth stating that these papers offer a model that can be used to test many scenarios, not just that of a single couple at our origin. The model will allow the examination of the effects of mutation rate, selection, recombination, population structure, and population history on patterns of genetic variability, in order to determine which scenarios best reproduce modern genetic diversity. As for the hypothesis of a single pair with created diversity, which Venema labels a “predetermined conclusion,” it is simply one hypothesis to be tested among many.

Moreover, initial “created diversity” is a legitimate, testable mechanism. We know how genetics works and we can decide whether (within the bounds of genetics) initial high diversity could account for present-day observations.

Unfortunately, critics of this work seem to want to reject the proposed model before it’s even been fully implemented. Dr. Venema complains of “predetermined conclusions.” But the criticism could be turned right around and applied to him, instead.