Darwinists try to get their theory off on a technicality

Biochemist Larry Moran Denies Darwin's Doubt, and We Doubt His Arguments

Ann Gauger September 3, 2015 5:44 AM

It has come to my attention that Larry Moran, professor of biochemistry at the University of Toronto, feels left out of the debate about Darwin's Doubt, documented in Debating Darwin's Doubt. He writes in a post on his blog that he's "a little miffed" about being omitted from the latter. Moran posted a number of critiques of Stephen Meyer's book, to which we offered no response at the time. No slight intended, Dr. Moran.

I have now taken a look at the first two of his posts, and noticed some biases. Moran showed a few illustrations that might impress the uninformed, but it's what he didn't say that is revealing.

Trees seeking to represent the history of life are drawn to convey different meanings. Moran's tree shows the diversity of life from a phylogenetic view. Of course, unicellular organisms represent the vast majority of this tree, leaving plants, animals, and fungi to one tiny portion of the tree, indicated by a circle. Moran implies that this indicates the Cambrian explosion was a mere blip. What he doesn't say is that the Cambrian explosion resulted in the sudden diversity of metazoa, or multicellular organisms like animals and seaweed, for which we have many fossils. As a portion of the diversity on the planet they may be a small fraction, but that doesn't mean the explosion wasn't real.

Take a look at Figure 1 from a paper on the subject ("The Cambrian 'explosion': Slow-fuse or megatonnage?") by Simon Conway Morris, an expert in the field. The first fossils for each group are indicated by solid circles. The branch points and putative common ancestors are indicated by asterisks, but have not been observed in the fossil record. To the left are the dates in millions of years. You can read across the tree and see that most of the phyla appear between about 525 and 535 million years ago. That is sudden in geologic time. The few groups present in the Vendian (pre-Cambrian) and still with us today include the fungi, the sponges, and sea anemones. All the rest of the phyla except one, which appears later, first come on the scene in the Cambrian. That is a short time for such basic differences in body plans to appear.

Morris ends his paper with this:

To conclude: The Cambrian explosion is real and its consequences set in motion a sea-change in evolutionary history. Although the pattern of evolution is clearer, the underlying processes still remain surprisingly elusive.

Moran's figure (where apparently a number of phyla have been demoted to classes) reveals the same problem. If you take into account where the circles (the crown groups) are, you will see that the major groups of animals first appear as fossils in the same narrow window. The rest of the branch points are phylogenetic inferences from molecular data, for which no fossils exist.

How did such diverse animals first appear? And how do we reconcile morphological data from fossils (and studies of modern representatives) with the molecular data that keeps pouring in? It is not so easy. A recent paper by Ronald Jenner ("Macroevolution of Animal Body Plans: Is There Science after the Tree?") acknowledges the problem. His abstract:

A renewed emphasis on the gaps in organization that exist between the crown-group body plans of higher-level animal taxa is a hallmark of the emerging consensus in metazoan phylogenetics. Bridging these gaps is the greatest hurdle that stands in the way of translating our knowledge of phylogeny into a renewed understanding of the macroevolution of animal body plans. Unless a good fossil record is available, there is little hope that we will be able to bridge many of these gaps empirically. We have, therefore, little choice but to resort to our more-or-less informed imagination to produce the historical narratives that are the ultimate goal of our studies of animal evolution. Only by fully engaging with the challenges of devising testable scenarios will we be able to tell where along the spectrum of science and fictionour understanding of animal body plan evolution will finally come to rest. [Emphasis added.]

Strong language. There's more in the paper:

The phylogenetic lineages of the major metazoan crown groups are discouragingly short in terms of the number of nodes available along each lineage for resolving the assembly of body plans. This seriously limits the resolution achievable by scenarios, especially in the absence of fossils, but before any evolutionary transformations between body plans can be traced, we must infer hypothetical ancestors. In their recent book on the Cambrian explosion, Erwin and Valentine (2013) likened our attempts to infer the body plans of ancient animal ancestors to séances. The older the nodes in question, the more apt this analogy is. The divergences between most pairs of higher-level crown-group-sister taxa are so significant that the inferences of hypothetical ancestral body plans are generally accompanied by substantial error bars. These become compounded as one integrates the inferences of increasing numbers of hypothetical ancestors to reach deeper and older nodes in the tree. Add to this matrix of uncertainty the potentially limitless play of our imagination, and our attempted explanatory historical narratives may end up being little more than untestable fiction.

Since these were some of the main points of Darwin's Doubt, perhaps it's fair to say there is reason to doubt that scientists have it all worked out. Sorry, Dr. Moran.

The end of the Wicked according to scripture

Carefully and prayerfully examine what these text of scripture state are destiny of the wicked and honestly ask yourself do the Holy scriptures support the Doctrine of eternal torment of the wicked,a thing that would necessitate their miraculous preservation or do the the scriptures indicate that the wicked will be eternally preserved or the reverse as their final punishment.


Psalm1:4-6NASB"The wicked are not so,
But they are like chaff which the wind drives away.Therefore the wicked will not stand in the judgment,

Nor sinners in the assembly of the righteous.For the Lord [a]knows the way of the righteous,

But the way of the wicked will perish."

Psalm7:9NASB"O let the evil of the wicked come to an end, but establish the righteous;

For the righteous God tries the hearts and [a]minds."

Psalm9:5NASB"You have rebuked the nations, You have destroyed the wicked;

You have blotted out their name forever and ever."

Psalm9:17NASB"The wicked will [a]return to [b]Sheol,
Even all the nations who forget God."

Psalm11:6NASB"Upon the wicked He will rain [a]snares;

Fire and brimstone and burning wind will be the portion of their cup."(Think Sodom and Gomorrah)

Psalm31:17ASV". Let me not be put to shame, O Jehovah; for I have called upon thee: Let the wicked be put to shame, let them be silent in Sheol."(Emphasis mine)

Psalm34:21NASB"Evil shall slay the wicked,

And those who hate the righteous will be [a]condemned."

Psalm37:10NASB"Yet a little while and the wicked man will be no more;

And you will look carefully for his place and he will not be there."

Psalm37:20NASB"But the wicked will perish;
And the enemies of the Lord will be like the [a]glory of the pastures,
They vanish—like smoke they vanish away."

Psalm37:28NASB"For the Lord loves [a]justice
And does not forsake His godly ones;
They are preserved forever,
But the [b]descendants of the wicked will be cut off."

Psalm37:ASV"Wait for Jehovah, and keep his way, And he will exalt thee to inherit the land: When the wicked are cut off, thou shalt see it."

Psalm37:38ASV"As for transgressors, they shall be destroyed together; The end of the wicked shall be cut off."

Psalm58:10ASV"The righteous shall rejoice when he seeth the vengeance: He shall wash his feet in the blood of the wicked;"

Psalm68:2ASV"As smoke is driven away, so drive them away: As wax melteth before the fire, So let the wicked perish at the presence of God."

Psalm75:8ASV"For in the hand of Jehovah there is a cup, and the wine foameth; It is full of mixture, and he poureth out of the same: Surely the dregs thereof, all the wicked of the earth shall drain them, and drink them."

Psalm75:10ASV"All the horns of the wicked also will I cut off; But the horns of the righteous shall be lifted up."

Psalm92:7NASB"When the wicked spring as the grass, And when all the workers of iniquity do flourish; It is that they shall be destroyed for ever."(Emphasis Mine)

Psalm94:23ASV"And he hath brought upon them their own iniquity, And will cut them off in their own wickedness; Jehovah our God will cut them off."(We see the issue proportionality being mentioned whatever suffering is brought upon the wicked must be proportional to the suffering they have caused even Satan himself has only been able to cause a finite amount of suffering)

Psalm101:8ASV"Morning by morning will I destroy all the wicked of the land; To cut off all the workers of iniquity from the city of Jehovah."

Psalm104:35ASV" Let sinners be consumed out of the earth. And let the wicked be no more. Bless Jehovah, O my soul. Praise ye Jehovah."

Psalm106:18ASV"And a fire was kindled in their company; The flame burned up the wicked."

Psalm112:10ASV"The wicked shall see it, and be grieved; He shall gnash with his teeth, and melt away: The desire of the wicked shall perish"

Psalm119:119ASV"Thou puttest away all the wicked of the earth like dross: Therefore I love thy testimonies."

Psalm139:19ASV" Surely thou wilt slay the wicked, O God: Depart from me therefore, ye bloodthirsty men."

Psalm141:10ASV"Let the wicked fall into their own nets, Whilst that I withal escape."(Again how much suffering can the wicked cause in a finite lifetime)

Psalm145:20ASV"Jehovah preserveth all them that love him; But all the wicked will he destroy."

Proverbs2:22ASV"But the wicked shall be cut off from the land, And the treacherous shall be rooted out of it."

Proverbs5:22ASV"His own iniquities shall take the wicked, And he shall be holden with the cords of his sin."(Jah's chastisement is justly proportionate)

Proverbs10:7ASV"The memory of the righteous is blessed; But the name of the wicked shall rot."(They will not even be mourned or memorialised in any way)

Proverbs10:25ASV"When the whirlwind passeth, the wicked is no more; But the righteous is an everlasting foundation."(See Jeremiah25:32,33)

Proverbs10:27ASV"The fear of Jehovah prolongeth days; But the years of the wicked shall be shortened."(The length of their existence will be cut short i.e the opposite of preserved.)

Proverbs10:28ASV" The hope of the righteous shall be gladness; But the expectation of the wicked shall perish."

Proverbs10:30ASV"The righteous shall never be removed; But the wicked shall not dwell in the land."(what would being excluded from the presence of an omnipresent God entail.)

Proverbs11:7ASV"When a wicked man dieth, his expectation shall perish; And the hope of iniquity perisheth." 

Proverbs11:8ASV"The righteous is delivered out of trouble, And the wicked cometh in his stead."

Proverbs11:10ASV" When it goeth well with the righteous, the city rejoiceth; And when the wicked perish, there is shouting."

Proverbs12:7ASV"The wicked are overthrown, and are not; But the house of the righteous shall stand."(Emphasis Mine)

Proverbs13:9ASV"The light of the righteous rejoiceth; But the lamp of the wicked shall be put out."

Ecclesiastes8:13ASV "but it shall not be well with the wicked, neither shall he prolong his days, which are as a shadow; because he feareth not before God."

So unfiltered by man made dogma.The wicked and their ways meet the same end.Both they and the distress they have caused vanish forever consigned by God and his messiah to the realm of dreams and shadows So that even their very memory will be no more i.e if words are to have definite contextually determined meanings.

On staying safe online

Darwinism vs the real world IX

Growing a Bone Requires Foresight
Evolution News & Views August 31, 2015 3:39 PM


Picture a linear bone growing. Say it's a leg bone, with attachment points for muscles and tendons along its length. Picture one such protrusion located a third of the way from one end. If the bone grows only at one end, the protuberance will migrate from its 1/3 position, causing problems for the tissues that need to attach there. If the bone grows at both ends, the same problem can occur.

How does the bone "know" to keep its structures at proper ratios along its length as it grows? That problem was investigated by a team of Israeli scientists publishing in PLOS Biology.

Although bidirectional elongation is a universal mechanism for bone growth, it nevertheless introduces a major challenge to bone morphogenesis. A fundamental characteristic of the unique morphology of each long bone is a set of protrusions of varying shapes and sizes, which are scattered along the exterior of the bone and thus break its morphological symmetry. These superstructures, known as bone ridges, tuberosities, condyles, etc., are necessary for the attachment of tendons and ligament as well as for articulation. To perform these functions they are located at specific positions along the bone. Bone superstructures emerge during early skeletogenesis. During growth, bones elongate extensively by advancement of the two growth plates away from the superstructures. It is therefore expected that during elongation, superstructures would remain at their original position near the center of the bone. Nevertheless, the end result is proper spreading of superstructures along the mature bone, which clearly implies the existence of a morphogenetic mechanism that corrects their locations. [Emphasis added.]
Bones end up with the right ratios, in other words, but how do they get that way? The team wanted to know if bone growth is isometric ("same-measure") or allometric ("other-measure"). If isometric, the bone's ratios should be maintained during growth. If allometric, the ratios should converge on the proper position at the end of growth. They were surprised at the result and the implications:

Strikingly, analysis revealed that the relative position of all superstructures along the bone is highly preserved during more than a 5-fold increase in length, indicating isometric scaling. It has been suggested that during development, bone superstructures are continuously reconstructed and relocated along the shaft, a process known as drift. Surprisingly, our results showed that most superstructures did not drift at all. Instead, we identified a novel mechanism for bone scaling, whereby each bone exhibits a specific and unique balance between proximal and distal growth rates, which accurately maintains the relative position of its superstructures. Moreover, we show mathematically that this mechanism minimizes the cumulative drift of all superstructures, thereby optimizing the scaling process. Our study reveals a general mechanism for the scaling of developing bones. More broadly, these findings suggest an evolutionary mechanism that facilitates variability in bone morphology by controlling the activity of individual epiphyseal plates.
It's strange to see "evolutionary" and "mechanism" juxtaposed, since the former means blind and unguided, but the latter means organized for a purpose. Indeed, there is a purposeful function going on in bone growth: to keep the bone's ratios to its superstructures constant. The mechanism required to achieve it implies that both of the growth plates have to "talk" to each other and continually adjust their growth rates so that the structures do not drift.

But that's not enough. The structures have to drift a little, because otherwise they would grow closer to the center as the ends elongate. Drift is achieved by a structure dissolving bone on the inner side and re-growing it on the outer side. In this way, the ratios between them are maintained from earliest embryonic stages through adulthood.

The level of control required to achieve isometric grown implies irreducible complexity and hierarchical control. Apparently the controls are different in different parts of the body. They point, for instance, to earlier findings that "forelimb bones tend to grow away from the elbow joint, whereas bones in hind limbs tend to grow toward the knee joint." Even though they are evolutionists, they admit there's no evidence this mechanism evolved.

These findings and ours clearly imply the existence of additional mechanisms that control the specific activity of each growth plate. Interestingly, some of these works were performed on other model animals such as rat, pig, rabbit, chick, and humans, suggesting that asymmetric growth of long bones is evolutionarily conserved across species.
Can their concluding summary be incorporated into a neo-Darwinian mechanism involving blind process of mutation and selection? Put yourselves in their shoes and try to imagine a way to Darwinize the findings:

In this work, we uncover the isometric nature of longitudinal scaling of long bones during growth. Using a newly developed algorithm, we recover for the first time, to our knowledge, the morphogenetic sequence of developing long bones from early embryonic stages to maturity. These data enabled us to provide accurate assessments of both the specific activity of the different growth plates and the drifting patterns of symmetry-breaking elements along the bone shaft. Based on these analyses, we conclude that longitudinal growth patterns in each bone are adjusted to preserve isometry. The constant tendency of the growth balance to protect element positions strongly suggest that symmetry-breaking elements are involved in the mechanism that regulates the differential activity of growth plates.
There's design hidden in their passive verbs; "patterns ... are adjusted"; "symmetry-breaking elements are involved in the mechanism that regulates" the activity. But how could a mutation to the growth plate at one end of a bone affect the regulation of a growth plate at the other end? How could a mutation that causes symmetry-breaking in the drift of one structure affect the coordinated outcome of the other structures? And how could mere chance orchestrate all the dynamic elements at play in the growth of a bone and its superstructures to end up with a functional adult bone, with all its muscles, tendons, and ligaments attached at the right places, so that the leg or arm actually works? When Haeckel drew those embryos, he had no idea what he was oversimplifying!

In a companion article in PLOS Biology, ("Make No Bones about It: Long Bones Scale Isometrically"), science writer Caitlin Sedwick mentions another interesting finding:

Unexpectedly, the authors' analysis showed that, while a few elements do drift, the rest do not. In fact, the researchers found that for each bone, a transverse plane can be drawn at the location where the ratio of the plane's distance to either end equals the ratio of growth rates at the respective ends (Fig 1, top panel). This "fixed plane" always falls nearby the non-drifting elements, and only the elements that are significantly distant from this plane show evidence of drift. However, the location of the fixed plane, and therefore an element's relationship to it -- which predicts the amount of drift needed to maintain the element's relative position on the bone -- will shift during development if the ratio of growth rates at the ends change.
The "fixed plane" is, therefore, another element that must also be under regulatory control. The two growth plates and the fixed plane are regulated together to minimize drift and optimize the energy needed to maintain isometric scaling.


What seems obvious here is an overarching design plan that operates with top-level control. The process needs to foresee a desired end point, and coordinate all the activities at multiple levels, from the body plan down to the cellular machines, to achieve it. Such mechanisms can be programmed to work autonomously, but are inaccessible to natural processes lacking foresight.

Yet more on life's anti-Darwinian bias III

Devolution: Getting Back to the Simple Life
Denyse O'Leary August 31, 2015 3:17 AM

As we have seen already in this series, evolution can occur via horizontal gene transfer and epigenetics, both of which add information to a life form by non-Darwinian means -- that is, not by natural selection acting on random mutation of the genome.

Talk to the Fossils.jpgThe information added by epigenesis and horizontal gene transfer is not random. For example, assume that male parents' alcoholism is consistently associated with disrupted patterns in children's genes. The effects of excess alcohol, far from being random, are a predictable, law-like chain of chemical cause and effect. Similarly, bacteria don't randomly share antibiotic resistance via horizontal gene transfer. Rapid development of resistance among whole colonies is a longstanding, law-like pattern that maintains a colony's ecology, a pattern recently traced back to millennia before humans began to develop antibiotics.

Today, we often hear that these non-random mechanisms of evolution are consistent with Darwinian evolution (the Modern Synthesis). So, nothing has really changed after all!

Not so fast. Darwinian evolution (Darwinism) had better be consistent with all demonstrated mechanisms of change. Unlike horizontal gene transfer, it has proven difficult to witness, and proponents have relied largely on the assumption that it is "the only known theory that is in principle capable of explaining certain aspects of life." What's changed is that it can no longer be considered equivalent to "evolution." It must compete with other known mechanisms.

Most of the time, when we think of evolution, we mean mechanisms for the growth of complex new information. After all, entropy (the tendency for disorder to increase over time) can satisfactorily explain loss of information. Yet, in the history of life, some forms survive while -- or even by -- losing information (devolution). Their history may tell us something useful too.

We all know devolution when we see it -- a jar of pennies becomes a doorstop, a computer becomes a boat anchor, the XYZ volume of the Encyclopedia props up a too-short table leg.

But interest in devolution of life forms spiked with the recent discovery of giant viruses, which a 2014 editorial at The Scientist considered a possible fourth domain of life.

The giant mimivirus for example, unlike conventional viruses, "carries many genes thought to be unique to cellular life, suggesting that it evolved from a cell."
If so, strictly speaking, it "devolved" from a cell. Information was lost, not gained. Perhaps the unicellular life form was unable to survive intact, but some remnant survives as a virus.

New Scientist announced in 2011 that, "World's largest virus proves giants came from cells." The idea is a reasonable one, though some, including National Geographic, now think that giant viruses preceded cells instead. We don't really know as yet.

The viruses have, however, infected researchers with incorrect thoughts. A discoverer of a giant virus encased in ice for 30,000 years observed (2014):

"We thought it was a property of viruses that they pack DNA extremely tightly into the smallest particle possible, but this guy is 150 times less compacted than any bacteriophage [viruses that infect bacteria]. We don't understand anything anymore!"
Didier Raoult, the discoverer of giant Marseillevirus said, provocatively, in 2009, "The idea of a common ancestor makes no sense in the light of viruses. That was Darwin's idea, but he was clearly wrong." Raoult, also the discoverer of the mimivirus (2003), considered "the most productive and influential microbiologist in France" according to Science, published a pop science book in 2011 that "flat-out declares that Darwin's theory of evolution is wrong."

Well, here are some things we can be reasonably sure of:

-- Sometimes, devolution offers an apparent advantage. Many plankton microbes eliminated the genes for producing key vitamins, and now outsource the function. One account suggests, "... most of the time, the fitness advantages of smaller genomes and lower cell replicating costs offset the potential fitness gains that would come from vitamin manufacture when the required nutrients are in short supply." Similarly, while functioning cell walls are thought to be critical to life forms, we are told that many bacteria can switch to a cell wall-deficient "L-form" state, "completely resistant to many antibiotics," and possibly ignored by our immune systems.

-- Similarly, some researchers believe that the Amanita mushroom group has devolved to a successful parasite on trees by losing the genes associated with breaking down cellulose. It's possible that the Amanitas were crowded by ground-level competitors and devolution enabled them to exploit a new niche.

-- Sometimes, however, the advantage is not clear. A brain part, the anterior sclerite, present in arthropods of 500 million years ago, is no longer extant. It is thought to be linked with bulbous eyes, but without further information, it's impossible to say why it is apparently no longer required.

-- Similarly, the Cambrian shrimp's heart (520 mya) was more complex than the modern one: "The level of complexity of the Fuxianhuia was extremely high, considering that we are studying some of the oldest animals on Earth." A 305-million-year-old harvestman (spiderlike arachnid) fossil has two sets of eyes (pictured above), but current descendants have one functional pair and one vestigial pair, apparently without suffering any adverse effect. But we would need to know much more than we do about the history of life to know why decreasing complexity was neutral or advantageous in each case.

-- One devolved amphibian is visually almost indistinguishable from an earthworm. Similarly, a newly discovered blind, legless lizard is described as having "evolved to live underground," though again, that should really be devolved.

-- Sometimes a pattern emerges. A study that investigated evolution in nematode worms, including the strain that survived the 2003 Columbia space shuttle crash, shows that under artificially stressed lab conditions, the worms all lost the same gene.

In some cases, particular aspects of Darwinian evolution have proved false by discoveries of devolution. One Darwinian doctrine, called Dollo's Law, formulated about 1890 by Belgian paleontologist Louis Dollo, states that a trait once lost cannot be regained.

No one seems to have told the life forms about it. For example, researchers were surprised to find one creature:

... in the aquifers beneath the Western Australian desert, which challenges the traditional Darwinian view of evolution. They have discovered that a species of blind predatory water beetles -- living underground for millions of years -- express vision genes (opsin) which are usually only found in species with eyes.
Losses can be reversed. Blind Mexican cavefish are considered an excellent model for studying evolution, with revealing results. In the lab, researchers have mated blind cave fish from separate and distant underwater caves and produced sighted offspring. Apparently, separate mutations had produced the blindness, and some hybrid offspring inherited a mix that includes enough genes for functioning sight. So no irrevocable devolution had taken place after all.

We are told that, with "dwindling evidence for the law-like nature of Dollo's Law" opinions are reversing because "large genomics databases and evo-devo studies are showing how the underlying developmental pathways and genetic architecture can be retained after the loss of a character."

Evolutionary biologists still have an odd relationship with devolution, to judge from items in Scientific American over the last two decades. First, we encounter obfuscation:

From a biological perspective, there is no such thing as devolution. All changes in the gene frequencies of populations -- and quite often in the traits those genes influence -- are by definition evolutionary changes.
...

Another misconception is that increasing complexity is the necessary outcome of evolution. In fact, decreasing complexity is common in the record of evolution. For example, the lower jaw in vertebrates shows decreasing complexity, as measured by the numbers of bones, from fish to reptiles to mammals. (Evolution adapted the extra jaw bones into ear bones.) Likewise, ancestral horses had several toes on each foot; modern horses have a single toe with a hoof.

This approach doesn't quite make sense. It fudges the fact that loss and gain of information are not the same thing. Loss needs no explanation other than entropy; gain requires new sources of complex, specified information.

Even writers in the same publication seem to contradict themselves about the existence of devolution. In 2012, a Scientific American blog reported on a new study that argued humans are devolving so as to be dumber: "Homo (Sans) Sapiens: Is Dumb and Dumber Our Evolutionary Destiny?"

Gerald Crabtree, a biologist at Stanford University, has put forward a provocative hypothesis that our cushy modern existence -- absent the ceaseless pressures of natural selection experienced during the Paleolithic -- makes us susceptible to the slow creep of random genetic mutations in the 2,000 to 5,000 genes needed to ensure that our intellectual and emotional makeup remains intact.
Others, we were told, disagree with Crabtree: The social world we live in is complex, so "we haven't in fact lost the selection process that kept the pressure on" to remain intelligent. But if Darwinian natural selection both produces high intelligence, and is needed to sustain it, why did it work only once, for humans? And does anyone really believe that social rejection today is the same as the life-and-death struggles of the Paleolithic?

In 2014, Scientific American, on a more serious note, informed us, with respect to those blind cave fish:

In the classic view of evolution, organisms undergo random genetic mutations, and nature selects for the most beneficial ones. A recent study in Science adds a twist to that theory: variability already present in a population's genome may remain hidden in times of plenty but come unmasked in stressful situations, ready to help with adaptation.
This is, we are told, still "a topic of active research." That is a good approach, better than insisting that traditional Darwinian concepts offer all the insight we need as long as we can cut the subject down to size. Because, one way or another, it's just not Darwin's evolution any more.


A variety of other non-Darwinian mechanisms of evolution may produce some change in some life forms, and we shall shortly give them each their turn in the spotlight.

The Watchtower Society's commentary on 'Antichrist'

ANTICHRIST

This word means “against (or instead of) Christ.” It occurs a total of five times, singular and plural, all of them in two of John’s epistles.

The subject was not new among the Christians when John wrote his letters (c. 98 C.E.). First John 2:18 states: “Young children, it is the last hour, and, just as you have heard that antichrist [Gr., an·tiʹkhri·stos] is coming, even now there have come to be many antichrists; from which fact we gain the knowledge that it is the last hour.” John’s statement shows that there are many individual antichrists, though all together they may form a composite person designated “the antichrist.” (2Jo 7) The use of the expression “hour” as referring to a period of time, either relatively brief or of undetermined length, is exemplified in other writings of John. (See Joh 2:4; 4:21-23; 5:25, 28; 7:30; 8:20; 12:23, 27.) He thus did not restrict the appearance, existence, and activity of such antichrist to some future time only but showed that the antichrist was then present and would continue on.—1Jo 4:3.

Identification. Although there has been much effort in the past to identify “the antichrist” with an individual, such as Pompey, Nero, or Muhammad (this latter person being suggested by Pope Innocent III in 1213 C.E.), or with a specific organization, as in the Protestant view of “the antichrist” as applying to the papacy, John’s inspired statements show the term to be broad in its application, embracing all those who deny that “Jesus is the Christ,” and who deny that Jesus is the Son of God who came “in the flesh.”—1Jo 2:22; 4:2, 3; 2Jo 7, NE, NIV; compare Joh 8:42, 48, 49; 9:22.

Denial of Jesus as the Christ and as the Son of God of necessity embraces the denial of any or all of the Scriptural teachings concerning him: his origin, his place in God’s arrangement, his fulfillment of the prophecies in the Hebrew Scriptures as the promised Messiah, his ministry and teachings and prophecies, as well as any opposition to or efforts to replace him in his position as God’s appointed High Priest and King. This is evident from other texts, which, while not using the term “antichrist,” express essentially the same idea. Thus, Jesus stated: “He that is not on my side is against me, and he that does not gather with me scatters.” (Lu 11:23) Second John 7 shows that such ones might act as deceivers, and hence the “antichrist” would include those who are “false Christs” and “false prophets,” as well as those who perform powerful works in Jesus’ name and yet are classed by him as “workers of lawlessness.”—Mt 24:24; 7:15, 22, 23.

In view of Jesus’ rule that what is done to his true followers is done to him (Mt 25:40, 45; Ac 9:5), the term must include those who persecute such ones, which means it would include the symbolic “Babylon the Great.”—⁠Lu 21:12; Re 17:5, 6.

John specifically mentions apostates as among those of the antichrist by referring to those who “went out from us,” abandoning the Christian congregation. (1Jo 2:18, 19) It therefore includes “the man of lawlessness” or “son of destruction” described by Paul, as well as the “false teachers” Peter denounces for forming destructive sects and who “disown even the owner that bought them.”—2Th 2:3-5; 2Pe 2:1; see MAN OF LAWLESSNESS.

Kingdoms, nations, and organizations are similarly shown to be part of the antichrist in the symbolic description at Revelation 17:8-15; 19:19-21.—Compare Ps 2:1, 2.


In all the above cases those composing the antichrist are shown to be headed for eventual destruction as a recompense for their opposing course.

Darwinism vs the real world VIII

Cardiovascular Function: Heart Failure Is a Problem for Patients -- and for Evolutionary Theory

Howard Glicksman August 28, 2015 11:41 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.

Since the body is made up of matter, it must live within the laws of nature. These laws demand that the body have enough energy to propel the amount of blood needed through the circulatory system to give its cells what they need to live. To do this, the heart must have enough power to overcome forces like inertia, friction, and gravity, which naturally prevent blood from moving anywhere.

The last few articles in this series have shown that the heart is a pump with its own blood supply, efficient one-way valves, and an electrical system that coordinates muscle contraction. In addition, experience teaches that the body uses the autonomic nervous system to control how hard and fast the heart pumps so it can meet its metabolic needs. Moreover, medical science has been able to determine the numerical values of these metabolic needs and how much blood the heart would have to pump out per minute to achieve them. The normal cardiac output at complete rest is about five liters per minute, but with maximal activity, the type our earliest ancestors would have needed to do to survive, the cardiac output needs to be at least 25 liters per minute.

Evolutionary biology may use its imagination to explain how human life and the cardiovascular system came into being, but it does so without taking into account the specific numbers that heart function must achieve so the body can survive. That's like trying to explain how the blueprints for a car and its assembly came about without taking into account its performance on the road. In other words, they explain how human life looks without taking into account how it actually works.

We have already seen that for the heart to perform well enough for our earliest ancestors to survive, their coronary arteries would need to have been wide enough to accommodate enough blood flow. How do we know this? Clinical experience shows that people with coronary artery disease and restricted blood flow to the heart muscle are incapable of performing the kinds of activities that would have been needed for survival.

We have also seen that for the heart to have been able to perform well enough for our earliest ancestors to survive, the valves within it would need to have been open wide enough to let enough blood flow forward and close tight enough to not let any blood go backwards. How do we know this? Because clinical experience shows that people with thickened valves, causing restricted forward blood flow, and/or weakened valves, causing leakage of blood backwards, have reduced cardiac efficiency, leading to weakness and shortness of breath often with limited activity. Now let's consider heart muscle function itself and its effect on survival capacity.

As you may recall, the cardiac cycle is made up of one-third systole and two-thirds diastole. During the diastolic phase, the heart relaxes and the ventricles fill up with blood. At rest, the volume of blood in the ventricle at the end of diastole (EDV) is usually about 120 mL. Systole then begins with ventricular contraction and the amount of blood pumped out with each heart beat is called the stroke volume (SV). At rest, the SV is usually about 70 mL. The ejection fraction (EF) is the ratio between the SV and EDV, showing what percentage of blood is pumped out of the ventricle with each heartbeat. The EF is a measure of how well the ventricle contracts. At rest the EF is usually about 60 percent (70/120) and the heart rate (HR) is about 72 beats per minute. The cardiac output (CO) is the amount of blood flowing out of the heart every minute. It can be calculated by the formula: CO = SV x HR. This means that the CO is directly related to the SV and HR. If the SV and HR both rise, so does the CO, and if they both fall, so does the CO.

Using this formula we can see that, at rest, the CO is usually about 5 L/min (70 times 72). Finally, with extreme levels of activity, the autonomic nervous system causes the heart to pump harder and faster. With maximum stimulation the EDV and EF can rise so the SV can be about 125 mL and the HR can rise to 200 beats per minute. This results in a CO of 25 L/min (125 times 200). Clinical experience teaches that if the heart of our earliest ancestors could not have achieved these high levels of cardiac output, they never could have survived to reproduce. How do we know this? Heart failure.

When the heart cannot meet the metabolic needs of the body it is said to be in heart failure. This common condition can involve either the left or right ventricle, or both at the same time. Left ventricular failure can also be systolic, with diminished contractility during systole, or diastolic, with reduced relaxation and filling of the ventricle during diastole. Coronary artery disease, resulting in diminished blood flow, and frequently damage to the heart muscle, is the commonest cause of systolic heart failure. The hallmark of this condition is an EF below normal, often with a lower SV, because the myocardium can't contract well. Coronary artery disease, hypertension, and aortic stenosis, which causes the heart muscle to thicken, are common causes of diastolic heart failure. This muscle thickening results in stiffening of the ventricular walls and limits the entry of blood during diastole which lowers the EDV and the SV as well.

Most people with heart failure can function well at rest. And for those who have mild heart failure, the heart can compensate by increasing the heart rate and size of the ventricular cavity, allowing for activities like slow walking. But for people with significant heart failure, increased levels of activity are physically impossible because their CO can't match their body's metabolic needs. In other words, real numbers can lead to debility.

People with heart failure must live relatively sedentary lives. They are incapable of performing at the high levels of activity that our earliest ancestors would need to have been able to perform to win the battle for survival. When trying to explain how human life came into being, there should be some discussion about how the heart just so happens to have the right amount of ventricular contractility and relaxation to allow its output to meet the metabolic needs of the body.

So far in this series I've demonstrated how impaired coronary blood flow, valve dysfunction, and heart failure can each lead to significant debility, and we have discussed related problems posed for evolutionary explanations of our biological origins. However, there is still one more cardiac problem to consider when it comes to how real numbers can result in debility. That's what we'll look at next time.