Monday, 31 August 2015
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.
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.
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.
Sunday, 30 August 2015
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.
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
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.
Saturday, 29 August 2015
Just another gatekeeper?
In Covering Intelligent Design, Wikipedia's Editors Engage in "Information Sabotage"
Thursday, 27 August 2015
Yet more on the ancient roots of Darwinism
The Ancient Philosophical Roots of Darwinism
Six centuries before the Christian era (B.C.E.), the Greek philosopher Anaximander asserted that the first living things emerged from formless matter and then underwent transmutations to produce a wide variety of forms. In what some commentators regard as a primitive form of evolutionary theory, Anaximander apparently held that humans descended from some other species of animal -- probably a fish.48 In the fifth century B.C.E., the Greek philosopher Empedocles taught that the chance interplay of earth, air, fire and water produced disconnected organs and limbs that wandered aimlessly about until they combined spontaneously to make whole creatures. Most of the resulting combinations were monstrosities -- with faces and breasts on the back as well as front, or half ox and half human -- that were so maladapted that they perished. Among the few that survived were creatures that eventually developed into modern humans.49
Leucippus and Democritus in the fifth century B.C.E. and Epicurus in the fourth century B.C.E. advocated a materialistic philosophy in which no gods exist -- only atoms and the void.50 In the first century B.C.E., the Roman philosopher Lucretius immortalized this view in his long poem “On the Nature of Things.” Book Five begins with an attack on religion and teleology, then it lays out a theory of survival of the fittest that is remarkably similar to Darwin’s. Although Lucretius did not suggest that all living things are descended from a common ancestor, he believed that all things -- including living organisms and human beings -- are products of aimless interactions among atoms. If they are well adapted to their environment, they survive and leave descendants; if not, they perish.51
Some modern followers of Charles Darwin regard these ancient thinkers as their intellectual forebears. According to a 1996 statement on a pro-evolution web site maintained by the University of California at Berkeley, “evolutionary theory begins” with Anaximander. Although his ideas “drew on the religious and mythical ideas of his time, he was still one of the first to attempt an explanation of the origin and evolution of the cosmos based on natural laws.” Thus Anaximander’s theory “bears some resemblance to evolutionary theory.” According to the same web site Empedocles proposed a theory that “seems a bit bizarre today” but was nevertheless “a sort of evolutionary theory: Past natural selection is responsible for the forms we see today. Empedocles also ascribed the origin of the life of today to the interplay of impersonal forces, in which chance, not the gods, played the major role.” Thus the Greeks “led the way in developing a general scientific worldview -- one in which natural, non-miraculous explanations for the causes of phenomena were sought.”52
Of course, there were differences between the ideas of the ancient Greeks and modern evolutionary theory, but they were similar in one fundamental respect: They attributed cosmic and biological origins to unguided natural processes rather than divine design. As modern evolutionary biologist Ernst Mayr put it, the ancient Greek theories “constitute the first scientific revolution, so to speak, a rejection of supernatural in favor of materialistic explanations.”53
For Mayr and the author of the Berkeley evolution web site, and for other followers of Charles Darwin, “science” is synonymous with “materialistic explanation.” In this respect, they are following in the footsteps of ancient materialistic philosophers.
This is why modern controversies over evolution are not really about empirical science. Although many of Darwin’s followers believe that he presented overwhelming evidence for his theory, nothing could be further from the truth. The Origin of Species is just warmed-over materialistic philosophy, decorated with illustrations borrowed from nineteenth-century science.
Six centuries before the Christian era (B.C.E.), the Greek philosopher Anaximander asserted that the first living things emerged from formless matter and then underwent transmutations to produce a wide variety of forms. In what some commentators regard as a primitive form of evolutionary theory, Anaximander apparently held that humans descended from some other species of animal -- probably a fish.48 In the fifth century B.C.E., the Greek philosopher Empedocles taught that the chance interplay of earth, air, fire and water produced disconnected organs and limbs that wandered aimlessly about until they combined spontaneously to make whole creatures. Most of the resulting combinations were monstrosities -- with faces and breasts on the back as well as front, or half ox and half human -- that were so maladapted that they perished. Among the few that survived were creatures that eventually developed into modern humans.49
Leucippus and Democritus in the fifth century B.C.E. and Epicurus in the fourth century B.C.E. advocated a materialistic philosophy in which no gods exist -- only atoms and the void.50 In the first century B.C.E., the Roman philosopher Lucretius immortalized this view in his long poem “On the Nature of Things.” Book Five begins with an attack on religion and teleology, then it lays out a theory of survival of the fittest that is remarkably similar to Darwin’s. Although Lucretius did not suggest that all living things are descended from a common ancestor, he believed that all things -- including living organisms and human beings -- are products of aimless interactions among atoms. If they are well adapted to their environment, they survive and leave descendants; if not, they perish.51
Some modern followers of Charles Darwin regard these ancient thinkers as their intellectual forebears. According to a 1996 statement on a pro-evolution web site maintained by the University of California at Berkeley, “evolutionary theory begins” with Anaximander. Although his ideas “drew on the religious and mythical ideas of his time, he was still one of the first to attempt an explanation of the origin and evolution of the cosmos based on natural laws.” Thus Anaximander’s theory “bears some resemblance to evolutionary theory.” According to the same web site Empedocles proposed a theory that “seems a bit bizarre today” but was nevertheless “a sort of evolutionary theory: Past natural selection is responsible for the forms we see today. Empedocles also ascribed the origin of the life of today to the interplay of impersonal forces, in which chance, not the gods, played the major role.” Thus the Greeks “led the way in developing a general scientific worldview -- one in which natural, non-miraculous explanations for the causes of phenomena were sought.”52
Of course, there were differences between the ideas of the ancient Greeks and modern evolutionary theory, but they were similar in one fundamental respect: They attributed cosmic and biological origins to unguided natural processes rather than divine design. As modern evolutionary biologist Ernst Mayr put it, the ancient Greek theories “constitute the first scientific revolution, so to speak, a rejection of supernatural in favor of materialistic explanations.”53
For Mayr and the author of the Berkeley evolution web site, and for other followers of Charles Darwin, “science” is synonymous with “materialistic explanation.” In this respect, they are following in the footsteps of ancient materialistic philosophers.
This is why modern controversies over evolution are not really about empirical science. Although many of Darwin’s followers believe that he presented overwhelming evidence for his theory, nothing could be further from the truth. The Origin of Species is just warmed-over materialistic philosophy, decorated with illustrations borrowed from nineteenth-century science.
On why Darwinism loses on every sale.
A Leaky Faucet: Why Darwinian Evolution Leads to Loss of Information
Ann Gauger August 26, 2015 11:03 AM
In 2010 biochemist Michael Behe published a paper in the Quarterly Review of Biology in which he concisely stated the first rule of adaptive evolution: "Break or blunt any functional coded element whose loss would yield a net fitness gain." By this he meant several things. First, there are indeed adaptive mutations -- that is, mutations that yield a benefit to the cell under a particular set of circumstances. Second, the primary way such adaptation occurs is by breaking or inactivating some non-essential pre-existing function, in order to make the cell more fit, more competitive than its neighbors.
Behe was talking about microbes -- viruses and bacteria -- but his rule also applies at the cellular level in higher organisms. The best example where this rule is played out is in cancer. Cancers develop when one or more normal functions in a cell are disrupted or broken. The ironic thing is that for the cancer cells, this breaking increases their fitness, their rate of growth and cell division, and thus is beneficial -- to them. Normal constraints have been removed, allowing uncontrolled growth. For the cancer cell that's good, but bad for us, of course. So one can say that cancer is a prime example of what adaptive evolution can accomplish on the multicellular level, by breaking or disrupting some normal function.
What does Behe's first rule of adaptive evolution say about evolution in general? If most "beneficial" mutations are due to the loss of something rather than a gain of something, we are losing information when most adaptations occur, sometimes irreversibly. Let me give an example.
Microbiologist Ralph Seelke and I published a paper in 2010 where we demonstrated that cells always, or nearly always, take the easiest road to success. Given a choice between a simple two-step path leading to repair of two genes needed to make tryptophan, versus a one-step path that eliminated expression of the those genes, only one out of a trillion cells went down the path toward making tryptophan, even though that path would ultimately be much more beneficial. Why did this happen?
The genes to be repaired were overexpressed -- too much of their products were made. Because one of the genes was broken in two places, no tryptophan could be made. Thus both genes were expensive to keep around. It was easier for the cell to break the useless genes than to repair them -- one step instead of two -- and the cells, having no foresight, took that path. Some of those cells deleted the genes, thus losing the information needed to make tryptophan for good.
Let me explain in everyday terms. A faucet leaking badly but with no way to hook it up to a hose is entirely useless. While it is relatively easy to repair the faucet, requiring only two parts, the owner of the faucet doesn't know that. Since he can do without the faucet, he is likely to cap it to stop the expense of the wasted water. But he has lost the ability to water his backyard using that faucet.
Like the clueless homeowner, evolution has no foresight and does not know there is a big payoff just two mutations away. If the cells can prevent the overexpression of the tryptophan genes or remove them in a single step, that's what they will do, especially since there are many more ways to inactivate a gene than to repair it. Any cell that does this instantly becomes more fit than its neighbors, because it is spending less energy making useless stuff.
In fact, that is what we observed. Nearly all the cells inactivated the genes (only one out of a trillion didn't). Some of the cells even deleted the genes, thus losing the capacity to make tryptophan for good. Darwinian evolution travels by the shortest road, without regard for where it's headed. And if the shortest road is to break an existing function -- to lose information -- that's the path it chooses.
I'm sure you can think of parallels in the business world, when only the bottom line, corporate fitness, is what matters, and executives have no long-term vision. They don't see how some things, if adjusted, may yield big payoffs. As a result, whole technologies can be decimated or lost in a push for efficiency, technologies that if maintained could prove vital in the future. But fortunately, unlike Darwinian evolution, we do have foresight and can plan ahead. We do have the capacity for innovation, and can make wise choices or correct our mistakes.
The process of innovation is the opposite of the first rule of adaptive evolution. In the biological world, the quickest road to adaptation may be to delete or inactivate genes that are not necessary. But you don't get new features by deleting information. Building something new, which is what is required to explain the diversity around us, requires more than the happenstance and selection of Darwinian evolution. It requires foresight, planning, and a clear picture of the goal. It requires intelligent design.
Ann Gauger August 26, 2015 11:03 AM
In 2010 biochemist Michael Behe published a paper in the Quarterly Review of Biology in which he concisely stated the first rule of adaptive evolution: "Break or blunt any functional coded element whose loss would yield a net fitness gain." By this he meant several things. First, there are indeed adaptive mutations -- that is, mutations that yield a benefit to the cell under a particular set of circumstances. Second, the primary way such adaptation occurs is by breaking or inactivating some non-essential pre-existing function, in order to make the cell more fit, more competitive than its neighbors.
Behe was talking about microbes -- viruses and bacteria -- but his rule also applies at the cellular level in higher organisms. The best example where this rule is played out is in cancer. Cancers develop when one or more normal functions in a cell are disrupted or broken. The ironic thing is that for the cancer cells, this breaking increases their fitness, their rate of growth and cell division, and thus is beneficial -- to them. Normal constraints have been removed, allowing uncontrolled growth. For the cancer cell that's good, but bad for us, of course. So one can say that cancer is a prime example of what adaptive evolution can accomplish on the multicellular level, by breaking or disrupting some normal function.
What does Behe's first rule of adaptive evolution say about evolution in general? If most "beneficial" mutations are due to the loss of something rather than a gain of something, we are losing information when most adaptations occur, sometimes irreversibly. Let me give an example.
Microbiologist Ralph Seelke and I published a paper in 2010 where we demonstrated that cells always, or nearly always, take the easiest road to success. Given a choice between a simple two-step path leading to repair of two genes needed to make tryptophan, versus a one-step path that eliminated expression of the those genes, only one out of a trillion cells went down the path toward making tryptophan, even though that path would ultimately be much more beneficial. Why did this happen?
The genes to be repaired were overexpressed -- too much of their products were made. Because one of the genes was broken in two places, no tryptophan could be made. Thus both genes were expensive to keep around. It was easier for the cell to break the useless genes than to repair them -- one step instead of two -- and the cells, having no foresight, took that path. Some of those cells deleted the genes, thus losing the information needed to make tryptophan for good.
Let me explain in everyday terms. A faucet leaking badly but with no way to hook it up to a hose is entirely useless. While it is relatively easy to repair the faucet, requiring only two parts, the owner of the faucet doesn't know that. Since he can do without the faucet, he is likely to cap it to stop the expense of the wasted water. But he has lost the ability to water his backyard using that faucet.
Like the clueless homeowner, evolution has no foresight and does not know there is a big payoff just two mutations away. If the cells can prevent the overexpression of the tryptophan genes or remove them in a single step, that's what they will do, especially since there are many more ways to inactivate a gene than to repair it. Any cell that does this instantly becomes more fit than its neighbors, because it is spending less energy making useless stuff.
In fact, that is what we observed. Nearly all the cells inactivated the genes (only one out of a trillion didn't). Some of the cells even deleted the genes, thus losing the capacity to make tryptophan for good. Darwinian evolution travels by the shortest road, without regard for where it's headed. And if the shortest road is to break an existing function -- to lose information -- that's the path it chooses.
I'm sure you can think of parallels in the business world, when only the bottom line, corporate fitness, is what matters, and executives have no long-term vision. They don't see how some things, if adjusted, may yield big payoffs. As a result, whole technologies can be decimated or lost in a push for efficiency, technologies that if maintained could prove vital in the future. But fortunately, unlike Darwinian evolution, we do have foresight and can plan ahead. We do have the capacity for innovation, and can make wise choices or correct our mistakes.
The process of innovation is the opposite of the first rule of adaptive evolution. In the biological world, the quickest road to adaptation may be to delete or inactivate genes that are not necessary. But you don't get new features by deleting information. Building something new, which is what is required to explain the diversity around us, requires more than the happenstance and selection of Darwinian evolution. It requires foresight, planning, and a clear picture of the goal. It requires intelligent design.
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