Sunday 17 July 2016
(Not so)Civil war?
When Atheists Attack (Each Other)
David Klinghoffer
The squabble between Darwin lobbyists who openly hate religion and those who only quietly disdain it grows ever more personal, bitter and pathetic. On one side, evangelizing New or "Gnu" (ha ha) Atheists like Jerry Coyne and his acolytes at Why Evolution Is True. Dr. Coyne is a biologist who teaches and ostensibly researches at the University of Chicago but has a heck of a lot of free time on his hands for blogging and posting pictures of cute cats.
On the other side, so-called accommodationists like the crowd at the National Center for Science Education, who attack the New Atheists for the political offense of being rude to religious believers and supposedly messing up the alliance between religious and irreligious Darwinists.
I say "supposedly" because there's no evidence any substantial body of opinion is actually being changed on religion or evolution by anything the open haters or the quiet disdainers say. Everyone seems to seriously think they're either going to defeat religion, or merely "creationism," or both by blogging for an audience of fellow Darwinists.
Want to see what I mean? This is all pretty strictly a battle of stinkbugs in a bottle. Try to follow it without getting a headache.
Coyne recently drew excited applause from fellow biologist-atheist-blogger PZ Myers for Coyne's "open letter" (published on his blog) to the NCSE and its British equivalent, the British Centre for Science Education. In the letter, Coyne took umbrage at criticism of the New Atheists, mostly on blogs, emanating from the two accommodationist organizations. He vowed that,
We will continue to answer the misguided attacks [on the New Atheists] by people like Josh Rosenau, Roger Stanyard, and Nick Matzke so long as they keep mounting those attacks.
Like the NCSE, the BCSE seeks to pump up Darwin in the public mind without scaring religious people. This guy called Stanyard at the BCSE complains of losing a night's sleep over the nastiness of the rhetoric on Coyne's blog. Coyne in turn complained that Stanyard complained that a blog commenter complained that Nick Matzke, formerly of the NCSE, is like "vermin." Coyne also hit out at blogger Jason Rosenhouse for an "epic"-length blog post complaining of New Atheist "incivility." In the blog, Rosenhouse, who teaches math at James Madison University, wrote an update about how he had revised an insulting comment about the NCSE's Josh Rosenau that he, Rosenhouse, made in a previous version of the post.
That last bit briefly confused me. In occasionally skimming the writings of Jason Rosenhouse and Josh Rosenau in the past, I realized now I had been assuming they were the same person. They are not!
It goes on and on. In the course of his own blog post, Professor Coyne disavowed name-calling and berated Stanyard (remember him? The British guy) for "glomming onto" the Matzke-vermin insult like "white on rice, or Kwok on a Leica." What's a Kwok? Not a what but a who -- John Kwok, presumably a pseudonym, one of the most tirelessly obsessive commenters on Darwinist blog sites. Besides lashing at intelligent design, he often writes of his interest in photographic gear such as a camera by Leica. I have the impression that Kwok irritates even fellow Darwinists.
There's no need to keep all the names straight in your head. I certainly can't. I'm only taking your time, recounting just a small part of one confused exchange, to illustrate the culture of these Darwinists who write so impassionedly about religion, whether for abolishing it or befriending it. Writes Coyne in reply to Stanyard,
I'd suggest, then, that you lay off telling us what to do until you've read about our goals. The fact is that we'll always be fighting creationism until religion goes away, and when it does the fight will be over, as it is in Scandinavia.
A skeptic might suggest that turning America into Scandinavia, as far as religion goes, is an outsized goal, more like a delusion, for this group as they sit hunched over their computers shooting intemperate comments back and forth at each other all day. Or in poor Stanyard's case, all night.
There's a feverish, terrarium-like and oxygen-starved quality to this world of online Darwinists and atheists. It could only be sustained by the isolation of the Internet. They don't seem to realize that the public accepts Darwinism to the extent it does -- which is not much -- primarily because of what William James would call the sheer, simple "prestige" that the opinion grants. Arguments and evidence have little to do with it.
The prestige of Darwinism is not going to be affected by how the battle between Jerry Coyne and the NCSE turns out. New Atheist arguments are hobbled by the same isolation from what people think and feel. I have not yet read anything by any of these gentlemen or ladies, whether the open haters or the quiet disdainers, that conveys anything like a real comprehension of religious feeling or thought.
Even as they fight over the most effective way to relate to "religion," the open atheists and the accomodationists speak of an abstraction, a cartoon, that no actual religious person would recognize. No one is going to be persuaded if he doesn't already wish to be persuaded for other personal reasons. No faith is under threat from the likes of Jerry Coyne.
David Klinghoffer
The squabble between Darwin lobbyists who openly hate religion and those who only quietly disdain it grows ever more personal, bitter and pathetic. On one side, evangelizing New or "Gnu" (ha ha) Atheists like Jerry Coyne and his acolytes at Why Evolution Is True. Dr. Coyne is a biologist who teaches and ostensibly researches at the University of Chicago but has a heck of a lot of free time on his hands for blogging and posting pictures of cute cats.
On the other side, so-called accommodationists like the crowd at the National Center for Science Education, who attack the New Atheists for the political offense of being rude to religious believers and supposedly messing up the alliance between religious and irreligious Darwinists.
I say "supposedly" because there's no evidence any substantial body of opinion is actually being changed on religion or evolution by anything the open haters or the quiet disdainers say. Everyone seems to seriously think they're either going to defeat religion, or merely "creationism," or both by blogging for an audience of fellow Darwinists.
Want to see what I mean? This is all pretty strictly a battle of stinkbugs in a bottle. Try to follow it without getting a headache.
Coyne recently drew excited applause from fellow biologist-atheist-blogger PZ Myers for Coyne's "open letter" (published on his blog) to the NCSE and its British equivalent, the British Centre for Science Education. In the letter, Coyne took umbrage at criticism of the New Atheists, mostly on blogs, emanating from the two accommodationist organizations. He vowed that,
We will continue to answer the misguided attacks [on the New Atheists] by people like Josh Rosenau, Roger Stanyard, and Nick Matzke so long as they keep mounting those attacks.
Like the NCSE, the BCSE seeks to pump up Darwin in the public mind without scaring religious people. This guy called Stanyard at the BCSE complains of losing a night's sleep over the nastiness of the rhetoric on Coyne's blog. Coyne in turn complained that Stanyard complained that a blog commenter complained that Nick Matzke, formerly of the NCSE, is like "vermin." Coyne also hit out at blogger Jason Rosenhouse for an "epic"-length blog post complaining of New Atheist "incivility." In the blog, Rosenhouse, who teaches math at James Madison University, wrote an update about how he had revised an insulting comment about the NCSE's Josh Rosenau that he, Rosenhouse, made in a previous version of the post.
That last bit briefly confused me. In occasionally skimming the writings of Jason Rosenhouse and Josh Rosenau in the past, I realized now I had been assuming they were the same person. They are not!
It goes on and on. In the course of his own blog post, Professor Coyne disavowed name-calling and berated Stanyard (remember him? The British guy) for "glomming onto" the Matzke-vermin insult like "white on rice, or Kwok on a Leica." What's a Kwok? Not a what but a who -- John Kwok, presumably a pseudonym, one of the most tirelessly obsessive commenters on Darwinist blog sites. Besides lashing at intelligent design, he often writes of his interest in photographic gear such as a camera by Leica. I have the impression that Kwok irritates even fellow Darwinists.
There's no need to keep all the names straight in your head. I certainly can't. I'm only taking your time, recounting just a small part of one confused exchange, to illustrate the culture of these Darwinists who write so impassionedly about religion, whether for abolishing it or befriending it. Writes Coyne in reply to Stanyard,
I'd suggest, then, that you lay off telling us what to do until you've read about our goals. The fact is that we'll always be fighting creationism until religion goes away, and when it does the fight will be over, as it is in Scandinavia.
A skeptic might suggest that turning America into Scandinavia, as far as religion goes, is an outsized goal, more like a delusion, for this group as they sit hunched over their computers shooting intemperate comments back and forth at each other all day. Or in poor Stanyard's case, all night.
There's a feverish, terrarium-like and oxygen-starved quality to this world of online Darwinists and atheists. It could only be sustained by the isolation of the Internet. They don't seem to realize that the public accepts Darwinism to the extent it does -- which is not much -- primarily because of what William James would call the sheer, simple "prestige" that the opinion grants. Arguments and evidence have little to do with it.
The prestige of Darwinism is not going to be affected by how the battle between Jerry Coyne and the NCSE turns out. New Atheist arguments are hobbled by the same isolation from what people think and feel. I have not yet read anything by any of these gentlemen or ladies, whether the open haters or the quiet disdainers, that conveys anything like a real comprehension of religious feeling or thought.
Even as they fight over the most effective way to relate to "religion," the open atheists and the accomodationists speak of an abstraction, a cartoon, that no actual religious person would recognize. No one is going to be persuaded if he doesn't already wish to be persuaded for other personal reasons. No faith is under threat from the likes of Jerry Coyne.
Enzymes v.Darwin.
When Enzymes Don't Lie
Evolution News & Views
New research published in Bio-Complexity calls into question some fundamental assumptions of neo-Darwinian theory and enzyme evolution.
Enzymes are proteins that catalyze reactions that are necessary for life. Enzymes play such a fundamental role in life that many researchers are interested in how they originated and how they have evolved. They are composed of strings of amino acids, and the particular sequence of amino acids determines what three-dimensional shape each protein has, and what enzymatic function it carries out. Biologists categorize enzymes into families based on similarity of structure. The more similar the structure, the closer the evolutionary relationship is presumed to be.
It is generally believed that these enzyme families arose by a process of gene duplication followed by divergence of the extra copies over time. If accumulating mutations in an extra gene led to a beneficial change in enzyme function, the gene encoding that enzyme would tend to be preserved. Over time, then, repeated rounds of duplication and divergence would produce the large multi-functional families we see today. Yet for this explanation to be true, converting enzymes to new functions must require only a few mutations in order for the process to be within reach of neo-Darwinian evolution.
Doug Axe and Ann Gauger from Biologic Institute recently published a paper that addresses this pervasive assumption about the ease of enzyme conversion :
Here, we explore this question by asking how many mutations are needed to achieve a genuine functional conversion in a case where the necessary structural change is known to be small relative to the change commonly attributed to paralogous divergence.
As the authors report, they focused "not on minor functional adjustments, like shifts in substrate profiles, but rather on true innovations -- the jumps to new chemistry that must have happened but which seem to defy gradualistic explanation." Their aim was not to establish ancestry between two particular enzymes, but to identify a functional innovation that should be relatively straightforward within a superfamily and then evaluate how evolutionarily feasible this modest innovation would be.
They began by looking at a large "superfamily" known as the pyridoxal-5'-phosphate (PLP) dependent transferases. This is a well-characterized family of enzymes that share a common fold (shape) but catalyze distinctly different reactions. They identified a pair within that superfamily with very close structural similarity but no functional overlap. Kbl2 is involved in threonine (a type of amino acid) metabolism, and BioF2 is part of the biotin biosynthesis pathway. They then used a three-stage process to identify the sequences mostly likely to confer a functional change.
The experimental question is: How many mutations are required to convert Kbl to BioF function?
Experimental Results:
There are about 250 different amino-acid differences between Kbl and BioF. This is a huge number, and probably many more than the minimum number of amino acids that are needed to convert one enzyme's function to the other's. In order to determine the minimum number of amino acid changes necessary for functional innovation to occur, Gauger and Axe followed a three stage process. First they used sequence and structural comparisons of the two enzymes to identify candidate amino acids most likely to be significant for function. Second, they mutated those amino acids in BioF, making them like Kbl, and checked for loss of BioF activity. They identified three groups of amino acids, each consisting of six or seven individual amino acids, and one single amino acid, H152, that were essential for BioF function. Finally, they tested whether changing these groups in Kbl to look like BioF would enable the mutated Kbl to substitute for BioF.
The experiment ended up showing that no functional conversion could be achieved, even when all identified changes were made, including every amino acid in the enzyme's active site (the place where the enzyme's chemistry is carried out). Gauger and Axe estimate that seven or more mutations would be required to convert Kbl to BioF function.
So what does this all mean?
Two major implications need to be noted from the results of this experiment. In a second post, we will have a further discussion on implications of this research for neo-Darwinism.
The first finding was that H152 was vital to the functionality of the BioF. Perhaps what is most interesting about this finding is that H152 is not within the active site but is on the enzyme surface away from the active site. It is generally believed that the active site is the area of interest for enzymes within a family and the rest of the enzyme (the "scaffold") just holds the active site. However, these experimental findings seem to indicate that the non-active site differences, however minimal they may be, need to be considered, and that these differences may be more important than the apparent similarities.
The second implication from this failure to convert functionality is the question of whether a neo-Darwinian process of step-by-step conversion from one enzyme to another is actually feasible. The two enzymes in this study were very similar enzymes, yet even with generous estimates for mutation rate, gene duplication rate, and no fitness cost for carrying the extra gene, there does not seem to be enough time for mutations of this sort to occur:
"...seven is a reasonable lower-bound estimate of the specific nucleotide substitutions required for conversion...this places the Kbl [to] BioF conversion outside the bounds of what can be achieved by the Darwinian mechanism." When using the established mechanisms and estimates, it would require 10^30 or more generations to elapse before any type of BioF-like conversion could be established. There is not enough time to accomplish this relatively small innovation! As Axe and Gauger aptly summarize:
This places the innovation well beyond what can be expected within the time that life has existed on earth, under favorable assumptions. In fact, even the unrealistically favorable assumption that kbl duplicates carry no fitness cost leaves the conversion just beyond the limits of feasibility.
These are not large leaps or large-scale changes, but small-scale changes. And other research, cited in this paper, have shown the same difficulty in achieving enzyme conversions. This calls into question a fundamental assumption in the neo-Darwinian paradigm, that similarity of structure or form means ease of conversion, and implies that a different paradigm is necessary to account for enzymatic functional conversion.
Evolution News & Views
New research published in Bio-Complexity calls into question some fundamental assumptions of neo-Darwinian theory and enzyme evolution.
Enzymes are proteins that catalyze reactions that are necessary for life. Enzymes play such a fundamental role in life that many researchers are interested in how they originated and how they have evolved. They are composed of strings of amino acids, and the particular sequence of amino acids determines what three-dimensional shape each protein has, and what enzymatic function it carries out. Biologists categorize enzymes into families based on similarity of structure. The more similar the structure, the closer the evolutionary relationship is presumed to be.
It is generally believed that these enzyme families arose by a process of gene duplication followed by divergence of the extra copies over time. If accumulating mutations in an extra gene led to a beneficial change in enzyme function, the gene encoding that enzyme would tend to be preserved. Over time, then, repeated rounds of duplication and divergence would produce the large multi-functional families we see today. Yet for this explanation to be true, converting enzymes to new functions must require only a few mutations in order for the process to be within reach of neo-Darwinian evolution.
Doug Axe and Ann Gauger from Biologic Institute recently published a paper that addresses this pervasive assumption about the ease of enzyme conversion :
Here, we explore this question by asking how many mutations are needed to achieve a genuine functional conversion in a case where the necessary structural change is known to be small relative to the change commonly attributed to paralogous divergence.
As the authors report, they focused "not on minor functional adjustments, like shifts in substrate profiles, but rather on true innovations -- the jumps to new chemistry that must have happened but which seem to defy gradualistic explanation." Their aim was not to establish ancestry between two particular enzymes, but to identify a functional innovation that should be relatively straightforward within a superfamily and then evaluate how evolutionarily feasible this modest innovation would be.
They began by looking at a large "superfamily" known as the pyridoxal-5'-phosphate (PLP) dependent transferases. This is a well-characterized family of enzymes that share a common fold (shape) but catalyze distinctly different reactions. They identified a pair within that superfamily with very close structural similarity but no functional overlap. Kbl2 is involved in threonine (a type of amino acid) metabolism, and BioF2 is part of the biotin biosynthesis pathway. They then used a three-stage process to identify the sequences mostly likely to confer a functional change.
The experimental question is: How many mutations are required to convert Kbl to BioF function?
Experimental Results:
There are about 250 different amino-acid differences between Kbl and BioF. This is a huge number, and probably many more than the minimum number of amino acids that are needed to convert one enzyme's function to the other's. In order to determine the minimum number of amino acid changes necessary for functional innovation to occur, Gauger and Axe followed a three stage process. First they used sequence and structural comparisons of the two enzymes to identify candidate amino acids most likely to be significant for function. Second, they mutated those amino acids in BioF, making them like Kbl, and checked for loss of BioF activity. They identified three groups of amino acids, each consisting of six or seven individual amino acids, and one single amino acid, H152, that were essential for BioF function. Finally, they tested whether changing these groups in Kbl to look like BioF would enable the mutated Kbl to substitute for BioF.
The experiment ended up showing that no functional conversion could be achieved, even when all identified changes were made, including every amino acid in the enzyme's active site (the place where the enzyme's chemistry is carried out). Gauger and Axe estimate that seven or more mutations would be required to convert Kbl to BioF function.
So what does this all mean?
Two major implications need to be noted from the results of this experiment. In a second post, we will have a further discussion on implications of this research for neo-Darwinism.
The first finding was that H152 was vital to the functionality of the BioF. Perhaps what is most interesting about this finding is that H152 is not within the active site but is on the enzyme surface away from the active site. It is generally believed that the active site is the area of interest for enzymes within a family and the rest of the enzyme (the "scaffold") just holds the active site. However, these experimental findings seem to indicate that the non-active site differences, however minimal they may be, need to be considered, and that these differences may be more important than the apparent similarities.
The second implication from this failure to convert functionality is the question of whether a neo-Darwinian process of step-by-step conversion from one enzyme to another is actually feasible. The two enzymes in this study were very similar enzymes, yet even with generous estimates for mutation rate, gene duplication rate, and no fitness cost for carrying the extra gene, there does not seem to be enough time for mutations of this sort to occur:
"...seven is a reasonable lower-bound estimate of the specific nucleotide substitutions required for conversion...this places the Kbl [to] BioF conversion outside the bounds of what can be achieved by the Darwinian mechanism." When using the established mechanisms and estimates, it would require 10^30 or more generations to elapse before any type of BioF-like conversion could be established. There is not enough time to accomplish this relatively small innovation! As Axe and Gauger aptly summarize:
This places the innovation well beyond what can be expected within the time that life has existed on earth, under favorable assumptions. In fact, even the unrealistically favorable assumption that kbl duplicates carry no fitness cost leaves the conversion just beyond the limits of feasibility.
These are not large leaps or large-scale changes, but small-scale changes. And other research, cited in this paper, have shown the same difficulty in achieving enzyme conversions. This calls into question a fundamental assumption in the neo-Darwinian paradigm, that similarity of structure or form means ease of conversion, and implies that a different paradigm is necessary to account for enzymatic functional conversion.
Friday 15 July 2016
Spiders in the dock for design.
Spiders Have Eight (Well-Designed) Eyes
Evolution News & Views
Have you ever wanted eyes in the back of your head? Spiders have eight eyes, compared to our two. They can boast of better vision than ours on some counts; sharp, color vision that extends into the ultraviolet. Their ample set of peepers allows for division of labor: the main pair in front helps them see detail, while the smaller eyes wrapped around their heads warn them of looming threats. Stephanie Pappas wrote about spider eyes on Live Science recently.
"We see that division of labor within that visual system... That's pretty cool if you think about it, because we only have one pair of eyes."
That was actually a quote from Skye Long, a doctoral student at the University of Massachusetts at Amherst, who decided to test and find out what the extra eyes are for. She outfitted an enclosure for her 46 jumping spider subjects and used paint to "blindfold" the principal eyes on a third of them, and the adjacent, smaller eyes (anterior lateral pair) on another third, leaving one third blindfold-free. (Don't worry about the spiders; the paint could be easily removed.)
Then she used an iPod Touch to create images of a black dot growing or shrinking in size. When seeing the "looming threat," the spiders backed up quickly and raised their front legs in defense, as if they felt scared -- even when the principal eyes were covered. This means the anterior lateral pair are crucial for alerting the spider to potential dangers. What are the other four eyes used for? That's what Long wants to find out next.
This would have been a "pretty cool" Halloween animal story, featuring a nice, experimental science project, had not Skye Long wandered off into evolutionary tale-telling:
That means the secondary eyes are crucial for alerting the spider to dangerous motion, Long said. Spider eyes are a "really cool step in evolution," she added; insects have compound eyes with multiple lenses, and some areas of those eyes have certain functions. Spiders, on the other hand, separate out visual functions across their heads.
"This is a different pathway that evolution has taken to allow a very small animal to have a very extensive visual system," Long said.
Right. No matter how cool or well-designed the adaption, just say it evolved. It's a "really cool step in evolution." It's a "different pathway evolution has taken." The blind, aimless, purposeless process of natural selection gave spiders a "very extensive visual system." Turn in your paper and get an A.
Here's a better way. Look what researchers at the Optical Society of America are doing with spiders. Incredible as it sounds, they are taking spider silk and using it for fiber optics. Spider silk is already prized as an ideal material: it's strong, flexible, and biodegradable. Now, a team has found it can also transmit and guide light almost as well as glass fibers.
One team is using it as a light guide in photonic chips, while another is trying to imitate the proteins in silk from spiders and silkworms to be able to manufacture it. This second team has already made a silk-based "plastic" that can be used for everything from biodegradable cups to implantable devices that dissolve in the body. Fiorenzo Omenetto presented his work in a superb TED Talk that raised the audience to their feet without him once mentioning evolution. And he is getting grants from the NSF!
Evolution is a straw scarecrow whenever it appears in biological research. The whole story is intelligent design, in the animals and plants studied, in the experiments devised to gain knowledge about them, and in the applications they lead to. Animal tricks become science's treats.
Evolution News & Views
Have you ever wanted eyes in the back of your head? Spiders have eight eyes, compared to our two. They can boast of better vision than ours on some counts; sharp, color vision that extends into the ultraviolet. Their ample set of peepers allows for division of labor: the main pair in front helps them see detail, while the smaller eyes wrapped around their heads warn them of looming threats. Stephanie Pappas wrote about spider eyes on Live Science recently.
"We see that division of labor within that visual system... That's pretty cool if you think about it, because we only have one pair of eyes."
That was actually a quote from Skye Long, a doctoral student at the University of Massachusetts at Amherst, who decided to test and find out what the extra eyes are for. She outfitted an enclosure for her 46 jumping spider subjects and used paint to "blindfold" the principal eyes on a third of them, and the adjacent, smaller eyes (anterior lateral pair) on another third, leaving one third blindfold-free. (Don't worry about the spiders; the paint could be easily removed.)
Then she used an iPod Touch to create images of a black dot growing or shrinking in size. When seeing the "looming threat," the spiders backed up quickly and raised their front legs in defense, as if they felt scared -- even when the principal eyes were covered. This means the anterior lateral pair are crucial for alerting the spider to potential dangers. What are the other four eyes used for? That's what Long wants to find out next.
This would have been a "pretty cool" Halloween animal story, featuring a nice, experimental science project, had not Skye Long wandered off into evolutionary tale-telling:
That means the secondary eyes are crucial for alerting the spider to dangerous motion, Long said. Spider eyes are a "really cool step in evolution," she added; insects have compound eyes with multiple lenses, and some areas of those eyes have certain functions. Spiders, on the other hand, separate out visual functions across their heads.
"This is a different pathway that evolution has taken to allow a very small animal to have a very extensive visual system," Long said.
Right. No matter how cool or well-designed the adaption, just say it evolved. It's a "really cool step in evolution." It's a "different pathway evolution has taken." The blind, aimless, purposeless process of natural selection gave spiders a "very extensive visual system." Turn in your paper and get an A.
Here's a better way. Look what researchers at the Optical Society of America are doing with spiders. Incredible as it sounds, they are taking spider silk and using it for fiber optics. Spider silk is already prized as an ideal material: it's strong, flexible, and biodegradable. Now, a team has found it can also transmit and guide light almost as well as glass fibers.
One team is using it as a light guide in photonic chips, while another is trying to imitate the proteins in silk from spiders and silkworms to be able to manufacture it. This second team has already made a silk-based "plastic" that can be used for everything from biodegradable cups to implantable devices that dissolve in the body. Fiorenzo Omenetto presented his work in a superb TED Talk that raised the audience to their feet without him once mentioning evolution. And he is getting grants from the NSF!
Evolution is a straw scarecrow whenever it appears in biological research. The whole story is intelligent design, in the animals and plants studied, in the experiments devised to gain knowledge about them, and in the applications they lead to. Animal tricks become science's treats.
The winged flocks v Darwin.
Starling Murmurations and Intelligent Design, Revisited
David Klinghoffer
A friend points out the bit of nice news that one of our favorite nature video clips, "Dylan Winter and the Starling Murmurations," from the Illustra film Flight: The Genius of Birds, has exceeded a million views on YouTube. Not bad. That's a million plus people exposed to one of the most remarkable demonstrations of the wonders of bird flight.
All those viewers may not know precisely how starling murmurations give evidence of intelligent design. We've discussed this in the past:
"Why Starling Murmurations Suggest Intelligent Design"
"'Not By Chance': Drone Engineers Try the Starling Trick"
"Fly Now; Swim Later"
As Dr. Timothy Standish explained, here in a nutshell is the challenge posed by starling murmurations to traditional evolutionary thinking:
In the cold hard world of survival of the fittest, starlings that stick with the group may enhance their odds of surviving predation. But such an effect is an emergent property of the murmuration. Attributing the origin of murmurations to enhanced survival requires first that murmurations exist, thus making for a circular argument. To circumvent this problem, a Darwinist might invoke cooption. Maybe the ancestors of modern starlings gathered together for some other practical purpose and then, in a lucky coincidence, gained the survival advantage provided by murmurations. But think about the resources consumed by daily migrations followed by considerable time flying about with other starlings. It's unclear why any other proposed reason for investing resources this way would not be equally vulnerable to the criticism of circularity.
Flying in formation has advantages that humans quickly recognized once we mastered powered flight. The most obvious of these involves multiple sets of eyes looking out for enemies or obstacles. If human intelligence can figure this out, perhaps clever starlings can as well. But if there is a genetic component to the behavior -- a reasonable assumption given that starlings form murmurations wherever they are in the world while other birds do not -- then a mechanism for creating the required genetic changes would need to anticipate the need fulfilled by murmurations. Darwinian evolution is blind and unguided, incapable by definition of anticipating anything. In the case of human flight, various types of formation flying were developed in anticipation of a need. Generally that was to survive during battles in the air. Formation flying is not something that pilots stumbled upon in the middle of a dogfight then stuck with; it is a solution to an anticipated need. Intelligence alone has been shown to have produced such solutions.
When it comes to design and murmurations, the elephant in the room is the other abilities birds must possess to achieve the phenomenon. They must have the inclination to fly long distances and to congregate. They must have the ability to navigate, the ability to fly, the ability to perceive and react to the other birds they are flying with, and any number of other wonders. Most people, scientists or not, can see this; but Darwinism demands that we turn a blind eye to such things.
David Klinghoffer
A friend points out the bit of nice news that one of our favorite nature video clips, "Dylan Winter and the Starling Murmurations," from the Illustra film Flight: The Genius of Birds, has exceeded a million views on YouTube. Not bad. That's a million plus people exposed to one of the most remarkable demonstrations of the wonders of bird flight.
All those viewers may not know precisely how starling murmurations give evidence of intelligent design. We've discussed this in the past:
"Why Starling Murmurations Suggest Intelligent Design"
"'Not By Chance': Drone Engineers Try the Starling Trick"
"Fly Now; Swim Later"
As Dr. Timothy Standish explained, here in a nutshell is the challenge posed by starling murmurations to traditional evolutionary thinking:
In the cold hard world of survival of the fittest, starlings that stick with the group may enhance their odds of surviving predation. But such an effect is an emergent property of the murmuration. Attributing the origin of murmurations to enhanced survival requires first that murmurations exist, thus making for a circular argument. To circumvent this problem, a Darwinist might invoke cooption. Maybe the ancestors of modern starlings gathered together for some other practical purpose and then, in a lucky coincidence, gained the survival advantage provided by murmurations. But think about the resources consumed by daily migrations followed by considerable time flying about with other starlings. It's unclear why any other proposed reason for investing resources this way would not be equally vulnerable to the criticism of circularity.
Flying in formation has advantages that humans quickly recognized once we mastered powered flight. The most obvious of these involves multiple sets of eyes looking out for enemies or obstacles. If human intelligence can figure this out, perhaps clever starlings can as well. But if there is a genetic component to the behavior -- a reasonable assumption given that starlings form murmurations wherever they are in the world while other birds do not -- then a mechanism for creating the required genetic changes would need to anticipate the need fulfilled by murmurations. Darwinian evolution is blind and unguided, incapable by definition of anticipating anything. In the case of human flight, various types of formation flying were developed in anticipation of a need. Generally that was to survive during battles in the air. Formation flying is not something that pilots stumbled upon in the middle of a dogfight then stuck with; it is a solution to an anticipated need. Intelligence alone has been shown to have produced such solutions.
When it comes to design and murmurations, the elephant in the room is the other abilities birds must possess to achieve the phenomenon. They must have the inclination to fly long distances and to congregate. They must have the ability to navigate, the ability to fly, the ability to perceive and react to the other birds they are flying with, and any number of other wonders. Most people, scientists or not, can see this; but Darwinism demands that we turn a blind eye to such things.
Wednesday 13 July 2016
File under 'well said' XXXI
Vague and mysterious forms of speech, and abuse of language, have so long passed for mysteries of science; and hard or misapplied words with little or no meaning have, by prescription, such a right to be mistaken for deep learning and height of speculation, that it will not be easy to persuade either those who speak or those who hear them, that they are but the covers of ignorance and hindrance of true knowledge.
John Locke
John Locke
Demythifying peer review.
For Critics of Intelligent Design, There's No Hiding Behind Claims of "Peer Review" Anymore
David Klinghoffer
Darwinists have had to back off considerably from the once-confident assertion that peer review in science journals constitutes, as Jerry Coyne put it in 2005 inThe New Republic, the "gold standard for modern scientific achievement." The whole institution of peer review is so besmirched now as to arouse, not even amusement anymore, but something more like pity.
In the same article, Coyne maintained that it was precisely by "By that standard" that advocates of the theory of intelligent design "have failed miserably." You mean by the standard of what is now revealed as the intellectual and scientific equivalent of insider trading? Or more like racketeering and simple fraud.
The existence of a blog like Retraction Watch is, in this respect, a sign of the times, a measure of the extent to which science publishing has fallen into derision. Their post from a couple of days ago, on a "peer review and citation ring at the Journal of Vibration and Control," has been widely reported, including the retraction of 60 papers from that journal. Sixty!
"This one deserves a 'wow,'" observes author Ivan Oransky. Indeed. The cat is really out of the bag.
Slate:
It may not be entirely fair to liken a "peer review and citation ring" to the academic version of an extortion ring, but there's certainly fraud involved in both. Retraction Watch, a blog dedicated to chronicling which academic papers have been withdrawn, is reporting that SAGE Publishing, a group that puts out numerous peer-reviewed journals, is retracting 60 papers from its Journal of Vibration and Control after an internal investigation uncovered extensive evidence of severe peer-review fraud.
Apparently researcher Peter Chen, formerly of National Pingtung University of Education in Taiwan, made multiple submission and reviewer accounts -- possibly along with other researchers at his institution or elsewhere -- so that he could influence the peer review system. When Chen or someone else from the ring submitted a paper, the group could manipulate who reviewed the research, and on at least one occasion Chen served as his own reviewer.
The Washington Post:
Now comes word of a journal retracting 60 articles at once.
The reason for the mass retraction is mind-blowing: A "peer review and citation ring" was apparently rigging the review process to get articles published.
You've heard of prostitution rings, gambling rings and extortion rings. Now there's a "peer review ring."
The publication is the Journal of Vibration and Control (JVC). It publishes papers with names like "Hydraulic enginge mounts: a survey" and "Reduction of wheel force variations with magnetorheological devices."
The Guardian:
An academic journal has retracted dozens of articles and apologised to readers after falling victim to what it described as a "peer review ring" that appears to have involved more than 100 bogus scholars.
The Journal of Vibration and Control (JVC), a leading publication in the field of acoustics, said it was withdrawing 60 papers published in print and online over the past four years, after discovering that articles were being approved and cited by academics with "assumed and fabricated identities".
The journal's publisher, Sage, said in a statement that the ring appeared to centre around Peter Chen, a researcher formerly of National Pingtung University of Education, in Taiwan. Chen provided an "unsatisfactory response" when confronted, and has since resigned from his post.
Oh, it's just one unfortunate lapse, you say, not representative of anything much beyond itself? If you want to comfort yourself with that idea, first try following the reporting at Retraction Watch, which commonly posts two or three accounts of scholarly fraud and slipshod science per day.
With respect to what this means for the theory of ID, go back and read Casey Luskin's post, "Intelligent Design Is Peer-Reviewed, but Is Peer-Review a Requirement of Good Science" Casey concludes:
Despite the attempted lockout, ID proponents have published their ideas in peer-reviewed scientific journals. This shows that ID has academic legitimacy whether or not one applies the dubious "peer-review" test of good science.
That's right. Going forward, if you want to argue against ID, you are going to have to actually argue against it, critically analyze its arguments and its evidence, as opponents of ID so commonly refuse to do. There's no hiding behind claims of "peer review" anymore.
David Klinghoffer
Darwinists have had to back off considerably from the once-confident assertion that peer review in science journals constitutes, as Jerry Coyne put it in 2005 inThe New Republic, the "gold standard for modern scientific achievement." The whole institution of peer review is so besmirched now as to arouse, not even amusement anymore, but something more like pity.
In the same article, Coyne maintained that it was precisely by "By that standard" that advocates of the theory of intelligent design "have failed miserably." You mean by the standard of what is now revealed as the intellectual and scientific equivalent of insider trading? Or more like racketeering and simple fraud.
The existence of a blog like Retraction Watch is, in this respect, a sign of the times, a measure of the extent to which science publishing has fallen into derision. Their post from a couple of days ago, on a "peer review and citation ring at the Journal of Vibration and Control," has been widely reported, including the retraction of 60 papers from that journal. Sixty!
"This one deserves a 'wow,'" observes author Ivan Oransky. Indeed. The cat is really out of the bag.
Slate:
It may not be entirely fair to liken a "peer review and citation ring" to the academic version of an extortion ring, but there's certainly fraud involved in both. Retraction Watch, a blog dedicated to chronicling which academic papers have been withdrawn, is reporting that SAGE Publishing, a group that puts out numerous peer-reviewed journals, is retracting 60 papers from its Journal of Vibration and Control after an internal investigation uncovered extensive evidence of severe peer-review fraud.
Apparently researcher Peter Chen, formerly of National Pingtung University of Education in Taiwan, made multiple submission and reviewer accounts -- possibly along with other researchers at his institution or elsewhere -- so that he could influence the peer review system. When Chen or someone else from the ring submitted a paper, the group could manipulate who reviewed the research, and on at least one occasion Chen served as his own reviewer.
The Washington Post:
Now comes word of a journal retracting 60 articles at once.
The reason for the mass retraction is mind-blowing: A "peer review and citation ring" was apparently rigging the review process to get articles published.
You've heard of prostitution rings, gambling rings and extortion rings. Now there's a "peer review ring."
The publication is the Journal of Vibration and Control (JVC). It publishes papers with names like "Hydraulic enginge mounts: a survey" and "Reduction of wheel force variations with magnetorheological devices."
The Guardian:
An academic journal has retracted dozens of articles and apologised to readers after falling victim to what it described as a "peer review ring" that appears to have involved more than 100 bogus scholars.
The Journal of Vibration and Control (JVC), a leading publication in the field of acoustics, said it was withdrawing 60 papers published in print and online over the past four years, after discovering that articles were being approved and cited by academics with "assumed and fabricated identities".
The journal's publisher, Sage, said in a statement that the ring appeared to centre around Peter Chen, a researcher formerly of National Pingtung University of Education, in Taiwan. Chen provided an "unsatisfactory response" when confronted, and has since resigned from his post.
Oh, it's just one unfortunate lapse, you say, not representative of anything much beyond itself? If you want to comfort yourself with that idea, first try following the reporting at Retraction Watch, which commonly posts two or three accounts of scholarly fraud and slipshod science per day.
With respect to what this means for the theory of ID, go back and read Casey Luskin's post, "Intelligent Design Is Peer-Reviewed, but Is Peer-Review a Requirement of Good Science" Casey concludes:
Despite the attempted lockout, ID proponents have published their ideas in peer-reviewed scientific journals. This shows that ID has academic legitimacy whether or not one applies the dubious "peer-review" test of good science.
That's right. Going forward, if you want to argue against ID, you are going to have to actually argue against it, critically analyze its arguments and its evidence, as opponents of ID so commonly refuse to do. There's no hiding behind claims of "peer review" anymore.
Thursday 7 July 2016
Monday 4 July 2016
Darwin of the gaps just so stories re junk DNA becomoing harder to sell
Junk DNA: Is Preventing Breast Cancer a Function?
Evolution News & Views February 6, 2016 4:33 AM
Each time a function is found for a piece of non-coding DNA, the "junk DNA" myth gets more mythological. Here's a function that has been revealed for a certain long, non-coding transcript of DNA into RNA (lncRNA). It helps prevent breast cancer and ovarian cancer.
Researchers at the University of Bath explain why it is difficult to find these functions for non-coding parts of the genome:
The human genome contains around three metres of DNA, of which only about two per cent contains genes that code for proteins. Since the sequencing of the complete human genome in 2000, scientists have puzzled over the role of the remaining 98 per cent.
In recent years it has become apparent that a lot of this non-coding DNA is actually transcribed into non-coding RNA. However, there is still a debate as to whether non-coding RNA is just 'noise' or whether it serves any function in the cell.
Part of the reason for this uncertainty is that it is very difficult to knock-out non-coding RNA without damaging the DNA, which can lead to off-target effects and false results.
They are clearly aware of the "debate" about junk DNA and the results of ENCODE that found that the majority of the genome is actually transcribed (they referenced ENCODE in the paper). As we have reported often, some members of the evolution side of the debate expect most of the DNA is junk. The design side expects that much of it (but not necessarily all) is functional. Thanks to this research, we have a new case that may point the way to future discoveries.
The news release is titled, "'Junk' DNA plays role in preventing breast cancer." It's based on an open-access paper in Nature Communications. Most readers scanning the paper will see what researchers are up against. Discussion of the complex interactions of parts -- lncRNAs transcripts, small interfering RNAs (siRNAs), promoters, exons, introns, alleles, interference in cis and trans and all the rest -- gets into the technical weeds fast. Thankfully, the release simplifies the essence of the finding. Basically, a piece of non-coding DNA "keeps cells healthy" by preventing a genetic "switch" from getting stuck.
Dr Adele Murrell, from the University of Bath's Department of Biology & Biochemistry, led the study. She explained: "The number of cells in our body are balanced by the level at which cells replicate and replace the ones that die. Sometimes the switches that control this growth get stuck in the 'on' position, which can lead to cancer.
"As the tumour grows and the cancer cells get crowded, they start to break away from the tumour, change shape and are able to burrow through tissues to the bloodstream where they migrate to other parts of the body, which is how the cancer spreads. This process is called metastasis and requires a whole network of genes to regulate the transformation of cell shape and mobilisation.
Dr Lovorka Stojic, from Cancer Research UK Cambridge Institute, the first author of this work identified that GNG12-AS1, a strand of non-coding RNA, prevents the growth switch getting stuck and suppresses metastasis. The specific genomic region where this non-coding RNA is located often gets damaged in breast cancer patients -- this control is removed and the cancer cells spread.
The researchers found that the lncRNA GNG12-AS1 acts as a molecular "rheostat" (their term) that controls the expression of an adjacent gene, DIRAS3, a tumor suppressor. It does it by two mechanisms. One is by regulating the number of transcripts of the tumor suppressor. But if that gets out of control, it can even suppress the "network of genes that prepare cells to change their shape and prepare for metastasis."
By experimentally reducing the amount of GNG12-AS1 produced, either by preventing its transcription or destroying the transcripts, they found that cells start becoming cancerous. This explains why in cancer patients, the switch is stuck:
DIRAS3 is downregulated in 70% of breast and ovarian cancer, and its loss of expression correlates with cancer progression and metastasis. The mechanism responsible for DIRAS3 downregulation to date involves different epigenetic mechanisms and loss of heterozygosity. We hypothesized that TI [transcriptional interference] by GNG12-AS1 could represent an additional layer of regulating DIRAS3 dosage.
The interactions are far more complex than can be described here. Suffice it to say that this long non-coding RNA, which would have been considered "junk" previously, plays a crucial role in regulating the amount of an important tumor suppressor gene. It's a "stable lncRNA localized in the nucleus" with a half-life of 20 to 25 hours, meaning it needs to be transcribed often. Other processes regulate the amount of the lncRNA in a very complex choreography of enhancers, suppressors, and feedback loops. Levels of expression also vary depending on the tissue involved.
It has become increasingly clear that non-coding parts of the genome play vital roles in regulating the coding parts. Regulation is an important function. A system that generates parts without regard to the amount needed is a system out of control. How cool is it to find a code that codes for products that regulate the amount of products in other parts of the code? Not only do we see function emerging for the non-coding regions, we see design on a more colossal scale than anyone could have imagined.
The University of Bath is an internationally recognized center of excellence in biological research. It's encouraging to see their biologists actively challenging the "junk DNA" myth:
Dr Kat Arney, science communication manager at Cancer Research UK, said: "Only a tiny fraction of our DNA contains actual genes, and we know that at least some of the bits in between -- often dismissed as 'junk' -- play important roles in controlling how genes get switched on and off at the right time and in the right place.
When the Human Genome project found that only 2 percent of the genome coded for proteins, the right question should have been, "What is all the rest doing?" Some evolutionists were too quick to dismiss it as a pile of useless leftovers from time and chance. Cancer patients around the world can be grateful that these researchers didn't buy that explanation, but looked beyond the unknown for greater understanding.
"Research like this is helping is to unpick the precise details about how these regions work, shedding light on their potential role in the development [or prevention] of cancer and pointing towards new approaches for tackling the disease."
If a system works, it's not happening by accident. That's the intelligent-design spirit that promises to shed more light into the genomic black box.
Evolution News & Views February 6, 2016 4:33 AM
Each time a function is found for a piece of non-coding DNA, the "junk DNA" myth gets more mythological. Here's a function that has been revealed for a certain long, non-coding transcript of DNA into RNA (lncRNA). It helps prevent breast cancer and ovarian cancer.
Researchers at the University of Bath explain why it is difficult to find these functions for non-coding parts of the genome:
The human genome contains around three metres of DNA, of which only about two per cent contains genes that code for proteins. Since the sequencing of the complete human genome in 2000, scientists have puzzled over the role of the remaining 98 per cent.
In recent years it has become apparent that a lot of this non-coding DNA is actually transcribed into non-coding RNA. However, there is still a debate as to whether non-coding RNA is just 'noise' or whether it serves any function in the cell.
Part of the reason for this uncertainty is that it is very difficult to knock-out non-coding RNA without damaging the DNA, which can lead to off-target effects and false results.
They are clearly aware of the "debate" about junk DNA and the results of ENCODE that found that the majority of the genome is actually transcribed (they referenced ENCODE in the paper). As we have reported often, some members of the evolution side of the debate expect most of the DNA is junk. The design side expects that much of it (but not necessarily all) is functional. Thanks to this research, we have a new case that may point the way to future discoveries.
The news release is titled, "'Junk' DNA plays role in preventing breast cancer." It's based on an open-access paper in Nature Communications. Most readers scanning the paper will see what researchers are up against. Discussion of the complex interactions of parts -- lncRNAs transcripts, small interfering RNAs (siRNAs), promoters, exons, introns, alleles, interference in cis and trans and all the rest -- gets into the technical weeds fast. Thankfully, the release simplifies the essence of the finding. Basically, a piece of non-coding DNA "keeps cells healthy" by preventing a genetic "switch" from getting stuck.
Dr Adele Murrell, from the University of Bath's Department of Biology & Biochemistry, led the study. She explained: "The number of cells in our body are balanced by the level at which cells replicate and replace the ones that die. Sometimes the switches that control this growth get stuck in the 'on' position, which can lead to cancer.
"As the tumour grows and the cancer cells get crowded, they start to break away from the tumour, change shape and are able to burrow through tissues to the bloodstream where they migrate to other parts of the body, which is how the cancer spreads. This process is called metastasis and requires a whole network of genes to regulate the transformation of cell shape and mobilisation.
Dr Lovorka Stojic, from Cancer Research UK Cambridge Institute, the first author of this work identified that GNG12-AS1, a strand of non-coding RNA, prevents the growth switch getting stuck and suppresses metastasis. The specific genomic region where this non-coding RNA is located often gets damaged in breast cancer patients -- this control is removed and the cancer cells spread.
The researchers found that the lncRNA GNG12-AS1 acts as a molecular "rheostat" (their term) that controls the expression of an adjacent gene, DIRAS3, a tumor suppressor. It does it by two mechanisms. One is by regulating the number of transcripts of the tumor suppressor. But if that gets out of control, it can even suppress the "network of genes that prepare cells to change their shape and prepare for metastasis."
By experimentally reducing the amount of GNG12-AS1 produced, either by preventing its transcription or destroying the transcripts, they found that cells start becoming cancerous. This explains why in cancer patients, the switch is stuck:
DIRAS3 is downregulated in 70% of breast and ovarian cancer, and its loss of expression correlates with cancer progression and metastasis. The mechanism responsible for DIRAS3 downregulation to date involves different epigenetic mechanisms and loss of heterozygosity. We hypothesized that TI [transcriptional interference] by GNG12-AS1 could represent an additional layer of regulating DIRAS3 dosage.
The interactions are far more complex than can be described here. Suffice it to say that this long non-coding RNA, which would have been considered "junk" previously, plays a crucial role in regulating the amount of an important tumor suppressor gene. It's a "stable lncRNA localized in the nucleus" with a half-life of 20 to 25 hours, meaning it needs to be transcribed often. Other processes regulate the amount of the lncRNA in a very complex choreography of enhancers, suppressors, and feedback loops. Levels of expression also vary depending on the tissue involved.
It has become increasingly clear that non-coding parts of the genome play vital roles in regulating the coding parts. Regulation is an important function. A system that generates parts without regard to the amount needed is a system out of control. How cool is it to find a code that codes for products that regulate the amount of products in other parts of the code? Not only do we see function emerging for the non-coding regions, we see design on a more colossal scale than anyone could have imagined.
The University of Bath is an internationally recognized center of excellence in biological research. It's encouraging to see their biologists actively challenging the "junk DNA" myth:
Dr Kat Arney, science communication manager at Cancer Research UK, said: "Only a tiny fraction of our DNA contains actual genes, and we know that at least some of the bits in between -- often dismissed as 'junk' -- play important roles in controlling how genes get switched on and off at the right time and in the right place.
When the Human Genome project found that only 2 percent of the genome coded for proteins, the right question should have been, "What is all the rest doing?" Some evolutionists were too quick to dismiss it as a pile of useless leftovers from time and chance. Cancer patients around the world can be grateful that these researchers didn't buy that explanation, but looked beyond the unknown for greater understanding.
"Research like this is helping is to unpick the precise details about how these regions work, shedding light on their potential role in the development [or prevention] of cancer and pointing towards new approaches for tackling the disease."
If a system works, it's not happening by accident. That's the intelligent-design spirit that promises to shed more light into the genomic black box.
Saturday 2 July 2016
Darwinism Vs.The real world.XXXVII
Puberty, Maturation, and Fertility: The Role of Information in Human Sexuality
Howard Glicksman
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 is delighted to offer this series, "The Designed Body." For the complete series, see here. Dr. Glicksman practices palliative medicine for a hospice organization.
The word sex comes from the Latin secare which means to separate or divide. Most one-celled organisms form offspring through asexual reproduction. It is asexual because there is no separation of genetic material. Therefore divided chromosomes do not need to be brought together and the new life produced is genetically identical to the original.
In contrast, most multi-cellular organisms form offspring in a much more complicated way called sexual reproduction. In humans, each of the chromosomes making up the 23 pairs containing the genetic material for life is separated from its partner and placed into gametes called male sperm and female eggs. Human reproduction involves sexual intercourse in which the male deposits sperm in the vagina of the female so they can move into the uterus and one of them can join its separated 23 chromosomes to the ones within the female egg in a process called fertilization. The fertilization of the female egg by the male sperm results in a one-celled zygote which then contains the full complement of genetic material and is distinct from its parents.
As difficult as it may be for evolutionary biologists to explain the blind and unguided development of the different organ systems and the body's ability to control them, because of the mechanism humans must use for reproduction they must also explain the simultaneous development of both males and females since neither is of any use to propagate the species without the other.
The three things needed for a human to reproduce are: (1) either be male or female and have all of the right sexual parts, (2) be able to produce enough sperm or release an egg into a fallopian tube, and (3) be able to participate in sexual intercourse so sperm is released into the vagina or have a clear path for sperm to swim toward the fallopian tubes.
In my last article, I showed that for the first few weeks of life the human embryo is asexual. That is because the primordial gonads have not declared themselves to be testes or ovaries yet. Notwithstanding where the embryonic structures that develop into mature sexual organs came from, the human embryo is destined to become female by default unless acted upon by specific chemicals. These include the Testis Determining Factor (TDF) (usually found on the Y chromosome), the enzymes needed to convert cholesterol into testosterone and testosterone into dihydrotestosterone, the androgen receptor on the Wolffian ducts and the tissue that will become male external genitalia, Anti-Mullerian Hormone (AMH) and the AMH receptor on the Mullerian ducts.
If all of these chemicals are present and working properly the human embryo will usually develop into a normal male. But if the TDF is absent it will usually develop into a normal female. However, if the TDF is present, directing the primordial gonads to become testosterone-producing testes, but the androgen receptor is absent or defective (Complete Androgen Insensitivity Syndrome (CAIS)), the result in an XY female. XY females occur in about one in twenty thousand "male" births and have testes instead of ovaries, no genital duct system and female external genitalia. So for the first decade of life they look like normal little girls. However, experience teaches that although humans are sexually differentiated as male or female at birth, they are not able to reproduce. Most children begin to show signs of their sexual development to come by the end of the first decade. Over the following years they will undergo sexual and bodily development in a process called puberty. Puberty is a constellation of physiological changes that, except in, for example, XY females, not only enables human beings to reproduce but also prepares them for their natural role in the family. Let's consider how this happens.
The hypothalamus and pituitary work to control many different vital hormones in the body. For example, the hypothalamus secretes Growth Hormone-Releasing Hormone, which stimulates the pituitary to release Growth Hormone (GH). As its name implies, GH is very important in the overall growth and development of the body. The hypothalamus also sends out Thyrotropin-Releasing Hormone (TRH), which tells the pituitary to send out Thyroid Stimulating Hormone (TSH). It is TSH that controls the production of thyroid hormone from the thyroid gland, which mainly affects the body's metabolic rate. Furthermore, the hypothalamus sends out Corticotropin-Releasing Hormone, which tells the pituitary to send out Adrenocorticotropin Hormone (ACTH). ACTH stimulates the adrenal glands to produce cortisol, another hormone that is important in the body's metabolism, in addition to androgenic hormones.
The hypothalamus and pituitary together control the production of a hormone such as thyroid hormone, or others, through a process called feedback inhibition. For example, the hypothalamus and the pituitary have specific receptors that allow them to sense the blood level of thyroid hormone. If it rises above what is needed the hypothalamus reduces its output of TRH and the pituitary lowers its output of TSH. The feedback of the thyroid hormone level in the blood serves to inhibit the release of TRH and TSH to maintain control of the blood level of thyroid hormone.
The production of the sex hormones is regulated in the same way by the hypothalamus and the pituitary. The hypothalamus secretes Gonadotropin-Releasing Hormone (GnRH) which attaches to specific receptors on certain cells in the pituitary and tells them to send out the gonadotropins, Follicle-Stimulating Hormone (FSH) and Luteinizing Hormone (LH). It is FSH and LH that attach to specific receptors on the testes or the ovaries to produce the sex hormones, testosterone and estrogen, respectively.
In the first decade of life it appears that the hypothalamus and the pituitary are very sensitive to the feedback inhibition of the sex hormones. This means that prior to puberty, very low levels of testosterone and estrogen are able to prevent the hypothalamus from releasing its GnRH and the pituitary its FSH and LH. This results in the blood levels of testosterone and estrogen being very low prior to puberty.
A few years before puberty the adrenals increase their output of androgenic hormones which causes a small growth spurt and the development of pubic and axillary hair. What actually triggers the beginning of puberty is, as yet, poorly understood. However, what is known to happen is that the hypothalamus and pituitary start to become progressively less sensitive to the sex hormones. The gradually diminishing feedback inhibition of the sex hormones on the hypothalamus and pituitary results in their slowly increasing their output of GnRH and the gonadotropins, FSH and LH, respectively. By the time puberty is in full swing, the levels of gonadotropins and the sex hormones have risen significantly.
During male puberty, more FSH and LH attach to specific receptors in the testes and cause an increase in testosterone production, while at the same time giving them the ability to produce sperm. Puberty in the male also results in the progressive increase and coarsening of facial, chest, axillary, abdominal, extremity, and pubic hair, with enlargement of the vocal cords and deepening of the voice. Moreover, with the associated increase in the pituitary output of Growth Hormone (GH), the male experiences a significant linear growth spurt and the development of his musculoskeletal system as well. Furthermore, along with the capacity for sperm production, puberty brings on enlargement of the penis, scrotum, and testes. Finally, testosterone not only plays a major role in sexual differentiation, development, and maturation, but also in the desire for sexual relations. In addition, testosterone is important in giving the male the ability to maintain an erection for adequate penetration into the vagina and ejaculation during sexual intercourse. All these developments prepare the boy to become a man and later a father.
During puberty in the female, more FSH and LH attach to specific receptors in the ovaries and cause an increase in estrogen production while at the same time giving them the ability to develop an egg. Puberty in the female results in an increase in mainly pubic and axillary hair that is not as coarse as in the male. Moreover, breast development takes place so that the potential mother will be able to provide breast milk for her infant. In addition, an increase in Growth Hormone (GH) results in a significant linear growth spurt and development of her musculoskeletal system as well. Puberty also brings on enlargement of the external genitalia and increased mucous production within the vagina and uterus. Finally, along with the capacity for egg development, the increase in FSH, LH, and estrogen allows for ovulation, where the egg is released and can enter the fallopian tube.
Inside the fallopian tube the egg can meet and join with the sperm, which has been deposited into the vagina by the male during sexual intercourse, to form new human life. After ovulation, the ovaries mainly secrete the pregnancy hormone called progesterone. The estrogen before ovulation, and the progesterone after ovulation, attach to specific receptors in the lining of the uterus to make it thicken up and produce more mucous helping it to prepare for pregnancy. If a pregnancy does not take place, the gonadotropins (FSH, LH) and the female sex hormone levels (estrogen, progesterone) drop precipitously to cause the lining of the uterus to shed in the process called menstruation. The first menstrual period generally marks the beginning of female fertility and usually takes place on a monthly basis for the next thirty or forty years.
All these developments prepare the girl to become a woman and later a mother. However, during puberty an XY female will develop normal breasts and in every way look like a normally maturing woman, except when she fails to menstruate. Investigation will then uncover her as yet unknown (even to her) secret.
Remember that an XY female has Complete Androgen Insensitivity Syndrome (CAIS). In this case, the testes form testosterone, but since the androgen receptors are absent or not working, the Wolffian ducts degenerate and the external genitalia become female. However, in addition to testosterone the testes also produce Anti-Mullerian Hormone (AMH), which attaches to specific AMH receptors on the Mullerian ducts and makes them degenerate as well. So the XY female has neither a male nor female genital duct system and her vagina ends in a blind pouch. If an XY female has testes instead of ovaries how can she develop breasts during puberty?
The answer lies in the fact that breast development does not, per se, depend only on estrogen but rather the ratio between estrogen and testosterone. Since during puberty the normal XY male produces lots of testosterone and relatively small amounts of estrogen, his breast tissue does not develop. During puberty the normal XX female produces lots of estrogen and only relatively small amounts of testosterone, so her breast tissue does develop. Although an XY female has testes that produce lots of testosterone, because there are no androgen receptors for it to take effect, this allows the small amount of estrogen she produces to dominate and cause breast development. In fact, without any androgenic effects in their bodies, XY females are some of the most femininely attractive women in the world.
As noted above, the human embryo is destined to become female by default unless several other chemicals swing into action to make it become a normal male. But that's only part of the story because for the first several years of life, humans, whether male or female, cannot reproduce. Puberty first involves an as yet unexplained reduction in feedback inhibition so there can be a significant increase in the release of GnRH from the hypothalamus and FSH and LH from the pituitary. This also requires the presence of specific receptors on their target tissues. It leads to the testes being able to produce sperm and more testosterone and the ovaries being able to release an egg and more estrogen (and progesterone) so males and females can reproduce.
It is information, wrapped in chemical signals, that makes the embryo become male or female and initiates puberty, thus making human reproduction possible. As Stephen Meyer observes in the Discovery Institute film The Information Enigma, the major discovery of the last half of the 20th century was that it is information that drives biology. In generating information, all human experience points to a mind rather than a random and unguided material process.
But clinical experience teaches that just having all of the parts present for reproduction doesn't automatically guarantee fertility and the natural ability to bring about new human life. That's what we'll begin to explore next time.
Howard Glicksman
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 is delighted to offer this series, "The Designed Body." For the complete series, see here. Dr. Glicksman practices palliative medicine for a hospice organization.
The word sex comes from the Latin secare which means to separate or divide. Most one-celled organisms form offspring through asexual reproduction. It is asexual because there is no separation of genetic material. Therefore divided chromosomes do not need to be brought together and the new life produced is genetically identical to the original.
In contrast, most multi-cellular organisms form offspring in a much more complicated way called sexual reproduction. In humans, each of the chromosomes making up the 23 pairs containing the genetic material for life is separated from its partner and placed into gametes called male sperm and female eggs. Human reproduction involves sexual intercourse in which the male deposits sperm in the vagina of the female so they can move into the uterus and one of them can join its separated 23 chromosomes to the ones within the female egg in a process called fertilization. The fertilization of the female egg by the male sperm results in a one-celled zygote which then contains the full complement of genetic material and is distinct from its parents.
As difficult as it may be for evolutionary biologists to explain the blind and unguided development of the different organ systems and the body's ability to control them, because of the mechanism humans must use for reproduction they must also explain the simultaneous development of both males and females since neither is of any use to propagate the species without the other.
The three things needed for a human to reproduce are: (1) either be male or female and have all of the right sexual parts, (2) be able to produce enough sperm or release an egg into a fallopian tube, and (3) be able to participate in sexual intercourse so sperm is released into the vagina or have a clear path for sperm to swim toward the fallopian tubes.
In my last article, I showed that for the first few weeks of life the human embryo is asexual. That is because the primordial gonads have not declared themselves to be testes or ovaries yet. Notwithstanding where the embryonic structures that develop into mature sexual organs came from, the human embryo is destined to become female by default unless acted upon by specific chemicals. These include the Testis Determining Factor (TDF) (usually found on the Y chromosome), the enzymes needed to convert cholesterol into testosterone and testosterone into dihydrotestosterone, the androgen receptor on the Wolffian ducts and the tissue that will become male external genitalia, Anti-Mullerian Hormone (AMH) and the AMH receptor on the Mullerian ducts.
If all of these chemicals are present and working properly the human embryo will usually develop into a normal male. But if the TDF is absent it will usually develop into a normal female. However, if the TDF is present, directing the primordial gonads to become testosterone-producing testes, but the androgen receptor is absent or defective (Complete Androgen Insensitivity Syndrome (CAIS)), the result in an XY female. XY females occur in about one in twenty thousand "male" births and have testes instead of ovaries, no genital duct system and female external genitalia. So for the first decade of life they look like normal little girls. However, experience teaches that although humans are sexually differentiated as male or female at birth, they are not able to reproduce. Most children begin to show signs of their sexual development to come by the end of the first decade. Over the following years they will undergo sexual and bodily development in a process called puberty. Puberty is a constellation of physiological changes that, except in, for example, XY females, not only enables human beings to reproduce but also prepares them for their natural role in the family. Let's consider how this happens.
The hypothalamus and pituitary work to control many different vital hormones in the body. For example, the hypothalamus secretes Growth Hormone-Releasing Hormone, which stimulates the pituitary to release Growth Hormone (GH). As its name implies, GH is very important in the overall growth and development of the body. The hypothalamus also sends out Thyrotropin-Releasing Hormone (TRH), which tells the pituitary to send out Thyroid Stimulating Hormone (TSH). It is TSH that controls the production of thyroid hormone from the thyroid gland, which mainly affects the body's metabolic rate. Furthermore, the hypothalamus sends out Corticotropin-Releasing Hormone, which tells the pituitary to send out Adrenocorticotropin Hormone (ACTH). ACTH stimulates the adrenal glands to produce cortisol, another hormone that is important in the body's metabolism, in addition to androgenic hormones.
The hypothalamus and pituitary together control the production of a hormone such as thyroid hormone, or others, through a process called feedback inhibition. For example, the hypothalamus and the pituitary have specific receptors that allow them to sense the blood level of thyroid hormone. If it rises above what is needed the hypothalamus reduces its output of TRH and the pituitary lowers its output of TSH. The feedback of the thyroid hormone level in the blood serves to inhibit the release of TRH and TSH to maintain control of the blood level of thyroid hormone.
The production of the sex hormones is regulated in the same way by the hypothalamus and the pituitary. The hypothalamus secretes Gonadotropin-Releasing Hormone (GnRH) which attaches to specific receptors on certain cells in the pituitary and tells them to send out the gonadotropins, Follicle-Stimulating Hormone (FSH) and Luteinizing Hormone (LH). It is FSH and LH that attach to specific receptors on the testes or the ovaries to produce the sex hormones, testosterone and estrogen, respectively.
In the first decade of life it appears that the hypothalamus and the pituitary are very sensitive to the feedback inhibition of the sex hormones. This means that prior to puberty, very low levels of testosterone and estrogen are able to prevent the hypothalamus from releasing its GnRH and the pituitary its FSH and LH. This results in the blood levels of testosterone and estrogen being very low prior to puberty.
A few years before puberty the adrenals increase their output of androgenic hormones which causes a small growth spurt and the development of pubic and axillary hair. What actually triggers the beginning of puberty is, as yet, poorly understood. However, what is known to happen is that the hypothalamus and pituitary start to become progressively less sensitive to the sex hormones. The gradually diminishing feedback inhibition of the sex hormones on the hypothalamus and pituitary results in their slowly increasing their output of GnRH and the gonadotropins, FSH and LH, respectively. By the time puberty is in full swing, the levels of gonadotropins and the sex hormones have risen significantly.
During male puberty, more FSH and LH attach to specific receptors in the testes and cause an increase in testosterone production, while at the same time giving them the ability to produce sperm. Puberty in the male also results in the progressive increase and coarsening of facial, chest, axillary, abdominal, extremity, and pubic hair, with enlargement of the vocal cords and deepening of the voice. Moreover, with the associated increase in the pituitary output of Growth Hormone (GH), the male experiences a significant linear growth spurt and the development of his musculoskeletal system as well. Furthermore, along with the capacity for sperm production, puberty brings on enlargement of the penis, scrotum, and testes. Finally, testosterone not only plays a major role in sexual differentiation, development, and maturation, but also in the desire for sexual relations. In addition, testosterone is important in giving the male the ability to maintain an erection for adequate penetration into the vagina and ejaculation during sexual intercourse. All these developments prepare the boy to become a man and later a father.
During puberty in the female, more FSH and LH attach to specific receptors in the ovaries and cause an increase in estrogen production while at the same time giving them the ability to develop an egg. Puberty in the female results in an increase in mainly pubic and axillary hair that is not as coarse as in the male. Moreover, breast development takes place so that the potential mother will be able to provide breast milk for her infant. In addition, an increase in Growth Hormone (GH) results in a significant linear growth spurt and development of her musculoskeletal system as well. Puberty also brings on enlargement of the external genitalia and increased mucous production within the vagina and uterus. Finally, along with the capacity for egg development, the increase in FSH, LH, and estrogen allows for ovulation, where the egg is released and can enter the fallopian tube.
Inside the fallopian tube the egg can meet and join with the sperm, which has been deposited into the vagina by the male during sexual intercourse, to form new human life. After ovulation, the ovaries mainly secrete the pregnancy hormone called progesterone. The estrogen before ovulation, and the progesterone after ovulation, attach to specific receptors in the lining of the uterus to make it thicken up and produce more mucous helping it to prepare for pregnancy. If a pregnancy does not take place, the gonadotropins (FSH, LH) and the female sex hormone levels (estrogen, progesterone) drop precipitously to cause the lining of the uterus to shed in the process called menstruation. The first menstrual period generally marks the beginning of female fertility and usually takes place on a monthly basis for the next thirty or forty years.
All these developments prepare the girl to become a woman and later a mother. However, during puberty an XY female will develop normal breasts and in every way look like a normally maturing woman, except when she fails to menstruate. Investigation will then uncover her as yet unknown (even to her) secret.
Remember that an XY female has Complete Androgen Insensitivity Syndrome (CAIS). In this case, the testes form testosterone, but since the androgen receptors are absent or not working, the Wolffian ducts degenerate and the external genitalia become female. However, in addition to testosterone the testes also produce Anti-Mullerian Hormone (AMH), which attaches to specific AMH receptors on the Mullerian ducts and makes them degenerate as well. So the XY female has neither a male nor female genital duct system and her vagina ends in a blind pouch. If an XY female has testes instead of ovaries how can she develop breasts during puberty?
The answer lies in the fact that breast development does not, per se, depend only on estrogen but rather the ratio between estrogen and testosterone. Since during puberty the normal XY male produces lots of testosterone and relatively small amounts of estrogen, his breast tissue does not develop. During puberty the normal XX female produces lots of estrogen and only relatively small amounts of testosterone, so her breast tissue does develop. Although an XY female has testes that produce lots of testosterone, because there are no androgen receptors for it to take effect, this allows the small amount of estrogen she produces to dominate and cause breast development. In fact, without any androgenic effects in their bodies, XY females are some of the most femininely attractive women in the world.
As noted above, the human embryo is destined to become female by default unless several other chemicals swing into action to make it become a normal male. But that's only part of the story because for the first several years of life, humans, whether male or female, cannot reproduce. Puberty first involves an as yet unexplained reduction in feedback inhibition so there can be a significant increase in the release of GnRH from the hypothalamus and FSH and LH from the pituitary. This also requires the presence of specific receptors on their target tissues. It leads to the testes being able to produce sperm and more testosterone and the ovaries being able to release an egg and more estrogen (and progesterone) so males and females can reproduce.
It is information, wrapped in chemical signals, that makes the embryo become male or female and initiates puberty, thus making human reproduction possible. As Stephen Meyer observes in the Discovery Institute film The Information Enigma, the major discovery of the last half of the 20th century was that it is information that drives biology. In generating information, all human experience points to a mind rather than a random and unguided material process.
But clinical experience teaches that just having all of the parts present for reproduction doesn't automatically guarantee fertility and the natural ability to bring about new human life. That's what we'll begin to explore next time.
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