Darwinism Vs. the real world XXIX

Muscles and Nervous System: Keeping the Body Moving
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.


To be able to sit and read this paragraph, your body must perform several actions all at once. Sitting upright requires continuous coordination of the spinal muscles and limbs to maintain your body's position in space. Scanning these words involves not only the neck and eye muscles, but also the vestibular apparatus to keep the picture in proper position as you move your head and your eyes track along the page. Your eyes must process the light reflecting off the screen and convert it into something called vision. To understand what you are reading, your brain must recognize the small dark figures it sees, identify them as words to be interpreted, and transform them into ideas.
So how does your body do it? The simple answer is that your nerves and muscles, working together, let you read and reflect on this paragraph and do much more besides. But that only answers the what, and not how. In my next several articles, I will explain how neuromuscular function allows the body to deal with the laws of nature. To begin with, we will briefly explore how nerve and muscle cells work at the molecular level and are organized within the body.
At rest, all human cells carry a negative charge inside and a positive charge outside the plasma membrane, creating what is called the resting membrane potential. Nerve cells (neurons) and muscle cells (myocytes) are excitable, meaning that when adequately stimulated, they can reverse this resting membrane polarity. By allowing sodium ions (Na⁺) to rapidly enter through specific channels, they make the inside positive relative to the outside. This process is called depolarization.
When depolarization of the neuron takes place, the electrical message moves along the cell and causes calcium ions (Ca⁺⁺) to enter as well. The sudden increase of Ca⁺⁺ ions in the cytosol of the neuron signals it to release its neurotransmitter. The neurotransmitter passes out of the neuron and affects either another neuron or a myocyte, which may be stimulated or inhibited.
When a muscle cell is adequately stimulated and Na⁺ ions suddenly enter to cause depolarization of its membrane, it releases Ca⁺⁺ ions from a reservoir called the sarcoplasmic reticulum. The sudden increase in Ca⁺⁺ ions within the cytosol of the myocyte enables the contractile proteins, actin and myosin, to interact. This interaction causes muscle contraction. This is relatively short-lived, because the Ca⁺⁺ ions are soon after pumped back into the sarcoplasmic reticulum, causing actin and myosin to disengage and contraction to cease.
Each skeletal muscle is made up of many individual myocytes that run parallel to each other and are grouped in bundles. At each end of these bundled muscle fibers there is fibrous tissue called the tendons that attach the muscle, usually to two different bones, across a joint. The end of the muscle attached to the bone that stays still during contraction is called the origin and the one that moves one bone toward the other is called the insertion.
Most joints have complementary pairs of muscles that allow it to be moved back and forth along a particular plane. This is how the body uses its muscles. For example, the origin of the biceps in the upper arm is attached to shoulder blade (scapula) just above the shoulder joint, while the insertion is attached to the inner aspect of the forearm. When the biceps contracts, this makes the forearm move toward the shoulder, flexing the elbow and bringing the fist up in the muscle-man pose. Try it and see: with the palm of your hand turned toward your face, maximally flex your elbow and put your other hand on your biceps to feel it contract.
In contrast, the origin of the triceps is located on the scapula just below the shoulder joint and its insertion is attached to the back of the elbow. When the triceps contracts this makes the forearm move away from the upper arm, straightening (extending) the elbow and moving the fist away from the shoulder. Try it and see: while maximally extending your elbow put your hand on your triceps and feel it contract.
The musculoskeletal system consists of over two hundred bones with about six hundred muscles attached to them, usually across a joint consisting of two or more bones. The bones that make up each joint can usually be moved in two or more directions by pairs of complementary muscles, like the biceps and triceps flex and extend the elbow. It is through controlled contraction and relaxation of the muscles that the bones can move to allow the body to breathe, move around, and manipulate things.
The nervous system is organized like a military operation in that a general and his staff must receive information from the reconnaissance team about where the enemy is located and what it is doing. This information is used by headquarters to help make decisions about strategy and to formulate the orders being sent out to the troops. But things don't end there. Headquarters has to constantly be kept informed of what is going on in the field so it can adjust to an ever-changing situation.
Similarly, the body's nervous system is divided into the central and peripheral nervous systems. The peripheral nerves have sensory neurons bundled within them that send information about what is going on inside and outside the body to headquarters. They also have motor neurons bundled within them, which take the orders from headquarters and tell the muscles what to do. The central nervous system, consisting of the brain and the spinal cord, is the headquarters where the sensory information is received, analyzed, and compared with other information. Then orders are sent out to perform coordinated actions that are purposeful and goal directed.
In general, the spinal cord organizes the sensory messages that it receives from the peripheral nerves and sends them to the brain. It also organizes the motor messages from the brain and sends them to the various regions of the body by way of the peripheral nerves. But since the laws of nature (like gravity) wait for no man, the central nervous system uses specific, quick-acting reflexes that work through the spinal cord and the brainstem to prevent injury or to maintain the body's posture while performing goal directed activities. This is how the body protects itself from the forces of nature so it can survive.
Now you understand how the nerve and muscle cells work at a molecular level and how they are organized within the body. Next time we will look at some of the sensory devices used to monitor the goings on both inside and outside the body.
Keep in mind that evolutionary biologists would have us believe that the multiple bones making up the numerous joints that can be moved in many different directions by complementary sets of muscles all under nervous control came into being by the forces of nature alone. As an experienced pediatrician has expressed to me in writing, "Dismissing a Creative Intelligence in favor of Darwinism defies any sense of reason, genuine intelligence, or just plain everyday common sense." I couldn't have said it better myself.  

On decanonising scientists.

Scientists Aren't Exempt from Feelings, Any More Than the Public Is
David Klinghoffer

Amanda Freise makes a fine point in a post for Scientific American, "It's Time for Scientists to Stop Explaining So Much." She's a PhD student in molecular and medical pharmacology at UCLA and has evidently made a study of research on science communication. She concludes that scientists shouldn't be shocked if loading more technical information on the public doesn't dissuade them from skeptical views on certain controversial issues.
She doesn't mention evolution, but she could have done so. Freise explains that many of her colleagues still hold a "widely discredited" idea, the "deficit model," which says that if only people could be supplied with enough of the right information, they would come around and believe what they are supposed to. It's not so, however.

[T]he reluctance of some scientists to accept the failure of the deficit model approach indicates that pure information isn't enough to convince them, either -- otherwise, they would acknowledge the research and look for new ways to talk to the public.
I do not place the blame solely on my stubborn colleagues. The science of science communication is rarely, if ever, discussed among academic researchers in many fields of "hard" science. They may not even be aware that the concept of the information deficit exists, much less that it's not an accepted model of science communication. Training in public communication for researchers is also rare -- so when they operate by the deficit model and share information directly, they're just doing what they know from speaking with colleagues. And although a majority of researchers agree that scientists should be actively engaged in public policymaking about science and technology, they may not want to do it themselves.
There are other approaches to communication which provide alternative methods to opening dialogue with skeptical audiences. For instance, contextualization suggests that science must be presented in the context of a person's values, beliefs, and personal experience. Scientists accustomed to making decisions purely based on evidence, without the influence of feelings or personal values, may find this to be an onerous task.

I don't expect that Amanda Freise will be sympathetic to this -- after all, she seems more interested in redirecting skepticism toward an embrace of orthodoxy -- but engaging with "personal experience" is exactly what some of the best evolutionary skeptics do.

Advocates of intelligent design appeal to the daily observation that only intelligent agents generate information of the kind we find in computer code, magazine articles, and the like, the very same kind of information we find in DNA. Douglas Axe in his new book, Undeniable: How Biology Confirms Our Intuition That Life Is Designed, shows that the intuition of design in nature is valid, being based on our "personal experience" of how expertise is brought to bear in invention. As he points out, a bed is not made, an omelet is not made, unless someone makes them. It's no different with organisms: with the design of an orca, a spider, or a crane. I love his example of the origami crane and the living crane. It defies not only science but personal experience to imagine that only one of the two came about through purposeful application of knowhow.
Again, this is not, I'm pretty certain, what Ms. Freise had in mind. I'm also not sure I can go along with her on this -- more of that precious overestimation of scientists, by the media and by scientists themselves:

We [scientists] place extraordinarily high value in data, with as little emotion involved as possible. Even a strong "gut feeling" about a scientific finding will be pushed aside when we see enough rigorously obtained evidence to the contrary. In contrast to many members of the public, a skeptical scientist can be convinced by giving them enough information. At least that's true when it comes to questions about our personal fields of research.

This seems to exempt scientists from the all too human tendency to be led by one's community, often to the exclusion of your own critical faculties. This tribalism -- which is what it really is -- applies not least when the context is your "personal field of research." You want to be thought well of especially by your colleagues. Another great lesson of Dr. Axe's book is that this applies to scientists too, no less than to the rest of us. You see this all the time in other areas of life -- political debates going on at the moment, for example. Why not in science, too? Why are scientists magically immune from a slavish regard for how others see you?
In the evolution controversy, the context we know best, here's how the dynamic works. So much hinges on the dread of "creationism." No one should ever forget the power of that scare word, "creationist," with all it implies by way of not only scientific but social opprobrium. Though ID is emphatically not creationism, being called "creationists" is something ID proponents face every day. This is the major way in which the orthodox, including scientists, confuse the public in order to tamp down dissent and skepticism.
In the minds of many, in science and in the media, merely to question the evidence that Darwinian processes explain life is to shame and taint yourself through association with "creationism." Of course this would make even Alfred Russel Wallace, co-discoverer with Darwin of the theory of evolution by natural selection, a "creationist."
However absurd, the term "creationist" is an effective prophylactic against thought, which is why, if I had my way, it would be retired from all discussion. Language should clarify and distinguish, not muddy and blur. Any lower standard is a hallmark of propaganda.
But propaganda is effective even with scientists. No, they are hardly more exempt from the "influence of feelings" than the public is. Recognizing that, and its flipside -- that intuition can sometimes be valid, cutting through reams of obscure technical data -- would help advance the conversation about evolution. Maybe about some other controversies in science, too.

Darwinism Vs. the real world. XXVIII

In Female Sexual Function, Irreducible Complexity and Natural Survival Capacity
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.


In previous articles I've explained that the human embryo is destined to become female by default unless several 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 involves an as yet unexplained reduction in the feedback inhibition of the hypothalamus and pituitary so they can increase their output of their respective hormones. This leads to the testes being able to produce sperm and more testosterone and the ovaries being able to develop and release an egg and produce more estrogen and also the pregnancy hormone, progesterone.
Once the sexual organs have matured so the male can produce sperm and the female can release an egg into the fallopian tube, all that is needed for new human life to come about is for them to join together to form a zygote. The natural way that human reproduction occurs is by the male and female physically coming together in sexual intercourse. This very intimate physical union requires the man to deposit semen containing sperm near the cervical opening of the woman's uterus. Over the next several hours, aided by the cervical mucus, the sperm use their flagella to swim through the body of the uterus toward the fallopian tubes. If one of the woman's ovaries has released an egg around that time then one of the sperm may be able to penetrate its outer shell to form a zygote in a process called fertilization. Over the next several hours the zygote develops into an embryo which over the next several days moves into the body of the uterus and implants in its endometrial lining. Once implantation takes place the embryo continues to develop and grow into the fetus in a process called gestation. It then exits the mother's body about nine months later as a newborn baby.
In my last article we looked at the two tasks the male must perform to reproduce and what can go wrong to prevent it. The male must produce enough healthy active sperm which is dependent on having, not only properly working testes, but the right amount of hormones and properly working receptors and he must have enough pelvic blood flow and nervous function to penetrate deep into the vagina and ejaculate his semen. Now let's look at what it takes for a woman to reproduce and what can go wrong to prevent it.
From the above it is evident that the female's fertility is mainly dependent on three tasks: developing and releasing an egg from the ovary, getting the egg to enter the fallopian tube while assisting the sperm to reach it for fertilization, and providing nutritional support for the developing new human life once it implants in the endometrial lining of the uterus.
All women have their full complement of immature eggs (ova) in their ovaries at birth. These are contained in sacs, with surrounding support tissue that are called follicles. The first task of the female, developing and releasing an egg from the ovary, is dependent on producing enough of the gonadotropins, Follicle Stimulating Hormone (FSH) and Luteinizing Hormone (LH), enough estrogen and having enough properly functioning specific receptors.
At the beginning of a woman's menstrual cycle the blood level of estrogen is low. This tells the hypothalamus to send out more Gonadotropin Releasing Hormone (GnRH) and the pituitary more FSH and LH. In particular, by attaching to specific receptors the rise in FSH stimulates some of the follicles in the ovaries to mature and make estrogen as well. At this point the ovary is said to be in the follicular phase. Throughout this phase the cells in the maturing follicles form more receptors for both FSH and estrogen which results in a positive feedback that makes the follicles even more sensitive to FSH and estrogen. This increased sensitivity enables them to produce more estrogen and causes the eggs to mature further. The dominant follicle that will ultimately release an egg (ovum) is the one that has been able to produce the most FSH and estrogen receptors and therefore has received the most hormonal stimulation.
However, during the follicular phase as the estrogen level rises higher and each of the developing follicles vies for the right to release their egg, something very surprising takes place in the pituitary. Remember that prior to puberty the release of FSH and LH is normally inhibited by a rising estrogen level. This in fact is how the body is able to keep control of its estrogen level. However, as the ovary nears the end of the follicular phase, when the level of estrogen is rising higher, this actually stimulates the pituitary to suddenly release more LH (and to a lesser degree FSH as well) in what is called the LH surge. This actually represents a positive feedback which as yet is still poorly understood. Clinical experience teaches that the LH surge is absolutely necessary for the dominant follicle to release the egg from the ovary so it can migrate toward the fallopian tube and have a chance of meeting up with a sperm in a process called ovulation.
There are several conditions that can result in anovulation, where the ovaries are not able to send out an egg toward the fallopian tube. One category involves inborn errors which results in the ovaries not developing and maturing properly. The vast majority however are acquired disorders which usually are intermittent and with medical intervention can be resolved. Consistent monthly ovulation is dependent on the delicate and complex interplay of the hypothalamus, the pituitary and the ovaries. Disruption of this hormonal balance by chronic emotional stress, malnutrition, significant fluctuations in weight, serious or recurrent illness and excessive physical exercise are some of the commoner reasons for anovulation.
Another not uncommon condition is polycystic ovary syndrome (PCOS). PCOS involves inappropriate negative feedback of the sex hormones on the pituitary gland. This causes a relatively low level of FSH which limits the cyclical development of the follicles in the ovaries so that a dominant one is not able to be released in ovulation. Also, there are numerous different glandular disorders, such as ones that affect the thyroid, the adrenals or the pituitary, which can lead to anovulation as well. Finally, it must be remembered that each woman begins her life with a full complement of egg follicles in her ovaries. Since, after puberty, during each month several follicles mature and vie for ovulation, this means there are that many less follicles available for ovulation and estrogen production in the future. A woman's fertility therefore eventually runs out and with it she no longer ovulates or has menstrual periods and has very low levels of estrogen. This is called menopause and usually takes place after thirty to forty years of menstruating.
If the female has had sexual intercourse around the time she has ovulated then her second task of getting the egg to enter the fallopian tube while assisting the sperm to reach it for fertilization comes into play. By attaching to specific receptors, the high levels of estrogen prior to ovulation makes the cells in the cervical opening of the uterus secrete lots of watery mucus. This watery mucus assists the sperm as they swim up through the body of the uterus to the fallopian tubes. At the same time the high levels of estrogen also causes the fallopian tubes to increase the movement of their cilia (small hair-like projections) and muscle contraction in an effort to try to coax the egg to enter. Once inside the fallopian tube the egg is swept along toward the body of the uterus by ciliary action and muscle contraction. It is here, within the relatively confined space of the fallopian tube, that the sperm usually meet up with the egg and fertilization takes place. The resulting zygote is then also swept along the fallopian tube into the body of the uterus on its way to implantation.
Some of the commoner causes of female infertility involve disorders of the fallopian tubes. Sexually transmitted diseases, like gonorrhea and chlamydia, cause pelvic infections which results in damage to the fallopian tubes and abnormal function. This causes them to either not be able to capture the egg, let the egg and sperm meet, or let the zygote pass through to the body of the uterus. Another not uncommon cause of fallopian tube malfunction, resulting in female infertility is a condition called endometriosis. This disorder involves the growth of tissue from the lining of the uterus (endometrium) in abnormal places, such as around the fallopian tubes and the ovaries. The presence of this abnormally placed endometrial tissue causes obstruction and damage of the fallopian tubes resulting in malfunction.
Recall, the second task of the female involves not only the fallopian tubes but also the cervical opening of the uterus where the sperm enter on their way to trying to fertilize the egg. Sexually transmitted diseases, like gonorrhea and chlamydia, can also cause inflammation and scarring of the cervix. This can lead to narrowing of the cervical canal and abnormal mucus production both of which can prevent the sperm from moving up into the uterus. In addition, certain hormone problems can cause the cervix to not produce the right amount or kind of mucus to adequately help the sperm move into the uterus.
If a sperm is able to fertilize an egg in the fallopian tube and the resulting zygote is able to move into the body of the uterus, then the third task of providing nutritional support for the developing new human life once it implants in the endometrial lining of the uterus becomes necessary. The increasing amounts of estrogen the ovary releases prior to ovulation attaches to specific receptors in the endometrial lining of the uterus and signals it to proliferate. This causes the endometrial lining to grow and develop resulting in it secreting large amounts of clear mucus which aids the sperm in their struggle to reach the fallopian tubes.
After ovulation the remaining cells of the dominant follicle become the corpus luteum (yellow body) and begin to form more LH receptors on their plasma membranes. The predominance of LH receptors on these cells results in the production of mostly progesterone, and to a lesser extent, estrogen as well, from continued FSH stimulation. Progesterone attaches to specific receptors on the endometrial lining and signals them to proliferate further and to secrete thicker and more nutrient-rich mucus in preparation for the implantation of the embryo. The corpus luteum normally has a lifespan of only about 10 to 14 days at which time a precipitous drop in the production of estrogen and progesterone takes place. This sudden drop in the levels of sex hormones results in the endometrial lining no longer being supported and it degenerates and dies. The endometrial tissue is then shed, with blood, out of the uterus and into the vagina and from there out of the woman's body in a menstrual period.
However, if pregnancy does take place the embryo produces a hormone called human Chorionic Gonadotropin (hCG) which acts like LH and is able to keep the corpus luteum alive and functioning until the placenta forms and takes over. From here on gestation takes place whereby the embryo develops into a fetus and continues to grow and develop within the uterus until it comes out into the world as newborn baby several months later.
For a healthy pregnancy to continue the embryo must implant in the lush endometrial lining of the uterus. The presence of uterine defects, such as abnormal shape, a dividing wall (septum), benign muscle tumors (fibroids), and abnormal mucosal growths (polyps) can interfere with either implantation or continued gestation resulting in infertility. If the corpus luteum does not secrete enough progesterone for an adequate amount of time the endometrial lining will not be prepared to properly nurture the embryo. Finally, one other rare cause of luteal phase insufficiency is the complete absence of progesterone receptors on the gland cells of the endometrium. Without these receptors the progesterone secreted by the corpus luteum cannot stimulate the endometrium, it cannot grow and develop properly and the uterine lining will be unable to perform the third task of female fertility.
In summary, human reproduction involves not only having the right tissues and organs in place, but also having them working together in a well-coordinated fashion. The female cannot be fertile unless at least one of her ovaries can release an egg, her fallopian tube can capture it and move it towards the sperm that have been assisted by the cervical mucus to swim toward it, and then provide a supportive haven for the implantation and gestation of new human life. These all require not only having the right tissues and organs in place, but also having the right amount of hormones and receptors that respond in the right way and at the right time. Any one permanent abnormality that leads to any one chronic malfunction is likely to make human reproduction impossible.
Of course, it goes without saying that all of the parts working together in a coordinated fashion, as directed by specific hormones and their receptors, to enable either the male or female to reproduce demonstrates not only irreducible complexity but natural survival capacity as well. However, the word sex comes from the Latin secare which means to separate or divide. This means that for every life form that reproduces sexually not only must all of its organ systems that allow for metabolic control but also its male and female components must have developed simultaneously. As for human life, whether it came about by the more plausible explanation of intelligent design or whether one believes the Darwinian narrative, it all had to start with just one male and just one female. 

A dose of humility re:junk DNA?

On Junk DNA Claim, Francis Collins Walks It Back, Admitting "Hubris"

David Klinghoffer

Count on Marvin Olasky at World Magazine not to miss something like this. In The Language of God, theistic evolutionary icon Francis Collins used so-called Junk DNA as homerun evidence against intelligent design. He has since backed down on that, honorably, admitting "hubris" in the process. Olasky:

Collins claimed on page 136 that huge chunks of our genome are "littered" with ancient repetitive elements (AREs), so that "roughly 45 percent of the human genome [is] made up of such genetic flotsam and jetsam." In his talk he claimed the existence of "junk DNA" was proof that man and mice had a common ancestor, because God would not have created man with useless genes.

Last year, though, speaking at the J.P. Morgan Healthcare Conference in San Francisco, Collins threw in the towel: "In terms of junk DNA, we don't use that term anymore because I think it was pretty much a case of hubris to imagine that we could dispense with any part of the genome, as if we knew enough to say it wasn't functional. ... Most of the genome that we used to think was there for spacer turns out to be doing stuff."

Good for Collins -- and maybe he'll go on to deal with other times scientists feel sorry for God as they look at His purportedly poor design. For example, evolutionists use the retina of the eye as evidence against creation, because nerve endings are at the front rather than at the back, which at first glance seems better placement. Yet, as Lee Spetner explains in The Evolution Revolution (Judaica Press, 2014), physicists now see front placement as the best one for "ingeniously designed light collectors."

The list of needed retractions should include what you probably learned in high school about apparently purposeless human vestigial organs. Robert Wiedersheim's 1895 list of 86 has shrunk, as almost all of them have proved to have functions. For example, the most famous vestigial organ -- the vermiform appendix -- is a crucial storage place for benign bacteria that repopulate the gut when diarrhea strikes. The appendix can be a life-saver.

By "hubris" perhaps he means the overweening tendency to assume that scientific opinion as constituted at the moment has got everything all figured out. The repeated need to retract and walk back previous certainties should be a lesson to all, a warning that we can't simply hand over our intellects to "science."

In briefest form, that's the message of Doug Axe's book Undeniable. When it comes to big-ticket science questions like evolution, not only do you get to think for yourself. You have a positive obligation to do so.

Why we need not idolise science for it to be of value.

Yes, There Can Be Science Without Scientism, and Without Relativism
Sarah Chaffee


In an article at Slate referring to Neil deGrasse Tyson's now famous #Rationalia tweet, sociologist Jeffery Guhin argues that "A rational nation ruled by science would be a terrible idea."

What? This, from popular media? Guhin makes his case against scientism, noting:

First, experts usually don't know nearly as much as they think they do....[T]he real problem is when we forget that scientists and experts are human too, and approach evidence and reasoned deliberation with the same prior commitments and unspoken assumptions as anyone else. Scientists: they're just like us.

Yes -- science, like any other human enterprise, is flawed.

"And second, science has no business telling people how to live," Guhin continues. Decrying scientific racism, he recalls that "Eugenics was science, as was social Darwinism and the worst justifications of the Soviet and Nazi regimes." Kudos to Guhin for recognizing that -- a point that many other commentators avoid facing squarely.

In fact, that sounds remarkably like what Discovery Institute's John G. West says in Darwin Day in America: How Our Politics and Culture Have Been Dehumanized in the Name of Science. As Dr. West summarizes in the Preface:

At the dawn of the last century, leading scientists and politicians giddily predicted that modern science -- especially Darwinian biology -- would supply solutions to all the intractable problems of American society, from crime to poverty to sexual maladjustment.

Instead, politics and culture were dehumanized as a new generation of "scientific" experts began treating human beings as little more than animals or machines:

In criminal justice, these experts denied the existence of free will and proposed replacing punishment with invasive "cures" such as the lobotomy.

In welfare, they proposed eliminating the poor by sterilizing those deemed biologically unfit.

In business, they urged the selection of workers based on racist theories of human evolution and the development of advertising methods to more effectively manipulate consumer behavior.

In sex education, they advocated creating a new sexual morality based on "normal mammalian behavior," without regard to longstanding ethical or religious imperatives.

But here Guhin abruptly changes direction with a weird foray into bashing creationism. He says that "creationism has a lot more in common with scientism than people such as Tyson or Richard Dawkins would ever admit." Where did that come from? My guess is it's tactical. At Slate, to get away with saying anything that could be seen as critical of materialism, you need to demonstrate your credibility by attacking the creationists.

He has no strong conclusion to his article; rather Guhin's last section is entitled "The elusive truth." Once creationism and scientism are gone, it turns out, what's left is relativism. He says, "Science may give us data, but it doesn't mean that data points to truth -- it's just what we currently understand as truth."

True, there's no science without faith, as Douglas Axe notes in Undeniable:

Science can't even conceivably give us anything more certain than the faith we place in the essential propositions undergirding science, which means science will never be the primary path to knowing, much less the only path to knowing.

But is there a third way? Can we reject the confines of pure materialism without rejecting the information-value of data? Can there be science without scientism?

Historically, science existed in a non-materialist framework. Intelligent design, unlike Darwinian evolution, provides a basis for believing that we are able to ascertain truth about the world while recognizing that some things may be beyond science's reach. ID aligns wells with a view affirming that humans are unique and it is consonant with the existence of ultimate meaning. At the same time, it affirms the importance of rationality and science -- which can help us to improve our quality of life through healthcare, technology, and more.


Accepting reality does not mean throwing away rationality -- just #Rationalia.

Scientists comment on "undeniable."

More Scientists Praise Douglas Axe's Undeniable
David Klinghoffer 

One of the refreshing things about Doug Axe's new book  Undeniable: How Biology Confirms Our Intuition That Life Is Designed is his confession that you don't have to take his word for it. Or anyone else's, for that matter.Despite being a molecular biologist who has done the lab research to confirm the impossibility of unguided nature chancing upon functional proteins, he shows how, even without that, the design intuition most of us share embodies sound science.

We don't need to rely slavishly on what scientists say because, in an important sense, we are all scientists, capable of judging a big scientific idea like evolution, if not necessarily the technical details, for ourselves. Evolution's defenders in the world of science love to overawe the public with those details, but we can look past and through them. Its defenders in the media tend toward a precious, almost worshipful regard for scientists, but as Dr. Axe reminds us, professionals in the sciences are human just like us.

All that having been said, it's interesting to hear from those professionals -- biologists especially -- who agree with Dr. Axe on his main point. And indeed endorsements for the book have continued to come in.

From Russell W. Carlson, Professor Emeritus, Department of Biochemistry and Molecular Biology, University of Georgia:

Many say we must accept that life is ultimately due to a grand cosmic accident, that evolution is an unguided purposeless process, and that we must deny our experience. Axe describes why the design we see in nature fits with scientific observation as well as with our "undeniable" experience.

From Matti Leisola, D.Sc., Professor Emeritus of Bioprocess Engineering, Aalto University, Finland:

Douglas Axe is one of the very few experimental scientists who has used his skills to test the validity of evolutionary mechanisms as a source of inventions. Here, he concludes that we can trust our common (universal) design intuition; it is supported by science, whereas evolutionary stories are anti-science.

From Mark C. Biedebach, Professor Emeritus, Department of Biological Sciences, California State University, Long Beach:

In Undeniable, Dr. Axe has carefully crafted a case that strongly favors our human intuition that life was designed. As a protein chemist, he gives numerous examples and reasons why unguided evolution (even of a cell's protein molecules) is improbable in the extreme. As I understand his case, its power to convince surpasses that of anything else I have ever read (on origins science) during my 65 years as an engineer, biophysicist, and physiologist.

Whoa. Frankly, those endorsements would be impressive from any scholar, or any thoughtful adult. They're all the more so from scientists who, you would have to agree even against your will (if you're a Darwinist), know what they're talking about.

Time for true separation of church and state in the U.K?Pros and cons.

A clash of titans XXIV

(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.

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.

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.

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.

The undeniable logic of the case for design.

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

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.

Miracles for sale.

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.