Biological Design Flaws?

Wisdom Teeth Reflect the Creator’s ForesightFebruary 1st, 2012 By Dr. Fazale Rana

Skeptics often point to human wisdom teeth as an example of a useless human body part. But a new study challenges this evolutionary account.

An impacted wisdom tooth is painful. The agony it causes, however, is not confined to the poor person destined for oral surgery. It also creates discomfort for Christian apologists.

Skeptics often point to human wisdom teeth as an example of a useless human body part. They claim the human body is beleaguered with bad designs (such as the appendix, tonsils, adenoids, the coccyx, body hair), asserting that these structures evince human evolution. Skeptics view these features as vestiges of biological evolution—structures that at one time had use, but lost it as humans descended from evolutionary ancestors.1

When it comes to wisdom teeth many people believe that they serve no useful purpose today. These “third molars” become impacted because of the relatively small size of the human jaw. When the teeth erupt (usually in young adulthood), there is no room for them. In contrast, the Neanderthal jaw was larger and could handle the onset of wisdom teeth. Evolutionary biologists interpret this characteristic to mean that wisdom teeth are leftovers (vestiges) from when humans were another hominid species.2

But a new study challenges this evolutionary account.3 A scientist from the UK studied the size and shape of the human jaw of eleven different people groups around the globe––six were agriculturalists and five engaged in a hunter-gatherer lifestyle.

The food that comprises the diet of these two broad categories varies significantly in consistency. Hunter-gatherers eat food that is raw, requiring longer and more intense bouts of chewing. Agriculturalists eat much softer food.

Research reveals that the jaw shape and size differs, depending on the means of subsistence. People who consume a soft diet (typified by an agriculturalist lifestyle) have shorter, broader jaws. Those who consume a hunter-gatherer diet exhibit longer, narrower jaws. The longer, narrower jaws of hunter-gatherers readily accommodate wisdom teeth. Conversely, wisdom teeth don’t easily fit into the mouths of people with shorter, broader jaws.

This result indicates that, fundamentally, the human jaw is designed to house wisdom teeth. For most of human history people employed a hunter-gatherer lifestyle, and impacted wisdom teeth and associated ailments were likely not present. It was only when humans implemented wide-scale agricultural practices that wisdom teeth caused problems. Still, shorter, broader jaws weren’t inevitably a problem. Without dental care until very recently, people throughout human history lost teeth. This tooth loss would provide room for wisdom teeth. And, of course, having replacement molars was welcome at a time when tooth loss was common.

Such advances take the teeth out of another evolutionary argument while sharpening the case for purposeful design.

Subjects: Bad Designs?

Does Inflammation after Injury Traumatize the Case for Intelligent Design?October 21st, 2010 By Dr. Fazale Rana

Nobody likes it when insult is added to injury. But when injury is compounded by inflammation, it is often fatal.

Researchers recently made progress in their understanding of the causes of life-threatening inflammation. It is hoped that this new insight might improve treatment for trauma patients.1 Others see this advance in a different light; it seemingly provides potent evidence for the evolutionary framework. They claim that the cause of inflammation is yet another example of a design flaw in nature—something unexpected if life stems from a Designer’s hand. But does this new discovery really cause injury to the case for a Creator?

Inflammation and TraumaPhysical trauma is a major cause of death. In many instances, the patient survives the injury because of medical intervention only to die from a post-traumatic complication known as systemic inflammatory response syndrome (SIRS). The symptoms of SIRS, including fever and shock (increased heart rate and low blood pressure), are highly similar to those caused by a severe bacterial infection.

Systemic inflammation caused by bacteria stems from the body’s response to biomolecules from a microbial agent. The materials generated by the body’s response are known as pathogen-associated molecular patterns (PAMPs). Biomedical scientists note that when patients suffer from traumatic injury, their bodies generate compounds that elicit the immune system in a way similar

to the reaction caused by PAMPs. These compounds are referred to as DAMPs (damage-associated molecular patterns). Presumably, severe tissue injury causes DAMPs to be released into the blood, exposing them to the immune system.

The Source of the Inflammatory ResponseResearchers from the United States and Great Britain, speculated that the source of DAMPs may be the mitochondria, organelles in the body’s cells. They reasoned—from an evolutionary standpoint—that these organelles, which are thought to have evolved from bacteria a billion years ago, should possess molecules that cause inflammation in the same way bacterial molecules cause sepsis-induced inflammation.

The researchers discovered that DNA and proteins from mitochondria form part of the repertoire of molecules that comprise the DAMPs. Presumably, these biocompounds are released when cells are damaged as a result of severe injury. For example, the researchers

1. measured increased levels of the mitochondrial biomolecules in human patients suffering from trauma;

2. demonstrated that these compounds attract white blood cells; and3. showed that these materials cause severe inflammation when injected into rats.

Of course, the hope is that this new discovery will stimulate advances that will improve trauma care.

Trauma, Inflammation, and the Case for Biological EvolutionAccording to the prevailing paradigm in evolutionary biology, mitochondria arose when a bacterial cell was ingested by a burgeoning eukaryotic cell and evolved to be a permanent internal symbiont. If this is the case, then it is reasonable to expect that mitochondrial compounds would, indeed, make up at least part of DAMPs.

It is impressive the evolutionary paradigm would make a prediction that successfully guided research efforts. But just because this prediction has been satisfied doesn’t mean that the similarity between PAMPs and mitochondrial DAMPs has to be understood exclusively from an evolutionary standpoint. This similarity can be readily accommodated as part of a creation model. The shared features of these molecules (which just happen to cause an immune response) could simply reflect the work of a Creator who designed the molecules in mitochondria with the same structural elements as those from bacteria.

It is tempting to view the existence of SIRS-causing materials within the mitochondria as a bad design—a flaw that would be expected only if evolution generated life. It is not a feature that one would anticipate if an all-knowing, all-powerful, all-good Creator made life. (For example, listen to the March 4, 2010 edition of the Nature Podcast, in which this work is described. The interviewer, Natasha Gilbert, states that the body’s response to mitochondrial DMAPs “seems like a bit of a design flaw.”)

In response to this challenge, however, Carl J. Hauser, who helped lead the investigation, disagrees. He argues that the immune response to mitochondria is a well-designed system, because SIRS doesn’t happen all the time, only when severe injury occurs. The SIRS response is avoided because the immune system doesn’t monitor activities inside cells.

In reality, the secondary inflammation that occurs after a severe injury should be inconsequential. It is only a concern because we now have the medical capabilities to keep people alive after trauma occurs. For much of human history this type of medical intervention simply wasn’t available. Even just a few decades ago, nearly everyone who experienced severe injury died. But the hope is that the number of deaths that result from traumatic injury will dramatically decrease now that we know the source of DAMPs.

And as we learn more about biological systems, I hope that the challenges to the design argument diminish as presumed design flaws in biological systems turn out to be elegant constructs.

Endnotes:

1. Qin Zhang et al., “Circulating Mitochondrial DAMPs Cause Inflammatory Responses to Injury,” Nature 464 (2010): 104–7.

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The Redundant Case for Intelligent Design: New Discovery Highlights the Robustness of the GenomeSeptember 9th, 2010 By Dr. Fazale Rana

I’m sure many of you have seen a reference at one time or another to “The Department of Redundancy Department.” 1

Image credit: Amazon.com.

It goes without saying that redundancy is generally not considered to be a “good” thing. If something is redundant it is, of course, unnecessary, useless, unneeded, wasteful, etc. Many skeptics view redundancy in biological systems as evidence that blind, undirected evolutionary processes, and not a Creator, formed living systems.

Redundancy does occur in organisms’ genomes. Evolutionary biologists believe redundant pieces of DNA result from biochemical processes that duplicate parts of the genome.

As a case in point, geneticists have discovered that many of the genes responsible for embryonic development also possess multiple enhancer sequences that each appear to control the gene’s expression in a similar fashion. At first glance, multiple enhancers appear a superfluous feature, but new research shows that this is not so. It seems that multiple enhancers actually impart robustness to the developmental process.2

Researchers studied a gene labeled shavenbaby, which plays a role in the embryonic development of the fruit fly, Drosophila. As part of their work, the investigators generated fruit flies that lacked two secondary enhancer sequences. At optimal growth temperatures, the fruit fly embryos with the missing enhancers developed in a normal manner, for the most part—but at higher and lower temperatures development was disrupted.

The researchers found that they could rescue the altered embryos at extreme temperatures if they added extra pieces of DNA to the embryos. Additionally, the researchers noted the same effect when they deleted the secondary enhancers associated with the developmental gene wingless. These results suggest that redundancy in the enhancer sequences imparts robustness to the development process (particularly when it occurs in non-optimal environments) and can be regarded as an elegant design feature of the Drosophila genome.

Redundancy and the Case for Intelligent Design

Even though redundancy is often viewed in a negative light, sometimes human engineers intentionally design systems with redundant components.  On this basis, as I point out in The Cell’s Design, it can be argued that biochemical redundancy is a good design feature. 

Redundancy is not incorporated into human designs in an aimless fashion; it’s well-thought out. Because of cost and efficiency concerns, engineers introduce redundant components into their designs judiciously, limiting them to only those parts that are critical for the systems operation.

When engineers incorporate duplicate parts into their designs, they typically engineer the system so that one of the duplicate parts functions as the primary system and the other as a backup. Only the primary system is active, while the backup system is held in reserve, kicking into operation only if the primary system fails. Engineers refer to this type of system as a responsive backup circuit.

And this appears to be how the secondary enhancers operate in the Drosophila genome. Rather than representing the unthinking randomness of evolutionary processes, secondary enhancers provide evidence that life is the product of a Creator’s thoughtful handiwork.

Endnotes:

1. To order a set of “Department of Redundancy Department” mugs, go here.

2. Nicolás Frankel et al., “Phenotypic Robustness Conferred by Apparently Redundant Transcriptional Enhancers,” Nature 466 (July 22, 2010): 490–93.

Design with a PurposeJuly 9th, 2010 By Guest Author

by Brad Sargent, PhD 

My back hurts this morning—another unwanted sign that my 50th birthday is rapidly approaching. And my eyesight—where are those reading glasses?

The human body is an amazing thing but, as I’m increasingly aware, it has its flaws. Some of the flaws in humans and all biological organisms are used as arguments against the divine design of life on Earth. After all, in Psalm 139, the Bible claims,

For you created my inmost being;you knit me together in my mother's womb.I praise you because I am fearfully and wonderfully made;your works are wonderful, I know that full well.

Atheists like Richard Dawkins and the late Stephen Jay Gould claim that if God is so good and so smart, then he would have done a better job designing the world around us. Gould’s book The Panda’s Thumb1 criticizes the design of the panda’s thumb as a case of poor engineering. Meanwhile in The Blind Watchmaker, Dawkins takes issue with the design of the human eye.2 A quick search of the Internet will produce more examples of so-called “bad designs.” For many people, the God they envision would have done a better job at creation; therefore, God can’t be responsible for life as we see it.

As a designer of medical devices, I believe that critics like Dawkins use the wrong criteria to decide what is and is not a good design. Every engineer tends to criticize how another engineer solved a problem. By nature, we like to believe we could have done a better job. But many times it turns out we just didn’t understand the problem well enough to judge. It is interesting to see how many supposed examples of bad design in nature turn out to be better than we initially understood. The complexity of a problem takes time to understand because of the subtle interaction between the parts of a system.

The panda’s thumb and the human eye are prime examples of misunderstood designs. The more we study them, the more they exhibit good design. For example, the panda’s thumb doesn’t have the versatility and capability of the human thumb, but it works well for the repetitive motion of stripping bamboo leaves. The human thumb couldn’t take that kind of constant stress.3

As another example, the high density of rods and cones in the human eye requires an increased blood flow to the retina. This requirement means the neural connections must face outward, toward incoming light.4 We now know that the human eye elegantly compensates for the inverted retina with special cells that channel light past the neurons and down to the rods and cones.5 Some researchers theorize that the inverted retina provides better blood flow to the rods and cones and allows for better neural processing.6

Both of these examples should serve as a warning to avoid being hasty in declaring a design “bad” simply because it wasn’t engineered the way we think it should have been. (The fault for other supposed design flaws—like my need for glasses—rests more on corrupted manufacturing instructions than an actual flaw.) 

We must also keep in mind that all designs require tradeoffs. At the company where I work, when a client brings us an idea for a new or improved product, the first step is defining the specifications for the new device. For medical devices, this is an essential part of the FDA Design Control process. The exercise usually starts like writing a wish list for Santa. Our experienced clients know they can’t have it all, but figure why not aim high? Everyone wants the new device to be better than the competition. The product must be smaller yet have longer battery life and a bigger display, be lighter yet more rugged and durable, be simpler and easier to use yet include more features. And, of course, it should be cheaper, too.

It can be fun trying to achieve what seems impossible. In the end, however, you have to prioritize the most important features. The key is clear understanding of the goals. I’ve seen many development projects lose focus because the design team didn’t understand the real goals of their project. Too often, good engineering effort goes into achieving unnecessary features while crucial ones are missed.

Interestingly, the FDA regulations for verification and validation testing of medical products does not focus on determining if a device is “perfect” in some absolute way. Rather, they require (1) that the product’s physical and operational requirements are specified clearly; and (2) that the device is tested thoroughly to see that it truly meets those specifications. In essence, the regulations ask, “Are the goals clearly defined and does the device meet those intended goals?”

Going back to “bad” designs in nature, I believe the comparison with man-made engineering should change the scope and focus of how we view organisms’ functions and operations. We need to avoid looking at whether a particular biochemical process is as efficient as it could be (according to us) or at whether a particular organism is as well suited to its environment as it could be. Instead, we need to ask, “Does that organism or process fulfill its purpose in the overall system we call life on Earth?”

In my work, if the part I design fulfills its purpose, then it is considered a “good” part. Yes, another engineer might have made improvements irrelevant to the function of the whole device but that doesn’t make it better. For example, the “improved” part might be lighter but if weight doesn’t matter, then this change is not an improvement. 

In regards to God’s designs in nature, we need to look at the big picture. We no longer need to debate whether the panda’s thumb is optimally designed. We need to ask, “What was God’s purpose for the panda?” If the panda is fulfilling that purpose, then there should be no complaint about its thumb. Imagine a creature optimized according to our standards. That animal would most likely overrun its environment and unbalance the ecosystem.

Complete understanding of God’s design for individual creatures (or any physical phenomena) is difficult, if not impossible. But we can look at the history of life and see how different organisms in different places and times have resulted in a planet wonderfully suited for humanity.  The individual pieces may seem, to us, flawed and insignificant, but take a step back and even those “flaws” add to the beauty of the whole picture. (See Hugh Ross’ book Why the Universe Is the Way It Is, as well as his list of evidences for supernatural fine-tuning, for further discussion of the incredibly delicate balance required for terrestrial life.)

The Bible reveals much about God’s purpose for mankind. My favorite passage is Romans 8:18–19 where Paul writes, “I consider that our present sufferings are not worth comparing with the glory that will be revealed in us. The creation waits in eager expectation for the sons of God to be revealed.”

Thinking about what God has planned for our future helps me put the supposed imperfections of this world in perspective—even that nagging pain in my back.

 

Endnotes:

1. Stephen Jay Gould, The Panda’s Thumb: More Reflections in Natural History (New York: W.W. Norton & Company, Inc., 1980).

2. Richard Dawkins, The Blind Watchmaker (New York: W.W. Norton & Company, Inc., 1986).

3. Hideki Endo et al., “Role of the Giant Panda’s ‘Pseudo-Thumb,’” Nature 397 (January 28, 1999): 309–10.

4. A. Wirth, G. Cavallacci, F. Genovesi-Ebert, “The Advantages of an Inverted Retina: A Physiological Approach to a Teleological Question,” Developments in Ophthalmology 9 (1984): 20–28.

5. A. M. Labin and E. N. Ribak, “Retinal Glial Cells Enhance Human Vision Acuity,” Physical Review Letters 104, 158102 (April 16, 2010).

6. L. M. Parver, C. Auker, and D. O. Carpenter, “Choroidal Blood Flow as a Heat Dissipating Mechanism in the Macula,” American Journal of Ophthalmology 89 (1980): 641–46.

Pseudogene Decoy Reveals Hidden Evidence for DesignJuly 8th, 2010 By Dr. Fazale Rana

Do you remember the movie Dave?

In this romantic comedy, the president of the United States suffers a stroke while having an extramarital affair and is in a coma. The chief of staff cooks up a scheme where Dave (Kevin Kline), an uncanny look-alike, is employed to impersonate the president.

Though the movie’s plot is a bit far-fetched, the premise has one foot in reality. Throughout history, heads of state, politicians, and military leaders have used political decoys to distract attention away from them and afford them some protection.

Decoys also play a role in biochemical systems. Recently, researchers discovered that the products of pseudogenes may function as biomolecular decoys, protecting the “real” gene products from breakdown.1 As it turns out, this new insight has important implications for the biology of cancer. It also provides potent evidence for the intelligent design of biochemical systems.

Pseudogenes

Evolutionary biologists consider pseudogenes the dead, useless remains of once functional genes. According to this view, severe mutations destroyed the capacity of the cell’s machinery to read and process the information contained in these genes. Still, pseudogenes possess the tell-tale signatures that allow molecular biologists to recognize them as genes, albeit nonfunctional ones.

Molecular biologists recognize several classes of pseudogenes. Duplicated pseudogenes are the largest class. Scientists posit that these DNA segments arose when gene(s) underwent duplication in the genome, after which the duplicated copies experienced severe mutations, rendering them unrecognizable as a functional gene by the cell’s machinery. Loss of duplicated gene function has little, if any, effect on an organism’s fitness since an intact copy of the functional gene still exists.

Pseudogenes and the Case for Biological Evolution

Evolutionary biologists traditionally have viewed pseudognes as “junk” DNA and consider them among the most compelling pieces of evidence for biological evolution. Identical (or nearly identical) segments of junk DNA often occur in a wide range of related organisms and reside in corresponding locations in these genomes. For evolutionists, this occurrence clearly indicates that these organisms shared a common ancestor. They believe these junk DNA segments arose prior to the time when the organisms diverged from their shared evolutionary predecessor.

Skeptics often ask, “Why would a Creator purposely introduce nonfunctional, junk DNA at the exact same location in the genomes of different, but seemingly related, organisms?”

Functioning Pseudogenes

However, as I’ve pointed out before, researchers are beginning to recognize that pseudogenes are not purposeless junk. (Go here, and here to read a couple of articles about the biological roles of pseudogenes.)

Adding to these earlier studies is new work indicating that pseudogenes control gene expression by acting as decoys to protect gene products from destruction.

The researchers who made this discovery focused on PTEN, a gene that suppresses tumors. When this gene is functionally impaired it leads to the onset of several different types of cancer. Furthermore, the researchers learned that cancer also results if mutations occur in PTEN’s corresponding pseudogene, PTENP1. This finding means that the PTENP1 pseudogene must be functional.

Researchers discovered that expression of PTEN can be down regulated by small RNA molecules (miRNA). The tiny molecules bind to messenger RNA produced from PTEN. The miRNA then directs the breakdown of the messenger RNA, and prevents the PTEN protein from carrying out its cellular role. Left unchecked, the miRNA molecules would direct the breakdown of most of the PTEN messanger RNA, thus suppressing the activity of PTEN gene products and leading to the onset of cancer.

However, the similarity between PTENP1 and PTEN allow the PTENP1 messenger RNA to also bind miRNA molecules. This means PTENP1’s messenger RNA breaks down instead of PTEN’s. In other words, the gene product of the PTENP1 pseudogene operates as a decoy, which allows for the appropriate levels of PTEN messenger RNAs production.

Such decoy mechanisms appear to be widespread among genes. The researchers also uncovered similar relationships for a number of gene/pseudogene pairs, including the KRAS gene and KRAS1P pseudogene, which are also implicated in the onset of certain cancers.

This new insight stands as a landmark discovery. It promises to prove an important advance in understanding the biology of cancer and in developing a fundamental understanding of how the genome is structured and how it operates.

Pseudogenes and the Case for Intelligent Design

The importance of functional pseudogenes (as well as other classes of junk DNA) undermines the best argument for evolution. If functional, then junk DNA sequences in genomes do make sense from a creation standpoint. So, too, does the corresponding location of junk DNA sequences in the genomes of related organisms. The common location likely reflects functional significance and could be understood as reflecting shared design instead of shared ancestry. In the case of pseudogenes, similarity to the “real” gene could be understood to reflect its functional role, not necessarily its evolutionary origin.

It looks as if pseudogenes are functional elements in the genome that have been merely impersonating junk DNA all along.

Endnotes:

1. Laura Poliseno et al., “A Coding-Independent Function of Gene and Pseudogene mRNAs Regulates Tumour Biology,” Nature 465 (2010): 1033–40.

New Research Highlights Elegant Design in the Inverted RetinaJune 4th, 2010 By Dr. Fazale Rana

Imagine sitting in an airport, waiting to board a plane. Thankfully you have something interesting to read as you wait for the flight. You glance up as someone walks by—it’s the pilot. To your dismay, you see he is wearing sunglasses and is escorted by a seeing-eye dog!

Some people claim this story is based on a real event. But of course, it’s just an urban myth.

The creation/evolution controversy is not immune to “urban myths.” Recent research has helped unravel one such “myth,” namely the belief that the vertebrate retina exhibits bad design.

Faulty wiringIn 1996, evolutionary biologist Richard Dawkins wrote in regards to the vertebrate retina, 

Any engineer would…laugh at any suggestion that the photocells might point away from the light, with their wires departing on the side nearest the light. Yet this is exactly what happens in all vertebrate retinas. Each photocell is, in effect, wired backwards.1

The retina is a thin layer of light-responsive neural cells lining the interior back wall of the eye. It consists of photoreceptor cells that generate an electrical signal when light impinges upon them. At first glance the retina appears to be based on a questionable design. The light-sensitive region of photoreceptor cells orients away from the source of light. Furthermore, the nerve cell conduits

to the optic nerve lie between the light source and photosensitive region of the photoreceptor cells—a design that would make any self-respecting engineer cringe.

Thus, vertebrates’ “backward-wired” retina became an exemplar of bad design. Evolutionary biologists like Dawkins consider faulty designs in biological systems as prima fascia evidence that life stems from undirected mechanistic processes, not from the activity of a Creator.

Debunking the mythBut further research into the construction and function of the vertebrate eye has unraveled the bad design myth. Most recently, a team of Israeli physicists performed modeling studies on the optical properties of radial glial cells. Their results confirm previous work by German scientists.2

In 2007, a team of German researchers demonstrated that radial glial cells associated with the retina act as optical fibers.3 That is, the radial glial cells (star-shaped cells that help maintain the structure of nervous tissue and transport nutrients to neurons) form fibers oriented in the direction of light propagation through the retina. This allows them to efficiently transmit light from the surface of the retina to the photoreceptors. Radial glial cells have a higher refractive index than the surrounding tissue matrix, serving as a low-scattering conduit for light, and thus transmitting images capably and with little distortion.

The work by the Israeli physicists supports the conclusion that these optical fibers compensate for the retina’s “bad design.”

In light of these new insights, it is easy to see that the inverted retina is a well-designed system, worthy of the Creator.

The Snopes.com website, devoted to debunking urban myths, has an entry for the “blind pilot,” but the last time I checked there was nothing about the vertebrate retina’s bad design. Looks like it’s time to update the site.

Subjects: Bad Designs?

Evidence for God’s Grace in Epilepsy Genes January 22nd, 2010 By Guest Author

Edward Glasscock, PhD 

Dr. Glasscock received his PhD in molecular and cell biology from the University of California at Berkeley in 2005, and currently serves as a research associate at Baylor College of Medicine in Houston, TX.

The old cliché “two wrongs don’t make a right” proves true in many situations, but in the genetics of the brain, two genetic wrongs can make a right. A few years ago, I participated in research at Baylor College of Medicine (Houston, TX) in which we discovered that inheriting two different epilepsy-causing gene mutations can actually make an individual less epileptic.1  These findings provide evidence that God has built grace into our genomes. And not only is this grace representative of

good design from an engineering standpoint, but it also reflects the character of God as our Creator.

Epilepsy is a chronic brain disease characterized by the repeated occurrence of spontaneous seizures. Although epilepsy can be acquired by brain damage such as head trauma, the disease is largely genetic, often caused by inheritance of multiple predisposing genetic risk factors. Of the more than a dozen genes known to underlie human idiopathic epilepsy (“idiopathic” means no known cause), almost all of them belong to a class of molecules called ion channels. In the brain, ion channels mediate signaling between neurons by regulating the flow of ions across the cell membrane. Studies in humans and mice have shown that individuals with more than one epilepsy-associated ion channel mutation usually have more severe seizures. However, since ion channels can have differing and often mutually opposing effects on neuronal signaling, my fellow researchers and I hypothesized that some combinations of ion channel gene mutations may actually exert mutually seizure-protective effects when present in the same individual. Such a result could explain the well-known sporadic nature of epilepsy in which the disease tends to skip generations despite the transmission of the epilepsy-associated mutation to the unaffected person.

In our study, we bred mice to carry two different gene mutations, both of which cause epilepsy independently. The first mutation disrupts a calcium ion channel gene (Cacna1a), causing mice to exhibit petit mal seizures, which are characterized by a non-convulsive, temporary cessation of activity. The second mutation deletes a potassium ion channel gene (Kcna1), causing mice to experience grand mal seizures, which cause severe shaking and convulsions. In addition, mice lacking Kcna1 die prematurely because of complications due to their severe epilepsy. When we examined mice carrying both the Cacna1a and Kcna1 mutations, they displayed a dramatic reduction in seizures and no longer showed the premature death characteristic of the Kcna1 mutation. These results demonstrate that in the appropriate genetic context, so-called “deleterious” mutations can actually be beneficial.

Although our study only pertained to a combination of two particular epilepsy genes in mice, evidence exists for “healthy” protective gene mutations in other human diseases. In studies of genetic risk factors for multiple sclerosis, a disease of the central nervous system, inheritance of certain gene variants (alleles) has been found to either confer disease susceptibility or protection. Whereas an allele called DRB1*15 is associated with a particularly high susceptibility to multiple sclerosis in carriers, four variants (DRB1*01, DRB1*10, DRB1*11 and DRB1*14) are linked to disease resistance, thus negating the harmful affects of the DRB1*15 variant.2,3 This principle of protective gene interactions is repeated again in age-related macular degeneration (AMD), where loss of vision in the center of the visual field (macula) leads to blindness. Studies looking for gene variants associated with resistance or susceptibility to AMD have found that not only do protective gene interactions occur at an appreciable frequency within the European-American population but also that the number of genetic combinations protective against AMD outnumber those linked to susceptibility.4, 5 Furthermore, the gene variants associated with resistance to AMD appear to exert protective effects of a magnitude comparable to that of disease-associated alleles (albeit in the opposite direction). Thus, although harmful mutations

exist that can cause multiple sclerosis and AMD, beneficial mutations also exist that can counteract the deleterious ones.

Sequencing of the human genome also provides indirect evidence for the presence of protective gene mutations. Craig Venter, cofounder of Celera Genomics, recently published his own personal genome DNA sequence.6 Examination of his DNA revealed that Venter carries many gene mutations that put him at risk for a variety of medical conditions, including myocardial infarction (heart attack), coronary artery disease, hypertension, obesity, lactose intolerance, and Alzheimer’s disease. Although he may develop one of these diseases eventually, to date Venter has not suffered from any of these ailments. This incongruity may be a result of the action of protective gene mutations, which are counterbalancing his harmful mutations.

In reality, each of us almost certainly carries many potentially harmful mutations for which we will never suffer disease, partly due to environmental factors, but also at least in part due to the effects of protective gene mutations. An individual’s genome is estimated to carry a minimum of about 500 potentially damaging mutations.7 In addition, one to three new harmful mutations can be generated at each generation in each individual.8 If we have so many genetic strikes against us, why then are most of us relatively healthy, all things considered? Geneticists at Case Western Reserve University School of Medicine put forth the following hypothesis aimed at this question:

“A long and healthy life could result from fortuitous absence of disease causing genetic variants (winning Mendel’s lottery), from longevity genes or, more likely, from modifier genes and protective alleles in individuals with genetic and environmental disease risks.” 9

The God of the Bible is a God of grace and the existence of protective gene mutations provides evidence of this grace built into our genomes. The psalmist describes God as “compassionate and gracious, slow to anger, abounding in love. He will not always accuse, nor will he harbor his anger forever; he does not treat us as our sins deserve or repay us according to our iniquities. For as high as the heavens are above the earth, so great is his love for those who fear him…” (Psalms 103:8–11). The same God that does not treat us as our sins deserve also designed our genomes so that we do not suffer disease as we deserve.

That two harmful mutations have the potential to mutually cancel one another in some cases brings to mind the biblical story of Joseph in the book of Genesis. Joseph was sold into slavery by his jealous brothers and years later Joseph, who was then second-in-command to the Egyptian Pharaoh, had the opportunity to confront them and exact his revenge. Instead of getting even, Joseph shows them grace saying, “But as for you, you meant evil against me; but God meant it for good, in order to bring it about as it is this day, to save many people alive” (Genesis 50:20, NKJV). Similarly, harmful genetic mutations which are “meant for evil” can sometimes be used for good. 

Endnotes:

1. E. Glasscock et al., "Masking epilepsy by combining two epilepsy genes," Nature Neuroscience 10 (2007): 1554–58.

2. D. A. Dyment et al., "Complex interactions among MHC haplotypes in multiple sclerosis: susceptibility and resistance," Human Molecular Genetics 14 (2005): 2019–26.

3. S.V. Ramagopalan et al., "The inheritance of resistance alleles in multiple sclerosis," Public Library of Science Genetics 3 (2007): e150.

4. B. Gold et al., "Variation in factor B (BF) and complement component 2 (C2) genes is associated with age-related macular degeneration," Nature Genetics 38 (2006): 458–62.

5. G. S. Hageman et al., "A common haplotype in the complement regulatory gene factor H (HF1/CFH) predisposes individuals to age-related macular degeneration," Proceedings of the National Academy of Sciences of the United States of America 102 (2005): 7227–32.

6. S. Levy et al., "The diploid genome sequence of an individual human," Public Library of Science Biology 5 (2007): e254.

7. K. E. Lohmueller et al., "Proportionally more deleterious genetic variation in European than in African populations," Nature 451 (2008): 994–97.

8. J. F. Crow, "The origins, patterns and implications of human spontaneous mutation," Nature Reviews Genetics 1 (2000): 40–47.

9. J. Nadeau and E. Topol, "The genetics of health," Nature Genetics 38 (2006): 1095–98. 

Subjects: Bad Designs?, Life Design

Viruses and God's Providence RevisitedNovember 26th, 2009

By Dr. Fazale Rana

New Research Suggests More Reasons Why God Created Viruses

Thanksgiving is the time of year that most people pause to celebrate their blessings. Christians understand that many of the good things they enjoy stem from God's providence.

In Christian theology, providence refers to God's continual role in: (1) preserving His creation; (2) ensuring that everything happens; and (3) guiding the universe. The concept of divine providence also posits that when God created the world He built into nature everything humans (and other living organisms) would need. Accordingly, every good thing that people possess has been provided and preserved by God, either directly or indirectly. (Scriptural support for this last point can be found in passages like Psalm 104.)

Sometimes God works in mysterious ways and sometimes His providence can be found in unusual places. A recent study suggests that maybe even viruses are part of God's provision for humanity. This notion may seem counterintuitive, because these nasty "bugs" are responsible for so much sickness and disease. Many people view viruses as an "evil" component of nature. But viruses are turning out to be quite practical for biomedical applications. A few months ago I wrote about proof-of-principle experiments performed by scientists from Harvard University and Howard Hughes Medical Center that describes the use of viruses to combat antibiotic-resistant strains of bacteria.

New work by a team of biomedical scientists from France adds further support for this idea. These researchers used the HIV-1 virus to successfully treat two boys with a rare brain disorder called adrenoleukodystrophy (ALD).

ALD is an x-linked genetic disorder that first appears in afflicted boys around six to eight years in age. This rapidly progressing disease almost always leads to death by adolescence. ALD results from a defect in the ABCD1 gene. This region of DNA encodes a protein that transports very long chain fatty acids into peroxisomes for destruction. Very long chain fatty acids take part in forming the myelin sheaths that encase axons of nerve cells. If very long chain fatty acids are not properly broken down, the maintenance of myelin sheaths is negatively impacted. As a consequence, demyelination takes place. ALD is characterized by the progressive widespread demyelination of neurons in the brain.

The French team of biomedical scientists developed and tested a clinical protocol to treat ALD by using a "disabled" HIV-1 virus to introduce a healthy ABCD1 gene into hemopoietic stem cells isolated from two seven-year-old patients suffering from ALD. After this genetic engineering step, the modified hemopoietic stem cells were introduced back into the patients. The modified cells produced healthy oligodendrocytes that halted the progression of the disease after 14 months. (For a more detailed discussion of the study go here to listen to an episode of Science News Flash that describes this work and its implications.)

It is provocative to think that researchers could use something as insidious as the HIV-1 virus to treat a horrible disease like ALD. Ironically, the same characteristics that make this virus harmful to life also turn out to be the ideal properties for gene therapy. In this way, viruses could be thought of as part of God's providence.

Does that mean God created pathogenic viruses? I suggest that the answer is yes. Pathogens control plant and animal populations and consequently play an important ecological role. What about viral pathogens that infect humans? In this case, I argue no. Rather, I propose that human viruses evolved from animal viruses, jumping hosts.

This cutting-edge work demonstrates that whether or not one sees a feature of nature as "evil" or "good" often depends on how comprehensively he or she views that particular aspect of creation. God does indeed work in mysterious ways. As researchers continue to develop new ways to use viruses, I foresee a day in which we view them as an indispensible part of our existence, part of God's provision, something that we thank Him for.

Viruses and God's ProvidenceJune 11th, 2009 By Dr. Fazale Rana

New Research Suggests a Reason Why God Created Viruses

As I mentioned last week, the Q&A sessions of our outreach events are usually pretty exciting. During this part of the program, it's not uncommon for skeptics to issue challenges to our scientific case for the Christian faith.

One frequently asked question goes something like this: "Why would God create viruses, since these nasty 'bugs' are responsible for so much sickness and disease?" Many people view viruses as an "evil" component of nature. If life stems from the work of a loving Creator, then we wouldn't expect to observe pain and suffering in nature. If, however, the blind, undirected process of evolution generated life, then cruel, troubling features in the natural realm could be easily explained.

So-called "bad" designs may not be as big a problem for the creation model as they first appear to be. Bad designs often turn out to be elegant systems and such is the case for viruses. Even though viruses cause disease, they actually comprise a vital component of nature. For example, recent work indicates that viruses play a key role in nutrient cycling in Earth's oceans.

New research that describes the use of viruses to combat drug-resistant bacteria also suggests another reason why God may have created viruses. Perhaps He made them to serve human needs.

The idea that God made aspects of nature to be of use to humanity is called divine providence. In Christian theology, this idea refers to God's continual role in: (1) preserving His creation; (2) ensuring that everything happens; and (3) guiding the universe. The concept of divine providence also posits that when God created the world He built into the creation everything humans (and other living organisms) would need. Accordingly, every good thing that people possess has been provided and preserved by God, either directly or indirectly.

On this basis, it could be argued that as part of His providence, God created viruses for humanity's use. This may seem counterintuitive, but viruses are turning out to be quite practical for biomedical applications. Recent proof-of-principle experiments performed by scientists from Harvard University and Howard Hughes Medical Center illustrate the utility of these microscopic entities. (To listen to an interview with one of the researchers, go here.)

These researchers are trying to develop a new approach to solving the obstacle of drug resistance in bacteria. Instead of looking for new antimicrobial agents, the scientists decided to make use of viruses that infect bacteria. Known as bacteriophages, some of these viruses can kill bacterial cells by infecting them and then causing them to break apart. The idea is to find viruses that will infect and kill drug-resistant microbes. Unfortunately, targeted cells can develop resistance to naturally lethal phages as well.

Due to of this confounding factor, the researchers decided to use phages nonlethal to microbes because the target cells aren't as likely to develop resistance to them. To make the phages lethal, the team re-engineered the viruses to produce proteins that target nonessential metabolic networks. Again, singling out nonessential metabolic networks makes it less likely that the bacteria will develop resistance to the phage.

As proof-of-principle, the researchers re-engineered a phage that infects E. coli. They inserted a gene into the phage, causing it to produce a protein that inhibits E. coli's so-called SOS response. This metabolic response kicks in when the bacterium's DNA sustains damage and it consists largely of a set of processes that repair the broken DNA.

The infected E. coli was also treated with a class of antibiotics called quinolones. These antibiotics produce compounds that damage DNA and would normally elicit the SOS response. Working together, the quinolones and re-engineered phage blocked DNA repair in the E. coli. Using this strategy, the scientists discovered that it took less antibiotic to kill off E. coli in culture with the phage present than without the phage. Additionally, this approach blocked biofilm formation in E. coli, which is associated with many diseases.

Furthermore, the researchers also showed that their method was effective at killing E. coli resistant to quinolones and, importantly, that it also frustrated the emergence of antibiotic-resistant cells. Two things account for the cell's inability to develop resistance: (1) the depletion of persister cells and (2) the inhibition of the SOS response. Persisters, usually resilient parts of a microbial infection, can evolve antibiotic resistance. The SOS response actually promotes the onset of antibiotic resistance because the DNA repair by the SOS system is error prone, introducing mutations to the DNA that can lead to antibiotic resistance.

Even more exciting, this technique is proven to be broadly effective. Its developers generated the same results using the re-engineered phage with other classes of antibiotics. Furthermore, they produced the same outcome using phages that were re-engineered to inhibit other metabolic systems as well.

But the utility of viruses doesn't stop here. Some researchers have proposed using retroviruses for gene therapy, in which a mutated gene is replaced with a healthy one. Other scientists used retroviruses to successfully transform adult skin cells into induced pluripotent stem cells) that may play a role in cell and tissue replacement therapies. (For an article on induced pluripotent stem cells and their potential biomedical use, go here.)

It's amazing to think that scientists have figured out how to use viruses to develop beneficial technologies. Ironically, the same characteristics that make viruses harmful to life also turn out to be the ideal properties for certain biomedical applications. And in this sense, viruses could be thought of as part of God's providence.

Does that mean that God created pathogenic viruses? I suggest that the answer is yes. Pathogens control plant and animal populations and consequently play an important ecological role. What about viral pathogens that infect humans? In this case, I argue no. Rather, I propose that human viruses evolved from animal viruses, jumping hosts. Recent examples of this phenomenon include the emergence of the HIV and SARS viruses.

This cutting-edge work demonstrates that whether or not one sees a feature of nature as "bad" or "good" often depends on how comprehensively he or she views that particular aspect of nature. As researchers continue to develop new ways to use viruses, I foresee a day in which we view them as an indispensible part of our existence, something that we thank God for.

The Appendix: Adding to the Evidence for Intelligent DesignSeptember 11th, 2009 By Dr. Fazale Rana

I am putting the finishing touches on a book about the quest to create artificial life in the lab. Going through this process makes it apparent that some material belongs in the book, but it doesn't quite fit in the main body.

So it winds up relegated to an appendix (defined by Merriam-Webster's dictionary as "supplementary material usually attached at the end of a piece of writing.")

Since Charles Darwin's time, biologists viewed the human vermiform appendix in the much the same way: A supplementary structure attached to the large intestine that isn't really needed. In fact, Darwin and evolutionary biologists since his time have argued that biological structures like the appendix stand as powerful evidence in favor of the theory of evolution. The human appendix is considered to be vestigial—once functional in evolutionary ancestors, but no longer needed by its descendents and experienced decay, losing its utility.

About seven percent of people in developed countries suffer from appendicitis. The inflamed appendix can be removed without any consequence. In fact, appendectomies help prevent ulcerative colitis. These facts seem consistent with the naturalistic view of the appendix as a useless evolutionary feature.

A team of researchers from Duke University recently challenged the idea that the human appendix is vestigial. They suggested that it might function as a storage chamber for bacteria that form beneficial biofilms in the upper part of the large intestine. The microbes stored in the appendix serve as a reservoir to replenish the biofilm that is lost as a result of diarrhea.

Interestingly, a comparative anatomy study published in 1980 (conducted from an evolutionary vantage point) demonstrated that the distribution of appendixes among primates and other mammals doesn't match the expected pattern if it was a vestigial structure. Instead, its occurrence suggests that it plays a useful role.

Revisiting the earlier study, the Duke University scientists confirmed the initial results generated in 1980. These researchers identified an appendix or an appendix-like structure in a number of mammals. From an evolutionary standpoint, it looks as if the appendix has been around for over 80 million years and appears to have originated independently multiple times, suggesting that it indeed is functional.

The human vermiform appendix is one appendix that doesn't belong at the back of the book. The fact that it is not a vestigial structure eliminates another popular argument for biological evolution.

Subjects: Bad Designs?

The Human Appendix: What Is It Good For?October 1st, 2008 By Dr. Fazale Rana

Absolutely nothing! That’s the answer soul singer Edwin Starr gave in 1970 to the question, “War, what is it good for?” It’s also the same response evolutionary biologists give when asked about the human vermiform appendix.

The human appendix is one of the prototypical examples for “bad” biological designs.1 According to skeptics, this structure is suboptimally designed. About 7 percent of people in developed countries suffer from appendicitis. And the inflamed appendix can be removed without any consequence. In fact, appendectomies help prevent ulcerative colitis.

Additionally, the human appendix is interpreted as vestigial by evolutionary biologists. Accordingly, this structure was once functional in evolutionary ancestors, but was no longer needed by its descendents and experienced decay, losing function.

Why would a Creator produce a poorly designed structure with minimal function that appears to have an evolutionary etiology (origin)? In response to this challenge, intelligent design advocates point out that, because of the lymphatic tissue associated with it, the appendix appears to serve a role in the immune system. Still, the exact nature of this putative function has never been fully established.

Researchers from Duke University Medical Center now think that they have figured out what the appendix is good for: as a storehouse for beneficial microbes.2 These scientists note that the human colon is coated with a biofilm that consists of helpful bacteria. This microbial coating may aid in digestion and participate in other biological activities. Perhaps most importantly, it excludes pathogenic bacteria from the surface of the colon. Occasionally the microbial content of the colon becomes imbalanced and pathogens gain a foothold and take over the biofilm. The body responds by flushing the colon. Bacteria from the appendix then repopulate the colon, reestablishing a healthy biofilm.

The Duke University scientists maintain that the human appendix is well designed to operate as a bacterial storage unit. Its thin, worm-like architecture and constricted opening prevent pathogenic bacteria from entering it. And its out-of-the-way location, attached to the caecum (the bulbous structure at the beginning of the colon that forms a cul-de-sac where the small intestine joins up with the colon), isolates it from the flow of fecal material through the digestive tract.

The association of lymphatic tissue with the appendix is also important. This tissue produces compounds that promote the growth of microbes within the appendix.

Interestingly, a comparative anatomy study published in 1980 (conducted from an evolutionary vantage point) demonstrated that the distribution of appendixes among primates and other mammals doesn’t match the expected pattern if it was a vestigial structure.3 Instead, its occurrence suggests that it is a structure that has utility.

It looks like the appendix is really good for something after all. Perhaps it’s just as well that Edwin Starr passed away. I doubt he would ever want to record a song about the vermiform appendix.

References:

1. Douglas Theobald, “The Vestigiality of the Human Vermiform Appendix: A Modern Reappraisal,” Talk Origins website, http://www.talkorigins.org/faqs/vestiges/appendix.html, accessed June 24, 2008.2. R. Randal Bollinger et al., “Biofilms in the Large Bowel Suggest an Apparent Function of the Human Vermiform Appendix,” Journal of Theoretical Biology 249 (2007): 826–31.3. G. B. D. Scott, “The Primate Caecum and Appendix Vermiformis: A Comparative Study,” Journal of Anatomy 131 (1980): 549–63.

Subjects: Bad Designs?

30% Inefficiency by Design April 1st, 2001 By Dr. Fazale Rana

Cells use a highly wasteful process when producing proteins.

Roughly 30 percent of all newly synthesized proteins must be degraded (broken down) by the cell immediately after formation because they are improperly made.1 On the surface, this new discovery seems to challenge the notion that an Intelligent Designer is responsible for life’s chemistry, but closer examination reveals a specific purpose for the “inefficiency” of protein synthesis.2-4

Anyone with experience in manufacturing would agree that a production process with a 30 percent defect rate needs much improvement. Yet, the seemingly wasteful process of protein synthesis actually plays a critical role in the ability of the immune system to respond rapidly to viral infections. Without this 30 percent defect rate, viral infections like the common cold could be much more severe.

A quick review of basic biochemistry will help demonstrate how inefficient protein production benefits the immune response. 5 To begin the process of protein production, a messenger RNA molecule carries information from a gene on one of the DNA strands to a structure in the cell called a ribosome. These ribosomes help assemble protein chains by linking together small, subunit molecules, called amino acids. Each of the myriad proteins found inside the cell possesses a unique sequence pulled from a pool of twenty different amino acids. The physical and chemical properties of the amino acid sequence determine how the protein chain folds to form its three-dimensional structure. Protein molecules called chaperones often play a key role in assisting the folding of the protein chain. The three-dimensional architecture of a protein determines its functional or structural role inside the cell.

After proteins have outlived their usefulness to the cell or have become damaged in the process of carrying out their cellular function, they are degraded. Upon degradation, the protein’s amino acids are released, and hence, become available for use in the production of new proteins.

The degradation process of any protein (including those defectively made) uses small fragments of the protein to communicate to the body’s immune system what is happening inside the cell. The cell uses a complex assembly of molecules called the class I major histocompatibility complex (MHC) to transport the fragment to the cell’s surface, where it is presented to the immune system.6, 7

In the case of virally infected cells, viral DNA takes over the cellular machinery and produces viral proteins. Before recent studies, experts thought that only viral proteins that had resided in the cell for some time were degraded and presented to the immune system through the class I MHC. This understanding of the process created a dilemma for researchers, because if the cell waited until well into the viral infection to communicate with the immune system, the body could not respond to the infection before the viral invasion progressed too far.

Enter the new discoveries.8, 9 It turns out that 30 percent of the viral proteins are also produced improperly and degraded immediately with the rest of the cell’s defective proteins. Fragments of the viral protein are then incorporated into the class I MHC and the immune system is quickly alerted to the presence of viral particles inside the cell.

This new discovery reveals that the high level of defective proteins produced by the cell is necessary to allow for a highly efficient immune response to viral infection. There is elegant design in the inefficiency of protein synthesis. This finding teaches an important lesson about so-called imperfections in nature. Without exception, an improved understanding of a “poorly” designed system and a proper viewing of the system from a broader context invariably reveal perfection that points to an Intelligent Designer.

Subjects: Bad Designs?, Biochemical Design

Kidney Stones- Evidence for Divine DesignOctober 1st, 2004 By Phil Chien

10/1/2004by Dr. Fazale ("Fuz") Rana

"It's the closest that a man will ever come to experiencing the pain of childbirth," the attending nurse proclaimed with a noticeable glee in her eyes. Her comment only added to my misery as I writhed in pain on a stretcher in the emergency room, waiting to pass a kidney stone.

Mineral deposits such as those that formed in my kidneys develop in one out of ten people during their lifetime and account for nearly ten out of every 1,000 hospital admissions.1 Stones can result whenever a chemical imbalance occurs in the kidney. The type of stone that forms depends upon the exact nature of the chemical imbalance and reflects different etiologies (causes). Calcium oxalate stones, the most common type, result from dehydration or excess levels of oxalate in the diet. (Oxalate is found in certain vegetables, nuts, berries, chocolate, and tea. 2) Sodium urate stones, a second type, are caused by an inborn error in metabolism that leads to excessive production of uric acid.3

Uric acid is the breakdown product of adenine and guanine (key components of DNA and RNA). As a normal metabolic activity, the cell turns over biomolecules-continually replacing "older" molecules with newly synthesized ones, thereby maintaining structural and functional integrity.

The cell recycles most of the adenine and guanine generated from the breakdown of nucleotides (the building blocks of DNA and RNA) through what biochemists call the salvage pathways. Still, the cell targets a significant portion of adenine and guanine for breakdown and secretion in the form of uric acid.4

Uric acid possesses low solubility in blood serum, causing it to readily precipitate into the urinary tract if the body dehydrates or generates an excessive amount of the product (which can occur if the enzymes of the salvage pathway are defective).5

Except for primates, including human beings, all mammals further metabolize uric acid to a more soluble derivative. Evolutionary biologists suggest that the enzymes responsible for this transformation were lost in the evolutionary process that gave rise to primates (and humans).6 For these scientists, the elimination of adenine and guanine in the form of uric acid argues potently for evolution, since it appears to reflect poor design.7 Why would an all-powerful and all-knowing Creator put into place an imperfect biochemical process that leaves human beings so susceptible to kidney stones (and other disorders, like gout)? Evolutionists would maintain that the adenine and guanine elimination pathways represent nothing more than an evolutionary "kluge" job, an imperfection that barely gets the job done-not a Creator's perfect handiwork.

This perspective fails to consider, however, uric acid's full range of metabolic properties, some of which are beneficial. This compound is a potent antioxidant that scavenges the chemically corrosive hydroxyl free radical, singlet oxygen, and superoxide anion, all produced by the metabolic pathways that the cell uses to harvest chemical energy.8 The high levels of uric acid in the blood serum, though precariously poised to form stones in the urinary tract, also help prevent cancer and contribute to long human life spans. For other mammals, the conversion of uric acid to more soluble forms before elimination deprives them of a key antioxidant and limits their life spans.

When considered more broadly, it turns out that the primate adenine and guanine elimination pathways reflect an elegant, rather than a poor, design that finds an important use for a waste product. Though inborn metabolic error in the salvage pathway enzymes accounts for the less-common type of kidney stone, the more-common type is largely preventable by a balanced diet-which seems a small price to pay for cancer prevention and long life spans.

When the pain-killers finally took effect and I'd had a chance to research and reflect on what happened to me, I was able to muster thanks to God for kidney stones. But I don't think anyone will want me to share my story at the Thanksgiving dinner table this year.

References

1. http://www.yourmedicalsource.com/library/kidneystones/KS_whatis.html, accessed March 11, 2003.

2. http://www.urologychannel.com/kidneystones/index.shtml, accessed March 11, 2003.3. Lubert Stryer, Biochemistry, 3d ed. (New York: W. H. Freeman, 1988), 619-22.4. Stryer, 619-22.5. http://www.urologychannel.com/kidneystones/index/shtml, accessed March 11, 2003.6. Stryer, 619-22.7. Stephen Jay Gould, The Panda's Thumb: More Reflections in Natural History (New York: W.

W. Norton, 1980), 19-26.8. Stryer, 619-22.

Subjects: Bad Designs?, Biochemical Design

"Junk" DNA Not so Junky

January 1st, 2000 By Phil Chien

1/1/2000by Dr. Fazale ("Fuz") Rana

A recent report by researchers from the University of British Columbia (UBC) provides new evidence that non-coding DNA (typically referred to as “junk” DNA or “selfish” DNA) is not useless. Instead it appears to serve an essential function in complex cells.1

The DNA content of complex cells (cells that possess a nucleus and internal membrane-bound organelles and compartments) varies enormously (as much as 80,000 times) among protozoans, fungi, animals, and plants. The widely varying DNA content results from the presence of non-coding DNA. Non-coding, or “non-specific,” DNA can make up anywhere from 30% to nearly 100% of an organism’s total DNA content (genome).2

Those seeking to explain life as the outworking of strictly natural processes have suggested that non-coding DNA is produced randomly. Either it is “junk” carried along with functional genes simply because it is physically attached, or it is “selfish,” a type of functionless parasite in the organism’s genome.3, 4 The “junk” or “selfish” DNA exemplifies the imperfection one would expect from random natural processes and is the preferred view among evolutionary biologists.

As far back as 1978, however, some researchers suggested that non-coding DNA may actually have a functional role. They developed a model in which the non-coding DNA determines the volume of a cell’s nucleus.5 As overall cell volume increases, the nuclear volume, and hence DNA content, too, must increase to give the cell’s nuclear contents room to communicate effectively with the cell’s cytoplasm (stuff outside the nucleus).

The UBC team has found experimental support for the usefulness of non-coding DNA in their study of cryptomonads (algae).6 The non-coding DNA appears to have kept the volume of the nucleus proportional to overall cell volume. Additionally, they found evidence refuting the “junk” or “selfish” model. A specialized cell part called the nucleomorph behaved opposite to what the naturalistic model predicts and exactly as the “purposeful” model predicts.

We still have much to learn about genome organization and non-coding DNA. Clearly, though, the more we uncover, the less likely the notion that an organism’s genome (including non-coding DNA) has been assembled by blind, chance processes, and the more likely it becomes that the genome is the work of an Intelligent Designer.

References:

1. Margaret J. Beaton and Thomas Cavalier-Smith, “Eukaryotic Non-Coding DNA is Functional: Evidence from the Differential Scaling of Cryptomonad Genomes,” Proceedings of the Royal Society of London B, 266 (1999), pp. 2053-2059.

2. Wen-Hsiung Li, Molecular Evolution, (Sunderland, Massachusetts: Sinauer Associates, Inc. Publishers, 1997), pp. 379-401.

3. W. Ford Doolittle and Carmen Sapienza, “Selfish Genes, The Phenotype Paradigm and Genome Evolution,” Nature, 284, (1980), pp. 601-603.

4. L. E. Orgel and F. H. C. Crick, “Selfish DNA: The Ultimate Parasite,” Nature, 284 (1980), pp. 604-607.

5. T. Cavalier-Smith, “Nuclear Volume Control by Nucleoskeletal DNA, Selection for Cell Volume and Cell Growth Rate, and the Solution of the DNA C-Value Paradox,” Journal of Cell Science 34, (1978), pp. 247-278.

6. Beaton and Cavalier-Smith, pp. 2053-2059.

Subjects: Bad Designs?, Biochemical Design, Junk DNA

Curvaceous Anatomy of the Female Spine Reveals Ingenious Obstetric DesignFebruary 14th, 2007 By Phil Chien

2/14/2007by Virgil L. Robertson, DC, QME, FAFICC

Bio: Dr. Robertson received his Chiropractic doctorate from Southern California University of Health Sciences in 1985, and currently serves as Clinical Director at Brea Canyon Pain Relief and Rehabilitation Center in Brea, California.

The arch in the small of your lower back is known as the “lumbar lordosis” and it plays an important role in allowing humans to stand upright and walk on two feet. If you’ve ever seen a pregnant woman negotiating her way down the aisle of a supermarket, you’ve surely noticed that the bigger the belly, the more the mother-to-be has to arch backward to keep her balance. Recently, researchers from Harvard University and the University of Texas examined this biomechanical phenomenon and made some fascinating discoveries, which were reported in the December 2007 edition of Nature.

As it turns out, the spines of men and women are not created equal. In fact, it now appears that women have been designed with specific anatomical features that enable them to safely carry the large asymmetric loads associated with pregnancy. Specifically, the research team headed by anthropologist Dr. Katherine Whitcome found that the lumbar spine of human females differs significantly from that of males. The female spine possesses an additional wedge-shaped vertebra, which substantially increases lordotic curvature in women (three wedge-shaped lumbar vertebrae in women vs. two wedge-shaped lumbar vertebrae in men). This feature allows expectant mothers to comfortably assume more extended (lordotic) postures during pregnancy. Additionally, the researchers found that the lumbar zygoapophyseal joint surfaces of women are proportionally larger and more coronally oriented than corresponding posterior joint structures in men. This distinctively female spinal configuration provides a more stable base for posterior weight bearing (hyperlordosis) and helps prevent anterolisthesis (fracture and forward slipping) of the lumbar vertebrae in pregnant women. As pregnancy proceeds and the fetus grows larger, mom simply leans back a little further (up to 28°) to balance the center of gravity over her hips—it’s a simple yet ingenious biomechanical system!

These new research findings indicate that women are particularly well equipped to safely bear the heavy anterior loads that come with pregnancy. Without these anatomical design features, pregnant women would have great difficulty balancing their unborn bundles of joy, and would be much more susceptible to myoligamentous (muscular) injuries and vertebral fractures during the third trimester of gestation.

The research team also reports that the spines of extinct hominid species (australopithecines) possessed the same kind of anatomical features and dimorphic disparities found in humans. The identification of anatomic features and biomechanical systems uniquely common to bipedal

primates is not surprising. Previous authors have identified numerous anatomical and physiological characteristics in bipeds that differ from those found in quadrupeds. While the authors of this new study interpret their findings in terms of an evolutionary framework, it should be noted that these findings are, likewise, fully consistent with the predictions of RTB’s Testable Creation Model. In fact, explaining why the unique features of bipedalism appear suddenly in the hominid fossil record some seven million years ago (in the absence of transitional intermediate forms), has proven to be a substantial challenge for evolutionary biologists.

When considering the abundance of elegantly engineered biomechanical systems found in the human body, it’s hard not to be impressed by the obvious hallmarks of design. To quote British physicist Paul Davies, “The impression of design is overwhelming.”

These latest research findings fall into a long line of evidences that provide support for the existence of an Intelligent Designer. The generation of such exquisitely engineered biosystems is simply beyond the scope and capability of random mutation and natural selection.

For more on the emergence of bipedalism see Who Was Adam?

Subjects: Bad Designs?, Lucy and Other Hominids, TCM - Human Origins