by Lloyd Pye
Next year, 1999, will be the 140th anniversary of the publication of Charles Darwin’s On The Origin Of Species. In that landmark volume he postulated that life on Earth had developed into its millions of forms through a long, slow series of fundamental changes in the physical structure of all living things, plants and animals alike. Though small and gradual, these changes would be relatively constant. Bit by imperceptible bit, gills would turn into lungs, fins would turn into limbs, scales would turn into skin, bacteria would turn into us. The problem for Darwin, and for all Darwinists since, came when the mechanism behind those changes had to be explained.
Because Darwin’s era was only beginning to understand cellular function (Gregor Mendel’s treatise on genetics did not appear until 1865), Darwin proposed a system of gradual physiological improvements due to small, discreet advantages that would accrue to the best-adapted progeny (his famous “survival of the fittest”) among all living things (a bit stronger, a bit swifter, a bit hardier), making them subtly different from their parents and producing offspring with similar advantages accruing in their physiological makeup. When enough small changes had compounded themselves through enough generations….voila! A new species would have emerged, sexually incompatible with the original parent stock, yet inexorably linked to it by a common physiological heritage.
Once cellular function came to be better understood, particularly the importance of DNA as the “engineer” driving the entire train of life, it was quickly embraced as the fundamental source of change in Darwin’s original model. Darwinian evolution, as it came to be called, was indisputably caused by mutations at the genetic level. Because such mutations were obvious to early geneticists, and could eventually be induced and manipulated in their laboratories, it seemed beyond doubt that positive mutations in DNA sequencing were the key to explaining evolution. That left neutral mutations exerting no effect, while negative mutations afflicted only the unlucky individuals who expressed them but had no lasting impact on a species’ collective gene pool.
In 1996 Michael Behe, a biochemistry professor at Lehigh University in Bethlehem, Pa., published a book called Darwin’s Black Box. He defined a “black box” as any device that functions perfectly well, but whose inner workings remain mysterious because they cannot be seen or understood. To Charles Darwin the living cell was an impenetrable black box whose inner workings he could not even imagine, much less understand. To scientists today the cell box is no longer quite as black, but it is still dark enough to leave them with only a faint understanding of how it works. They know its basic components and the functions of those components, but they still don’t know how all those pieces fit together to do what cells do–live.
Life is still every bit the profound mystery it was in Darwin’s day. Many additional pieces of the puzzle have found their way onto the table since 1859, but scientists today are not much closer to seeing the whole picture than Darwin or his cronies. That is an ironic reality which few modern Darwinists will accept in their own hearts and minds, much less advertise to the world in general. So they supply the media with intellectual swill that the media, in turn, unknowingly palms off as truth, while the scientists edgily cross their fingers and hold their breath in the hope that someday, maybe even someday soon, but certainly before the great unwashed get wise to the scam, they will finally figure out the great secret…they will see into the heart of the universe’s blackest box…they will understand how life actually works, from the first moment of the first creation to evolution itself.
Darwinists teach and preach that life began spontaneously in a mass of molecules floating freely in the Earth’s earliest rivers and seas. Those molecular precursors somehow formed themselves into organic compounds that somehow formed themselves into the very first living organism. This incredible feat of immaculately choreographed bioengineering was, Darwinists insist, accomplished without the aid of any outside agency, such as a Prime Mover (what some would call “God”), and especially not anything extraterrestrial. It was done using only the materials at hand on the early Earth, and accomplished solely by the materials themselves, with a probable assist from a perfectly timed, perfectly aimed lightning bolt that, in the most serendipitous moment imaginable, swirled tens of thousands, or even hundreds of thousands of inanimate molecules into a living entity.
For as glibly as Darwinists have fashioned and promoted this scenario in schools to this day, the complexity of its mechanics might challenge the creative skills of a busload of Prime Movers. Countless lipids have to somehow be coaxed to form a membrane that somehow surrounds enough strands of DNA to create a cell that can manage life’s two most basic functions: it must absorb organic and inorganic compounds in its environment and turn them into proteins, which can then be converted into energy and excreta; and it must have the ability to reproduce itself ad infinitum. If all of those varied factors, each a bona fide miracle in itself, do not occur in the precise order demanded by all living cells for their tightly orchestrated, step-by-step development, then the entire process becomes laughably improbable.
British astronomer Fred Hoyle has offered the classic analogy for this scenario, stating that its actual likelihood of being true and real equals “that of a tornado sweeping through a junkyard and correctly assembling a Boeing 747.” It did not and could not happen then, just as it cannot be made to happen now. The very best our biochemists can do today is construct infinitesimal pieces of the puzzle, leaving them little nearer to seeing how life truly works than Darwin and his cohorts 140 years ago. But why? What’s the problem? Haven’t we cracked the atom? Haven’t we flown to the moon? Haven’t we mapped the ocean floors? Yes, yes, and yes. But those things were easy by comparison.
If the Darwinists are so wrong, where are they wrong? What is the fundamental mistake they are making? It has to do with where they are looking, which is the cell, inside the cell, and specifically at the functioning of DNA. Because the twisting double-helix of DNA contains the instructions for all of life’s processes, the assumption has always been that disruptions in the patterns of those instructions are the only logical explanation for how physiological changes at both the micro (small) and macro (large) level must be created and executed. In other words, changes in DNA (mutations) must be the engine driving all aspects of evolutionary change. Nothing else makes sense.
Sensible or not, however, it is wrong. Why? Because in 1984 a group of British researchers decided to do an experiment utilizing what was then considered to be a universal truth about genes, handed down from Gregor Mendel himself: the idea that genes are sexless. Mendel had postulated that a gene from either parent, whether plant or animal, was equally useful and effective throughout the lifetime of the individual possessing it. This was taken as gospel until those British researchers tried to create mouse embryos carrying either two copies of “father” genes or two copies of “mother” genes. According to Mendel’s laws of inheritance, both male and female embryos should have developed normally. After all, they had a full complement of genes, and if genes were indeed sexless they had all they needed to gestate and thrive.
The researchers were stunned when all of their carefully crafted embryos were dead within a few days of being transferred to a surrogate mother’s womb. How could it happen? What could have gone so wrong in a scenario that couldn’t go wrong? They were completely baffled. What they didn’t know, and what many refuse to accept even now, fourteen years later, is that they had unwittingly opened their own–and their icon’s–darkest, blackest box. They had ventured into a region of the cell, and of the functioning of DNA, that they hadn’t imagined was off-limits. By taking that inadvertent journey they ended up forging an entirely new understanding of Mendelian inheritance, while driving a stake through the already weakened heart of Darwinian evolution.
Normally, father genes or mother genes control the expression of their own activity. A father gene might give, for example, the signal for a crop of head hair to grow–to “express” itself–and to stop expressing when the follicles had been constructed in their proper places in the scalp. The cessation of the expressing process is called methylation, which is the surrounding of expressing genes with clusters of chemicals that shut them off (picture the cap being put back on a toothpaste tube). In the same way, a mother gene might express a pair of eyes and then, when they were completed, “methylate” the gene’s growth processes into inactivity.
Until 1984, it was believed that all genetic function operated the same way. If a gene or suite of genes came from Dad’s side of the mating process, then those genes managed their own affairs from birth until death. And the same held true for genes coming from Mom’s side of the mating. But certain genes turned out to exhibit radical differences, depending on whose side of the mating process they came from. When the female mouse embryos died, it was found that genes vital to their growth had inexplicably never been turned on at all, while still others were never turned off (methylated) and spiraled unchecked into cancers. Even more baffling, the fatal processes in the all-male embryos were entirely different from those in the all-females. The embryos were dying for reasons that were clearly sex-biased. What could it possibly mean?
Imprinted genes were found to be the culprit. Imprinted genes, it turned out, could be expressed by either parent and, incredibly, methylated by the other parent! Somehow, someway, by means not clearly imagined, much less understood, genes from one parent had the ability to independently begin or end processes that were critical to the lives of forming embryos. In the world of genetics as it had always been perceived, that was impossible. Only a localized (sexless) gene should be able to control its own destiny or purpose, not a separate gene from an entirely different parent. Cooperating genes broke all the rules of physical inheritance that had been written by Gregor Mendel. Yet imprinted genes do, in fact, disregard Mendel’s rules; and by doing so they provide the above mentioned stake that will inevitably be driven through the heart of classic Darwinian evolution.
So far geneticists have identified about 20 imprinted genes embedded within the 80,000 to 100,000 believed to comprise the entire human genome. New ones are discovered on a regular basis, with many geneticists predicting the final tally will reach hundreds, while others suspect the total might reach into the thousands. But whether hundreds or thousands, any imprinted genes at all means that classic Darwinism can no longer count on mutations in DNA as a plausible mechanism for fundamental physical change.
For mutations to be acceptable as the engine of Darwinian change, they have to be able to occur in isolation and then, as stated earlier, pass themselves intact to succeeding generations. By definition that means they have to be able to regulate their own functions, both to express and to methylate their genetic processes. Whenever a trait mutates, whether a longer limb, a stronger muscle, or a more efficient organ, it should pass into the gene pool whole and complete, not half of it being expressed from the male side of a pairing and half from the female side. Why? Because both parents would have to mutate in complementary ways at the same time to the same degree…and then they would have to find each other and mate in order to have even a chance to pass the mutation on!
Natural mutations, while statistically rare, are clearly documented. They can be neutral, negative, or positive. So when geneticists contend that isolated mutations in DNA can occur and be passed on to succeeding generations, they first assume the individual with the mutation has been fortunate enough to have the correct one out of the three possibilities. They further assume the individual survives the brutal winnowing process Darwin so correctly labeled “survival of the fittest.” But fittest or not, any fledgling animal or plant must contend with an infinite number of ways to miss the boat to maturity. Assuming that passage is safe, the lucky individual with the positive mutation has to get lucky several more times to produce enough offspring so that at least a few of them possess his or her positive mutation and also survive to maturity to pass it along. It is a series of events that, taken altogether, are extremely unlikely but at least they are feasible, and they do, in fact, happen.
Imprinted genes, however, neatly sever those threads of feasibility by making it literally impossible for any mutation, positive or otherwise, to effect more than the individual expressing it. There is certainly no way for it to work its way into a gene pool regulated by imprinted genes. Why? For the reasons just stated above: for a mutation to be implemented, it must be beneficial and it must be paired with a similar change in a member of the opposite sex. Thus, if only a handful of genes are capable of being turned on and off by different parents, then Darwinian evolution has no place in the grand scheme of life on Earth. Imprinting shoves Darwinists well beyond any hope of feasibility, to a region of DNA where change is incapable of being positive.
What we are really talking about with imprinting processes is timing, the most exquisite and incomprehensible faculty any gene possesses. By knowing when–and being able–to turn on and off the millions to billions of biological processes that create and sustain living organisms, genes control the switches that control life itself. In effect, whatever controls the timing switches controls the organism. If, for example, only one methyl group misses its turn-off signal on an expressing gene, the resultant non-stop expressing will lead to cellular overproduction and, ultimately, cancer. Conversely, if only one gene fails to express when it should, at the very least a seriously negative event has occurred, and at worst the organism has suffered a catastrophe that will terminate its life.
The “evolution” of a timing sequence in the development of an embryo or a growing offspring simply cannot be favorable in the Darwinian sense. Why? Because in terms of results it is already perfect. And how do we know it is perfect? Because the parents both reached maturity. What is so special about their reaching maturity? It means their own timing sequences performed perfectly in their own embryos, with their initial sperm and egg differentiating in millions of ways to become their bodies. (In plants the same principle holds true). Then their growing period developed perfectly, with its millions of different timing events leading to their limbs and organs growing to their proper sizes and carrying on their proper functions.
Any alteration of that perfection can be, and nearly always is, devastating. In golf a putt drops or it doesn’t. In timing sequences, they are started and stopped precisely, or not. There is no room for error or improvement (no third condition called “better”). Thus, no genetic alteration to timing can create the faster legs, larger horns, sharper teeth, etc., called for by Darwin’s theory of piecemeal change. This is why gills cannot become lungs, why fins cannot become limbs, why scales cannot become fur or skin. No single timing mechanism can “evolve” without altering the perfection that has been passed to offspring by parents through untold generations.
A good analogy is the building of a house. We start with a blueprint. Analogize this with the genetic blueprint provided by DNA. The former outlines the physical materials that go into a house: wood, nails, sheetrock, doors, etc. The latter outlines the physical materials that go into creating a body: blood, bones, skin, hair, etc. Next, we bring in the carpenters who will build the house. It is they who, following our carefully drawn blueprint, will determine everything that will be done to create our house. More importantly, they will determine when all parts of the house will be built, when any particular process will start and when it will stop. They will build the floor before the walls, the walls before the roof, etc.
Building our house is thus a two-part project: what to build, and how and when to build it. It is the same with living organisms, whose carpenter genes (the mysterious timing mechanisms that turn growth processes on and off) determine their success. Now it becomes easy to understand Darwin’s fundamental error. While examining the widely varied houses of living organisms, he saw no trace of the invisible carpenters who have the decisive hand in their creation. Therefore, his theory did not–and so far cannot–account for the fact that carpenter genes invariably prohibit alterations.
As with a house, DNA contains or provides everything necessary to create a particular organism, whether animal or plant. DNA has the further capacity to define and manufacture the physiological materials needed to create the entirety of the organism, precisely when they are needed and to the exact degree they are needed. And, perhaps most wondrous of all, DNA contains the ineffable carpenter genes that determine when each phase of the organism’s construction will begin and end. Any organism’s parents will have passed to it a set of DNA blueprints of what to build and how to build it, which are nearly always perfect with respect to timing, but allowing slight variations in what is built. On the occasions when faulty timing does lead to tragedy, the imperfections are due to sperm-egg misconnects, or molecular anomalies in DNA caused by radiation or chemicals.
Where classic Darwinian evolution completely breaks down is in not allowing carpenter genes to exist separately from end results. Darwinism contends that when any aspect of an organism’s materials change (i.e., a mutation in some strand of DNA which changes some aspect of physical structure), that organism’s carpenter genes smoothly accommodate the change (alter the blueprint) by adjusting the timing sequences (beginning and end) of that structure’s development. This is not reality. A Watusi’s thighbone takes just as long to form as a Pygmy’s thighbone (about 18 years), so only the end results–their respective sizes–have changed, not their timing processes. This is one reason why all human beings can so easily interbreed, even the unlikely combination of Watusis and Pygmies. Our vast array of underlying genetic timing mechanisms, including our imprinted genes, have been handed down intact (unevolved!) since the beginning of our existence as a species.
Thus, what is built can be slowly, gradually altered; how it is built cannot. This obvious fact…this undeniable truth…has the most profound implications: In the carpenter genes of successful organisms, no improvement is possible! And without improvement, via Darwinian change, how could they have evolved? Not just into something from nothing, but into millions of interlocking, tightly sequenced commands that smoothly mesh over extended periods as organisms develop from embryo to birth to sexual maturity? The short answer is, “They can’t.”
What all this means, of course, is that everything we think we know about how life develops on Earth is flatly wrong. It means all of our “experts” are totally mistaken when they tell us that Darwin’s theory of gradual mutations has led to the development of all species of plants and animals on the planet. Nothing could be further from the truth. Darwinism cannot work now, it has never been able to work, and the time has come for its supporters to stop their intellectual posturing and admit they need to go back to their drawing boards to seek a more plausible explanation for what is surely life’s greatest single mystery.