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Madame Curie Bioscience Database [Internet]. Austin (TX): Landes Bioscience; 2000-2013.

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Steven Weinberg once said that the complexity of physics today reaches very close to the edge of the human intellect.1 Where would that leave us,the biochemists and biologists, who study a subject many times more complex than physics? Biology has invented physics, and with that invention it has been possible to chip one equation of physics after another from the “ephemeral eternity” that marks our universe at each instant. Presently physics has reached a level of power and sophistication that makes it possible to predict, with fair confidence, when the universe began, how it started, how the galaxy formed that is the home for our sun and its planets, and where all of it is flying at what speed. We even know at what time our planet will be burned up in the solar corona. From the slow down of binary systems we can calculate the power of gravity to the 12th decimal place2 and we are beginning to uncover ‘quintessence’, a different force that takes over when gravity diminishes in the distant power fields of space.3 Is quintessence the gravitational pull of a neighboring universe? You see our protein-based computer is tempted to spark off at the slightest cue and will work on a problem until a new concept can be tacked onto our quilt of science.

Yes, we also know what we are made of. We know the electric fields of atoms that caused molecules to assemble, the rules whereby they assembled to form self-perpetuating units, some of which have reached such complexity as to be able to do all the incredible feats described in the previous paragraph. Should we be satisfied with the suggestion that all of this is based upon chance processes such as mutations? An unending string of lucky mutations at the beginning of quantum theory and relativity is certainly not one of our better ideas.

A hypothesis of evolution exerts influence on the development of biological sciences of which biochemistry in turn provides major parameters for anchoring concepts, connecting them to reality, as it were. During the development of the Darwinian model the discipline of biochemistry did not exist and genetics had just been, started but logic, the very basis of scientific discourse, was there. Thus Darwin replaced God by logic but put chance, the hand of divinity, right back into the core of the model. The Genomic Potential Hypothesis purges constructive chance events from the equation and returns the problem to biochemistry in the true sense of the term. As a consequence evolution seems more complex but, in exchange, it has become a legitimate target of scientific pursuit. Instead of tranquilizing the human mind with fortunate accidents, the new direction calls for answers. Is there a higher order code in the genome, did the beginning nucleic acid polymer show some sequence-dependent tendency to collect compatible sequences to make possible that one full percent of nucleic material of the human genome would carry functioning messages? How is morphology expressed, how do sets of dependent functions get organized such as food intake, digestion distribution, or reproduction or locomotion? These functions are all finished when the first macro-organisms enter the fossil beds; they were assembled by rules other than needs that were still unexpressed. The complexity of these interactions is staggering but they came about by self-assembly based upon structural features, i.e., they are ultimately discoverable! Questions of this kind will guide the research effort of evolutionists back to the problems that are subject to the falsification test.

The phrase ‘in principle’ falsifiable4 or discoverable means that a model is contiguous. Interaction of historically uncoupled events (chance) are by definition unpredictable regardless of whatever level of supernatural expertise one might bring to bear on such a problem. For example, the old theory holds that the organisms present at the Cambrian edge represent the total biological pool, and that among them must be the stock for the whole post-Cambrian world, for the fauna and flora that developed from these early life forms by gene duplication and mutations.5 Inspecting a genome of one of these animals closely one would not be able to predict where or if the required mutations would occur to produce a new species. And that is not a matter of ignorance or overwhelming complexity but rather of principle. In other words, even if we knew a genome to the most profound level and with supernormal facilities, nothing in that structure can tell us what mutation would hit next. In this case predictions become “in principle impossible” and to make respectable extrapolations from such a process is, in fact, impossible. Causality and contiguity are the quintessence of science and mutations are not contiguous. They cannot be constructive for all the reasons given in this book, and it does not matter that everybody in evolution seems quite happy with mutations as the modulator of biological form. Science is, in the final analysis, decided neither by majorities nor by prominence of the proponent. Not too long ago a mathematics-supported origin of life scenario was published that, at the end, decayed into a mutation-driven diversification scheme.6

It takes but one mutation to cause a disease and that mutation does not even need to occur at one specific place in a gene. About 30 different mutations have been identified that cause osteogenesis imperfecta, and the same is true for many other genetic diseases. If it were possible to convert a zebra into a horse (to keep it impersonal) how many mutations would it take and how precisely would they have to be placed and in what sequence must they occur and lastly, how many deadly mutations must the convert avoid? So, why is it not reasonable to build life from a series of lucky reactions and sort out that which failed? Because the number of failures would be larger than the number of particles in this universe!

Perhaps the gambler can make a positive contribution to this discussion. Dice have only 6 surfaces and the chance of winning is 1:6, which by biological standards are high odds. The odds of losing, of course, are 5 times higher so his fate, which cannot be influenced by skill, is no surprise. Although frowned upon in that trade, “fate” can be influenced by breaking the symmetry of the system (loading the dice). Nature has done it legitimately and the Genomic Potential Hypothesis is based upon the realization that the ‘dice’ have been loaded when energy condensed into atomic structures. In such a setting randomness comes about only when there is no structural discriminator in the interacting system.

The loaded dice will not show the winning number at every throw but will do so rather more frequently than an unmodified one. That is precisely what happens in chemistry where complex reactions always yield an approximately normal distribution around a major product and where repeats under similar conditions are a very likely event, hence the multiple origin scenario.

The way life produced itself is the way it persists. Mass action, affinity constants, and competition produce all our pathways of control in conjunction with stochastic movements of proteins.7 Affinity constants are the loaded dice in biological control processes and even these can be modulated stochastically by increasing or decreasing the affinity for a target by, say, phosphorylation. The regulatory site of DNA will be occupied by inhibitors or promoters depending upon the amounts and affinities of the various molecules in the nucleus. Of course, this condition holds for other reactions in the cell and explains why life, why the cell needs membranes which prevent loss of solutes and permit control over the concentration of regulatory components. Affinity constants dictate how many molecules have to be in a fixed volume to cause 50% occupancy of the binding site. Mass action and molecular structure have produced organisms in the Genomic Potential Hypothesis and that is the principle whereby they have to function. In a roundabout way the cellular metabolism provides a hint as to how self-assembly produced cells during primordial times.

The genomist will look at the first animals and predict that all of them will remain just what they were in the Cambrian until the present or extinction.8,9 New forms will come from species-specific precursors at later times. The fossil record gives a nod to the new world.

The Genomic Potential Hypothesis raises the spectre that all species have shown up by now. Any “new” form that is reported off and on has merely escaped notice or is the result of hybridization. Truly new species should be more complex than H. sapiens (H. sapiens super sapiens) which we, after deep self-analysis, readily admit to be unlikely. Perhaps potentially more advanced clone members are living among us, analogous to the cohabitation of H. erectus and H. sapiens on the island of Java. This scenario is not impossible but difficult to confirm considering the extensive global mixing of genes that comes with technology. The Genomic Potential Hypothesis carries within its conceptual core the prediction that evolutionary development is finite. Species wax and wane in numbers but diversity is on a steady decline.

After a 150-year grace period evolutionary biology must get back to basics or risk being ostracized from science by the science it created. We are not playing in a sandbox by ourselves; we cannot forever nurture and protect a miniature pontifical college that will preach to us on matters of evolution and suppress the turmoil, which is such a fertile ground for advancement of knowledge.


Weinberg S. The First Three Minutes 1977. Basic Book Inc. New York. 1977.
Taylor JH, Fowler LA, McCulloch PM. Measurements of general relativistic effects in the binary pulsar PSR1913+16. Nature. 1979;277:437.
Ostriker JP, Steinhardt PJ. The quintessential universe. Sci Am. 2001;284:46–53. [PubMed: 11132422]
Miller DW. Popper Selections Princeton University Press, 1985. (Miller DW, ed.
Benton MJ. Diversification and extinction in the history of life. Science. 1995;268:52. [PubMed: 7701342]
Eigen M, Schuster P. The Hypercycle Berlin Heidelberg New York: Springer Verlag, 1997.
Misteli T. Protein dynamics: implications for nuclear architecture and gene expression. Science. 2001;291:843. [PubMed: 11225636]
Schwabe C, Warr GW. A polphyletic view of evolution: the genetic potential hypothesis. Perspectives in Biology and Medicine. 1984;27:465. [PubMed: 6374609]
Schwabe C. Evolution and chaos. Computers Math Applic. 1990;20:287.
Copyright © 2000-2013, Landes Bioscience.
Bookshelf ID: NBK6592


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