Does this theory satisfy the definition of a scientific theory?
It all depends on the definition you wish to start with. My theory is based on all the essential criteria according to David Hilbert's philosophy of science. See The Quintessential Language of Science. I believe it is well within the range of the most popular definitions of a scientific theory.
What are your postulates?
My theory is both a tweak and a refinement of standard evolutionary theory.
According to the New World Encyclopedia, Neo-Darwinism, also called the modern evolutionary synthesis, generally denotes the integration of Charles Darwin's theory of evolution by natural selection, Gregor Mendel's theory of genetics and mathematical population genetics. I accept the theory of genetics and mathematical population genetics. To those two pillars I add the tautology, "Whatever survives, survives." In my revised theory I call that tautology the principle of natural selection. And last, I also refine the Darwinists' principle of random variation in the same way that geneticists do. Errors occur in the DNA copying process. At this point my theory inherits all the observational and predictive success of the modern evolutionary synthesis.
To all that wonderful success I add two new postulates that I claim are stronger than the postulates that I have just enunciated.
To those unfamiliar with David Hilbert's philosophy of physics, I must digress to state a definition first. By definition, if we adjoin a scientific hypothesis to a scientific theory such that it refines the old theory and is logically consistent with it, then the refined theory is also a scientific theory.
The principle of refinement is a mere tautology but it's useful. This principle is just as self-evident in mathematics as it is in Hilbert's logical approach to science. Every refinement of a scientific theory is a scientific theory.
Formally then, the theory of descent with modification (devolution) is based on two postulates, in addition to my preferred definition of a scientific theory and the minor adjustment to the modern evolutionary synthesis.
1. All life forms are molecular machines. I don't believe that any scientist doubts this scientific hypothesis. [1][2][3].
2. The second postulate, the devolution hypothesis, stipulates that all models of molecular machines are becoming less robust over time. As genetic code in all life forms continues to get corrupted and degrades through copying errors and other mutations, successive generations of machines, in all series, must plod along with increasing inefficiency and sometimes features are entirely lost. [4]
The theory of devolution is now being recognized as a legitimate science:
Evolution may provide us with the most abundant phenotypes (observable genetic characteristics) rather than the fittest, according to a new theory published on July 18 in the open-access journal PLoS Computational Biology. That is, natural selection may be optimal for choosing the most fit organism of the moment, but evolutionary biologists question if the process leads to the optimal organisms in the long run. Researchers from The University of Texas at Austin, led by Drs. Matthew Cowperthwaite and Lauren Ancel Meyers, propose a new theory: life may not always be optimal.
Natural selection is driven by genetic mutations, and we usually can predict and understand the short-term fate of a mutation. If a mutation makes the organism more fit, it tends to last through the years; if the mutation is harmful, it usually dies off with its host organism. Evolutionary biologists, however, do not have such a complete understanding of the long-term consequences of mutations. Is it possible that what is good now may be not-so-good later? — Evolution May Yield Most Abundant Traits, Not Best
Yes. The theory of devolution is a logical possibility.
IF YOU want to know how all living things are related, don't bother looking in any textbook that's more than a few years old. Chances are that the tree of life you find there will be wrong. Since they began delving into DNA, biologists have been finding that organisms with features that look alike are often not as closely related as they had thought. These are turbulent times in the world of phylogeny, yet there has been one rule that evolutionary biologists felt they could cling to: the amount of complexity in the living world has always been on the increase. Now even that is in doubt.
The idea of loss in evolution is not new. … However, the latest evidence suggests that the extent of loss might have been seriously underestimated. Some evolutionary biologists now suggest that loss - at every level, from genes and types of cells to whole anatomical features and life stages - is the key to understanding evolution and the relatedness of living things. — Evolution: hacking back the tree of life.
Another article in the same journal is titled, Evolution myths: Natural selection leads to ever greater complexity. Please note the subtitle: "natural selection often leads to ever greater simplicity."
If you don't use it, you tend to lose it. Evolution often takes away rather than adding. For instance, cave fish lose their eyes, while parasites like tapeworms lose their guts.
Such simplification might be much more widespread than realised. Some apparently primitive creatures are turning out to be the descendants of more complex creatures rather than their ancestors. For instance, it appears the ancestor of brainless starfish and sea urchins had a brain.
These newscientist articles unquestionably support the theory of devolution!
Experimental support for the theory of devolution is just beginning to be noticed. Consider the article, Evolution of Penicillin-Binding Protein 2 Concentration and Cell Shape during a Long-Term Experiment with Escherichia coli, in the Journal of Bacteriology, 2009 February; 191(3): 909–921. The Abstract states: "In a long-term experiment, 12 populations of Escherichia coli having a common ancestor were allowed to evolve for more than 40,000 generations in a defined environment." The abstract specifies the "physiological trade-offs and ecological specialization during experimental evolution" and identifies them precisely. The trade-offs were that "both mutations that evolved were beneficial in the environment used for the long-term experiment and that … both mutations decreased cellular resistance to osmotic stress."
That's a very precise confirmation of the theory of descent with modification (devolution). Yes, the mutant Escherichia coli that survived were better adapted to the new environment and could outcompete the more robust ancestral strains in that new environment. However, the more robust ancestral strains were more robust in their preferred environment than the mutant Escherichia coli were in their specialized environment. That's exactly what the theory of devolution predicts. As the theory of devolution affirms, along with evolution (change), which is due to accumulated mutation, there is devolution (the decrease in robustness).
The Inveritable Encyclopedia of Universal Evolutionary Knowledge highlights this essential point:
"Another adaptation that occurred in all these bacteria was an increase in cell size and in many cultures, a more rounded cell shape. This change was partly the result of a mutation that changed the expression of a gene for a penicillin binding protein, which allowed the mutant bacteria to out-compete ancestral bacteria under the conditions in the long-term evolution experiment. However, although this mutation increased fitness under these conditions, it also increased the bacteria's sensitivity to osmotic stress and decreased their ability to survive long periods in stationary phase cultures." [5].
Obviously, in the background, there is a rather unsurprising principle. Escherichia coli and their descendants can adapt to eating junk food but it's not good for them. They would have been better off in their original environment.
A second clear example of devolution is nitrofurantoin-resistant E. coli mutants. The fitness of susceptible and resistant strains was measured as growth rate in the presence and absence of nitrofurantoin in rich culture medium. The mutant E. coli showed a reduction in fitness when compared with the susceptible parent strain.
"Conclusions: Nitrofurantoin resistance confers a reduction in fitness in E. coli in the absence of antibiotic. In the presence of therapeutic levels of nitrofurantoin, even resistant mutants are so disturbed in growth that they are probably unable to become enriched and establish an infection." — Nitrofurantoin resistance mechanism and fitness cost in Escherichia coli.
"Mutations that confer antibiotic resistance affect essential processes and often reduce fitness, manifesting as decreased virulence, transmission and growth rate (reviewed in ANDERSSON and LEVIN 1999)." [6]. There are no known examples of mutants that are unquestionably intrinsically healthier than the ancestral strains.
Clearly then, robustness is a measure of the "fitness for life," not the ability to spread genes. Niles Eldredge makes this point in his book, Why We Do It: Rethinking Sex and the Selfish Gene. [7].
The Eldredge anti-Darwinian emphasis also appears in Life on Earth: An Encyclopedia of Biodiversity, Ecology, and Evolution:
"Fitness is not equivalent to survival or the number of offspring that an organism produces, but in the long run individuals that are more fit are more likely to survive and produce more offspring." Vol. 1, p. 521.
Here is another interesting thought: Eldredge characterizes robust species as generalists. Logically then, generalists becoming specialists would imply a loss of robustness.
"In any case, if the ability of an ecosystem to persist or rebound after disturbance is exceeded, the system degrades and collapses; it finally undergoes ecosystem replacement, as a new system is built up at the same location either from the durable remnants of the previous system (the physiologically robust species, resource generalists, organisms with resting stages) or from invading species able to exploit or tolerate the new environmental factors." Ibid., pp. 306-7.
The logic is undeniably correct. Specialization is speciation. The generalists are more robust. Therefore speciation implies devolution.
Here is a powerful confirmation of the theory of devolution, published in Hum Mutat. 2003 Jan;21(1):12-27:
Kondrashov AS wrote: Direct estimates of human per nucleotide mutation rates at 20 loci causing Mendelian diseases.
National Center for Biotechnology Information, NIH, Bethesda, Maryland 20892, USA.
I estimate per nucleotide rates of spontaneous mutations of different kinds in humans directly from the data on per locus mutation rates and on sequences of de novo nonsense nucleotide substitutions, deletions, insertions, and complex events at eight loci causing autosomal dominant diseases and 12 loci causing X-linked diseases. The results are in good agreement with indirect estimates, obtained by comparison of orthologous human and chimpanzee pseudogenes. The average direct estimate of the combined rate of all mutations is 1.8x10(-8) per nucleotide per generation, and the coefficient of variation of this rate across the 20 loci is 0.53. Single nucleotide substitutions are approximately 25 times more common than all other mutations, deletions are approximately three times more common than insertions, complex mutations are very rare, and CpG context increases substitution rates by an order of magnitude. There is only a moderate tendency for loci with high per locus mutation rates to also have higher per nucleotide substitution rates, and per nucleotide rates of deletions and insertions are statistically independent on the per locus mutation rate. Rates of different kinds of mutations are strongly correlated across loci. Mutational hot spots with per nucleotide rates above 5x10(-7) make only a minor contribution to human mutation. In the next decade, direct measurements will produce a rather precise, quantitative description of human spontaneous mutation at the DNA level. Published 2002 Wiley-Liss, Inc.
There are no beneficial Mendelian diseases.
HERVs
Human endogenous retroviruses (HERVs) are a family of viruses within our genome with similarities to present day exogenous retroviruses. ERVs provide marvelous support for the theory of devolution. They have no known biological benefits.
HERVs have been inherited by successive generations and several HERVs have been implicated in certain cancers and autoimmune diseases. Over 20 HERV families have been identified during the past two decades. Although many are defective through the accumulation of mutations, deletions, and termination signals within coding sequences, a limited number of HERVs have the potential to produce viral products and, indeed, to produce viral-like particles. Furthermore, some HERVs have been implicated in certain autoimmune diseases and cancers and might have a role in the aetiology and pathology of disease.
HERV insertion mutation, molecular mimicry, superantigen motifs, and recombination with other viruses could be responsible for the development and pathology of disease.
It has been suggested that HERV-K may be important in the progression of testicular germ cell tumours through inhibition of an effective immune response.
HERV-K might be important in the pathogenesis of human breast cancer.
Although the exact function of HERVs in the carcinogenic process is still under investigation, the evidence implicating HERVs in the carcinogenic process is substantial and further investigation will be required to elucidate the contribution of HERVs to the development of malignancy. [8].
The modern evolutionary synthesis has met the criteria of a scientific theory. It explains the observable phenomena of biological diversity, and can make specific predictions about it via the study of populations and gene sequencing.
Fine. I'm delighted that you're so comfortable. But now you have a competing theory to contend with.






