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J. G. Mendel: Why his discoveries were ignored for 35 (72) years?


Some critical comments about the effects of Darwinism on Biological Research by Pioneers of Genetics as well as further Biologists and Historians of Biology.

Especially in the decade after the publication of Darwin’s ORIGIN (1859) the scientific world was eagerly awaiting the discovery of the laws of heredity by some experimental or other scientist(s). After two lectures in 1865, Mendel published his famous Pisum-treatise VERSUCHE ÜBER PFLANZEN-HYBRIDEN in 1866. His work was quoted at least 14 times before 1900, the year of its ‘rediscovery’. There were references in such widely distributed works as Focke’s DIE PFLANZEN-MISCHLINGE (1881), THE ENCYCLOPAEDIA BRITANNICA (1881) and the CATALOGUE OF SCIENTIFIC PAPERS OF THE ROYAL SOCIETY (1879).The treatise had been sent to the libraries of some 120 institutions including the Royal and Linnean Society of Great Britain. Moreover Mendel had 40 additional reprints at his disposal, many of which he sent to leading biologists of Europe. In fact, professor Niessl (1903 and 1906) emphasized that Mendel’s work was “well known” at his time. So in the face of the expectations just mentioned, – why was the discovery of the laws of heredity ignored by most scientists for more than 35 years, until 1900, and by the “true Darwinians” (Mayr) for another 37 years? That is 72 years in all!

The reasons have been hinted at or clearly stated by several pioneers of genetics as de Vries (1901), Bateson (1904, 1909, 1924), Johannsen (1909, 1926) as well as several historians of biology and/or biologists as Niessl (1903, 1906), Richter (1941, 1943), Stern (1962), Lönnig (1982, 1986, 1995), Callender (1988) and Bishop (1996):

All the evidence points to the main reason as follows: Mendel’s ideas on heredity and evolution were diametrically opposed to those of Darwin and his followers. Darwin believed in the inheritance of acquired characters (and tried to back up his ideas with his pangenesis hypothesis, which even Stebbins called an “unfortunate anomaly”) and, most important of course, continuous evolution. Mendel, in contrast, rejected both, the inheritance of acquired characters as well as evolution. The laws discovered by him were understood to be the laws of constant elements for a great but finite variation, not only for culture varieties but also for species in the wild (Mendel 1866, pp. 36, 46, 47). In his short treatise EXPERIMENTS IN PLANT HYBRIDIZATION mentioned above Mendel incessantly speaks of “constant characters”, “constant offspring”, “constant combinations”, “constant forms”, “constant law”, “a constant species” etc. (in such combinations the adjective “constant” occurs altogether 67 times in the German original paper). He was convinced that the laws of heredity he had discovered corroborated Gärtner’s conclusion “that species are fixed with limits beyond which they cannot change”. And as Dobzhansky aptly put it: “It is…not a paradox to say that if some one should succeed in inventing a universally applicable, static definition of species, he would cast serious doubts on the validity of the theory of evolution”.

As the Darwinians won the battle for the minds in the 19th century, there was no space left in the next decades for the acceptance of the true scientific laws of heredity discovered by Mendel and further genetical work was continued mainly by Darwin’s critics among the scientists. In agreement with de Vries, Tschermak-Seysenegg, Johannsen, Nilsson, et al., Bateson stated (1909, pp. 2/3):

“With the triumph of the evolutionary idea, curiosity as to the significance of specific differences was satisfied. The Origin was published in 1859. During the following decade, while the new views were on trial, the experimental breeders continued their work, but before 1870 the field was practically abandoned.

In all that concerns the species the next thirty years are marked by the apathy characteristic of an age of faith. Evolution became the exercising-ground of essayists. The number indeed of naturalists increased tenfold, but their activities were directed elsewhere. Darwin’s achievement so far exceeded anything that was thought possible before, that what should have been hailed as a long-expected beginning was taken for the completed work. I well remember receiving from one of the most earnest of my seniors the friendly warning that it was waste of time to study variation, for “Darwin had swept the field“” (emphasis added).

The general acceptance of Darwin’s theory of evolution and his ideas regarding variation and the inheritance of acquired characters are, in fact, the main reasons for the neglect of Mendel’s work, which – in clear opposition to Darwin – pointed to an entirely different understanding of the questions involved (see above).

However, the idea of Bishop (1996) and Di Trocchio (1991) as to Mendel that “most of the experiments described in Versuche are to be considered fictitious” or “…we are today forced by a series of anomalies and incongruities to admit that Mendel’s account of his experiments is neither truthful nor scientifically likely, and that the strategy he really followed must have been completely different” (Di Trocchio 1991, p.487 and p. 491, emphasis added) is in my opinion for several reasons untenable. (1) It does not match Mendel’s character which is distinguished by humility, extreme modesty and accuracy in handling things. (2) Too much is known about his life, work and correspondence to simply deny the existence of the work he has described (see the publications of Orel, Stern, Weiling and many others). (3) Fisher’s claims of fraud in Mendel’s data have already been disproved by several geneticists and historians of biology (Lamprecht 1968, Pilgrim 1986, Weiling 1995, Vollmann and Ruckenbauer 1997, and many other authors, see below). Working with Pisum for 7 years, I myself have found very similar data for several characters as Mendel had. In an answer to Edward, Ira Pilgrim commented (1986, p. 138): “…one had better have a good deal more evidence (such as a set of loaded dice or perhaps the information that the man is a known cheat) before accusing someone of cheating, which is what Fisher did to Mendel, and those who cite Fisher are doing now.”

On the other hand, if not only the accusations of Fisher but also those of Di Trocchio and Bishop were true, they would make Mendel’s work one of the greatest hoaxes in the whole history of science (“he counted 19,959 individuals” etc., Zirkle) – and at the same time the most ingenious fiction ever produced: an invention hitting directly upon the truth of the laws of heredity with many basic repercussions on nearly all biological and medical areas and our understanding of the living world. However, as long as there are no real foundations for these suspicions and as long as no convincing proofs can be advanced, – proofs which could stand the test of any honest court trial, the accusations fall back on those who produce them: fiction, invention and/or lies in the minds of the inventors (according to A. Kohn, Mendel belongs to the “false prophets”, M. Gardner states that “even Brother Mendel lied” (emphasis added) and V. Orel (1996, p. 207) lists further such examples).

The more I ponder and test the accusations regarding Mendel’s works, the more improbable and absurd the accusations appear to me, and the question comes to my mind: Could it be that now – after the creation position of a scientific giant like Mendel has become clear to so many observers – these accusations are the last resort of a more or less unconscious method of evolutionary philosophy to discredit Mendel and his work after all? 

Hubert Markl comments on the accusations of dishonesty against some renowned scientists (1998, p. VII): “Even if Galilei, Newton or Mendel had cheated when presenting the reasons and evidence for the natural laws they had discovered, that which they had recognized as being true, is nevertheless true, because it was found to be right in multiple tests” (see the original German sentence in the next chapter).

Although this is in principle correct, – being deeply impressed by another study of Mendel’s VERSUCHE ÜBER PFLANZEN-HYBRIDEN (1866), – concerning Mendel I think that this comment is unnecessary (as for Galilei and Newton, I do not want to give an opinion here). I presume the proof for the authenticity and precision of Mendel’s work is to be found in – among other things – the paragraph concerning the seventh of the characters studied by Mendel. He writes (p. 11) [English Version according to]:

“With regard to this last character it must be stated that the longer of the two parental stems is usually exceeded by the hybrid, a fact which is possibly only attributable to the greater luxuriance which appears in all parts of plants when stems of very different lengths are crossed. Thus, for instance, in repeated experiments, stems of 1 ft. and 6 ft. in length yielded without exception hybrids which varied in length between 6 ft. and 7 [and] 1/2 ft.”

Thus, in this paragraph Mendel clearly describes a case of heterosis, hybrid vigour, over- or superdominance (as the phenomenon was later named from 1914 [heterosis] onward) (as for the history of the term, the genetical basis of the phenomenon and further examples, see Lönnig 1980:Heterosis bei Pisum sativumL.). Moreover, Mendel describes a second case of heterosis when continuing (pp. 11/12):

“T h e    h y b r i d    s e e d s    in the experiments with seed-coat are often more spotted, and the spots sometimes coalesce into small bluish-violet patches. The spotting also frequently appears even when it is absent as a parental character” (spaced by Mendel).

Without a theoretical basis (which is still controversial for many cases of heterosis even in our age of molecular biology) and in the absence of any experiments, it is not possible to simply ‘invent’ such unexpected phenomena of science. Rather one must “stumble over” such totally unaccustomed and unpredictable curiosities of nature to report them to an amazed audience. Dominance in all of the characters Mendel described was already astonishing enough, but the two cases of overdominance (heterosis, superdominance) represent strong evidence that Mendel had exactly done what he described. (Mendel’s explanation of the superdominant plant length found, “which is possibly only attributable to the greater luxuriance which appears in all parts of plants when stems of very different lengths are crossed” is hardly more than a tautology [here a more inclusive restatement of the phenomenon to be explained: it does not answer the question why the greater luxuriance occurs in all plant parts, of which the unusual plant length is an ingredient]. Mendel’s statement shows that he was really at a loss for any theoretical/genetical answer for the heterosis-phenomenon he had encountered and precisely described.)

One could, perhaps, object that the phenomenon of hybrid vigour had been mentioned before Mendel. However, to describe heterosis for definite characters and organs in definite sizes and quantities in definite species and culture varieties (and all that without any knowledge of the genetical and/or molecular basis of the phenomena reported), so that the experiments not only appear unlikely (in fact, unlikely!), but also prove to be entirely reproducible and true – without really having made them at all – is so improbable that we can confidently forget this objection.

Concerning Mendel’s paper, I agree on the scientific level with Mayr and Stern. Curt Stern stated (1966, p. v): “Gregor Mendel’s short treatise, ‘Experiments on Plant Hybrids’ is one of the triumphs of the human mind. It does not simply announce the discovery of important facts by new methods of observation. Rather, in an act of highest creativity, it presents these facts in a conceptual scheme which gives them general meaning. Mendel’s paper is not solely a historical document. It remains alive as a supreme example of scientific experimentation and profound penetration of data” (Stern and Sherwood 1966). Mayr concurs (1982, p. 726) that by this comment Stern has “so well” characterized Mendel’s achievement.

Human DNA less diversified than that of chimps: evidence for Noah’s flood?



In recent years, researchers have discovered that the DNA of humans, even among (geographically) distant ethnics, such as native Americans and Chinese people, or Europeans, it’s much less genetically varied than the genes of chimps living in a same group! How could this be? The evidences points to the occurrence of a “bottleneck”, i.e., when a population undergoes a near-extinction event, and as such, loses most of its individuals.  The following are excepts of some articles relating to this fact (of course, with a lot of evolutionary wishful thinking and nonsensical dates permeating the texts) :


Pascal Gagneux, an biologist at the University of California at San Diego, and other members of a research team studied genetic variability among humans and our closest living relatives, the great apes of Africa.  
     Humanoids are believed to have split off from chimpanzees about 5 million to 6 million years ago. With the passage of all that time, humans should have grown at least as genetically diverse as our cousins. That turns out to be not true.  
     We actually found that one single group of 55 chimpanzees in west Africa has twice the genetic variability of all humans, Gagneux says. In other words, chimps who live in the same little group on the Ivory Coast are genetically more different from each other than you are from any human anywhere on the planet.

“The family tree shows that the human branch has been pruned,” Gagneux says. “Our ancestors lost much of their original variability.” 
     “That makes perfectly good sense,” says Bernard Wood, the Henry R. Luce Professor of Human Origins at George Washington University and an expert on human evolution. 
     “The amount of genetic variation that has accumulated in humans is just nowhere near compatible with the age” of the species, Wood says. “That means you’ve got to come up with a hypothesis for an event that wiped out the vast majority of that variation.” 
     The most plausible explanation, he adds, is that at least once in our past, something caused the human population to drop drastically. When or how often that may have happened is anybody’s guess. Possible culprits include disease, environmental disaster and conflict.  

“The evidence would suggest that we came within a cigarette paper’s thickness of becoming extinct,” Wood says.

They compared the DNA variability of apes and chimps to that of 1,070 DNA sequences collected by other researchers from humans around the world. They also added the DNA from a bone of a Neanderthal in a German museum. The results, the researchers say, are very convincing. 
     “We show that these taxa [or species] have very different amounts and patterns of genetic variation, with humans being the least variable,” they state. 
     Yet humans have prevailed, even though low genetic variability leaves us more susceptible to disease. (Why? What’s wrong with the story of evolution; mutations and natural selection bringing forth new genetic information out of thin air?)


Another article, from the Oxford University website, reiterates the substantial genetic variety among chimps:


Common chimpanzees in equatorial Africa have long been recognized as falling into three distinct populations or sub-species: western, central and eastern chimpanzees. A fourth group, the Cameroonian chimpanzee, has been proposed to live in southern Nigeria and western Cameroon, but there has been considerable controversy as to whether it constitutes a distinct group.

Oxford University researchers, along with scientists from the University of Cambridge, the Broad Institute, the Centre Pasteur du Cameroun and the Biomedical Primate Research Centre, examined DNA from 54 chimpanzees. They compared the DNA at 818 positions across the genome that varied between individuals.

Their analysis showed that Cameroonian chimpanzees are distinct from the other, well-established groups.

Dr Rory Bowden from the Department of Statistics at Oxford University, who led the study, said: ‘These findings have important consequences for conservation.[…] The fact that all four recognized populations of chimpanzees are genetically distinct emphasizes the value of conserving them independently.’ (Again, what’s wrong with evolution giving rise to new genetic content ex-nihilo?) 

The researchers also contrasted the levels of genetic variation between the chimpanzee groups with that seen in humans from different populations.

Surprisingly, even though all the chimpanzees live in relatively close proximity, chimpanzees from different populations were substantially more different genetically than humans living on different continents. That is despite the fact that the habitats of two of the groups are separated only by a river.


‘That chimpanzees from habitats in the same country, separated only by a river, are more distinct than humans from different continents is really interesting. It speaks to the great genetic similarities between human populations, and to much more stability and less interbreeding over hundreds of thousands of years in the chimpanzee groups.’ (When something damages their accepted theory, they use attenuating terms such as “very, really interesting”)


And a lot more articles talk about this intriguing fact, and of course, about the supposed catastrophic event which caused the bottleneck, such as a volcano eruption or asteroid impact, 70.000 years ago:


There is one near-extinction event that is fairly well-known, although it remains controversial. Roughly 70,000 years ago, give or take a few thousand years, an enormous eruption occurred in what is now Sumatra, leaving behind Lake Toba). The eruption coincides with a population bottleneck that is often cited as the reason for the relatively low genetic diversity across Homo sapiens sapiens. Research suggests as few as 2,000 humans were left alive by the eruption and its aftereffects.

A recent paper in the Proceedings of the National Academy of Sciences found another population bottleneck much farther back in human history. Genetic studies found that 1.2 million years ago there were as few as 55,000 members of genus Homo, including pre-human hominids like Homo erectus and Homo ergaster. This one is interesting because we don’t have solid evidence of a catastrophic event during that period, so we’re not sure what might have caused the population crash or where to look for more evidence.

The really interesting thing about a population bottleneck is the effect it has on evolution. With a small population, mutations get passed through a very large percentage of the species’ members. Detrimental mutations could be devastating and lead to outright extinction. (Why are they afraid of mutations? They (the mutations) have allegedly caused the origin of millions of perfectly fit species, countless features, limbs, organs…)

“When humans faced extinction.” BBC News.

“Humans Might Have Faced Extinction.” Scientific American.


Others say that the bottleneck event occurred in the Pleistocene era:

It is our conclusion that, at the moment, genetic data cannot disprove a simple model of exponential population growth following a bottleneck 2 MYA at the origin of our lineage and extending through the Pleistocene. Archaeological and paleontological data indicate that this model is too oversimplified to be an accurate reflection of detailed population history, and therefore we find that genetic data lack the resolution to validly reflect many details of Pleistocene human population change. However, there is one detail that these data are sufficient to address. Both genetic and anthropological data are incompatible with the hypothesis of a recent population size bottleneck. Such an event would be expected to leave a significant mark across numerous genetic loci and observable anatomical traits, but while some subsets of data are compatible with a recent population size bottleneck, there is no consistently expressed effect that can be found across the range where it should appear, and this absence disproves the hypothesis.


Okay, it’s a fact that humans has undergone a period on which they were almost vanished from Earth. And this has caused the current small genetic diversity. So, why can’t we conceive the idea of a global flood? Surely a flood explains it quite well, and also explains some amazing fossils found, depicting unusual scenes:










Ichthyosaur Giving Birth





Those scenes, and delicate physical details can only be explained by a rapid burial, because organisms are quickly decomposed in nature…

Any other suggestion other than a flood?

What about natural selection?

“Nature encourages no looseness, pardons no errors”
– Ralph Waldo Emerson

“I have called this principle, by which each slight variation, if useful, is preserved, by the term Natural Selection.” – Charles Darwin, The Origin of Species

 According to evolutionists, the so-called Natural Selection has four main components:

  1. Variation.  Organisms (within populations) exhibit individual variation in appearance and behavior.  These variations may involve body size, hair color, facial markings, voice properties, or number of offspring.  On the other hand, some traits show little to no variation among individuals—for example, number of eyes in vertebrates. 
  2. Inheritance.  Some traits are consistently passed on from parent to offspring.  Such traits are heritable, whereas other traits are strongly influenced by environmental conditions and show weak heritability.
  3. High rate of population growth.  Most populations have more offspring each year than local resources can support leading to a struggle for resources.  Each generation experiences substantial mortality.
  4. Differential survival and reproduction.  Individuals possessing traits well suited for the struggle for local resources will contribute more offspring to the next generation. 

Source: Global Change

Well, these four points are in fact undeniable, provided they actually occurs in nature (yet, not to the extent of causing the “macro-evolution”, it simple causes sick, old, weak organisms to be eliminated, whereas the most health, strong ones succeed in reproduction, a process that only causes the maintenance of the already existent genetic content). Read, for example, this AiG link telling the reality of natural selection (also: ICR article  “Natural” Selection versus “Supernatural” Design; CMI’s Q&A; Creationscience).

The article proceeds:

“During the twentieth century, genetics was integrated with Darwin’s mechanism, allowing us to evaluate natural selection as the differential survival and reproduction of genotypes, corresponding to particular phenotypes.  Natural selection can only work on existing variation within a population.  Such variations arise by mutation, a change in some part of the genetic code for a trait.  Mutations arise by chance and without foresight for the potential advantage or disadvantage of the mutation.  In other words, variations do not arise because they are needed.”

Oh yeah, mutations.. What are they?

“In genetics, a mutation is a change of the nucleotide sequence of the genome of an organismvirus, or extrachromosomal genetic element. Mutations result from unrepaired damage to DNA or to RNA genomes (typically caused by radiation or chemical mutagens), from errors in the process of replication, or from the insertion or deletion of segments of DNA by mobile genetic elements. Mutations may or may not produce discernable changes in the observable characteristics (phenotype) of an organism. Mutations play a part in both normal and abnormal biological processes, including evolution,cancer, and the development of the immune system.” Wikipedia

When the genetics was integrated with ToE, mutations  became thus the  driving forces of evolution (even despite the fact they are mostly harmful or neutral!). The Wikipedia article goes on, and later it mentions some “beneficial” mutations, such as the CCR5-Δ32, which causes HIV-resistance; the defective gene which causes sickle-cell anemia, but also causes malaria resistance, and the bacterium that became resistant to vaccines, etc. Surely these aren’t the best examples for a process allegedly causer of improvement, enhancement on living beings, driving to “uphill” evolution. However, this is the “best” mutations can do, aside from being neutral. 

But, in the evolutionist world, mutations are dandy! As the Wikipedia states:

“Mutations can involve large sections of DNA becoming duplicated, usually through genetic recombination. These duplications are a major source of raw material for evolving new genes, with tens to hundreds of genes duplicated in animal genomes every million years.”

Not only the Wikipedia, but also renowned scientific papers, such as the Nature, which describes:

“Mutations can have a range of effects. They can often be harmful. Others have little or no detrimental effect. And sometimes, although very rarely, the change in DNA sequence may even turn out to be beneficial to the organism.”

What are the probabilities of an OFTEN HARMFUL/NEUTRAL factor actually leading to the origin of millions and millions of species, extant and already extinct?

The same Nature article declares some lines later:

Mutations are essential to evolution. Every genetic feature in every organism was, initially, the result of a mutation. The new genetic variant (allele) spreads via reproduction, and differential reproduction is a defining aspect of evolution. It is easy to understand how a mutation that allows an organism to feed, grow or reproduce more effectively could cause the mutant allele to become more abundant over time.”

Of course, “it’s easy to understand” that mutations are enhancing, except, of course, for the numberless genetic diseases, deformations, sterility, etc (it’s expected that any mutant organism should be ripped off by natural selection for not being “fit”). But nothing poses as a problem for a theory as plastic as the ToE!

Before proceeding with the article, I could not leave this part go unnoticed:

“For instance, genes control the structure and effectiveness of digestive enzymes in your (and all other vertebrate) salivary glands. At first glance, mutations to salivary enzymes might appear to have little potential for impacting survival. Yet it is precisely the accumulation of slight mutations to saliva that is responsible for snake venom and therefore much of snake evolution. Natural selection in some ancestral snakes has favored enzymes with increasingly more aggressive properties, but the mutations themselves have been random, creating different venoms in different groups of snake.”

The famous evolutionist’s ability to “flight on fancy” about non-testable, imaginary scenarios on evolution… Do not notice the “might appear”, or “if” when they do their fantasy, regardless of these subjective words, they are actually  totally sure that these scenarios really happened! How trustworthy…

Returning to the main subject, the term “Natural selection” was derived from the “artificial” one, i.e., selective breeding made by men, in the agriculture, animal/plant breeding, selecting the most agreeable, productive, resistant varieties and discarding these with uninteresting features. Darwin himself inspired in this millennial custom to draw the main driving force of his original theory. Verily, selective breeding has “created” more productive plants and animals, improving the production of food and grains,  among other things. But, with respect to genetic variety, new content, etc, what artificial selection has proven therefore? Did the (artificial) selection caused the arising of new genetic information? The answer definitely is NOT!

If so, we would not face some intriguing problems, like it happens with dog breeding. Over many hundreds of years, humans have produced the various breeds by specifically selecting different traits to breed for; there are currently over 200 distinct varieties of dog, but all belong to the same species, and could theoretically breed with each other, though size difference between larger and smaller breeds renders some combinations unlikely.

Over time, breeding only for certain traits allows great predictability in what a dog’s offspring will look like—a Dalmatian mated with a Dalmatian will produce Dalmatian puppies, and so on. When this occurs regularly, the type of dog becomes an official breed. But this predictability comes at a genetic cost. The breeders have drastically reduced the amount of genetic information in the population of dogs—such as for other coat colours and lengths, or different sizes or temperaments. This caused painstaking problems for some breeds..

The bigger dog breeds become susceptible to hip dysplasia, others are plagued by heart problems. The King Charles Spaniel is prone to an extremely nasty condition, syringomyelia (SM), in which the skull is too small to house the brain. In the documentary, veterinary neurologist Clare Rusbridge described the condition: “A burning pain, a piston-type headache, abnormal sensations to even light touch, even items of clothing, a collar, for example, can induce discomfort for these animals.” She believes up to one-third of the breed could be affected by this condition.

Overall, there are 500 genetic diseases which are known to occur in dogs. This is fewer than those documented in humans, but in dogs they occur at a much higher rate. The problem is that when the gene pool has been so depleted, it is not possible to avoid breeding diseased dogs, because that would be impoverishing the gene pool even more, and could lead to new diseases and disorders in a breed. Rusbridge acknowledged this to be true. (source)

“Mutts”, or even crossbred dogs, have a much lower chance of having these diseases, because many are genetically recessive—a healthy copy of the gene will override a diseased gene. Because the diseases are also often breed-specific, even breeding two purebred dogs of different breeds will normally produce much healthier offspring than a purebred mating. The mutts will have lower instances of disease as well as being slightly longer-lived on average.

In Britain, an already bad situation has been compounded in many ways by the Kennel Club’s breeding and show dog practices. First, the gene pool of the breeds is artificially restricted to the descendants of the originally-registered dogs from the mid-nineteenth century—in some cases, only a handful of dogs. This means that genetic diversity cannot be re-introduced into a breed, even if this means making the population healthier.

Second, there is extreme selection for absolute perfection in appearance—breeders seek to produce dogs which adhere to the breed standard as closely as possible. This causes them to remove dogs that fall short of that standard, such as Dalmatians with non-standard markings, albino dogs, or Rhodesian Ridgebacks with no ridge, from the gene pool of the species, either by simply not mating them, or by culling them as puppies. This renders the overall population even more genetically impoverished.

Third, extreme inbreeding has been the norm—it is common to mate littermates, or to mate a female dog with her “grandfather”, or “mother” to “son”. Evolutionary geneticist Steve Jones criticized the practice: “People are carrying out breeding which would be, first of all, it’s illegal in humans, and second of all, it’s absolutely insane from the point of view of the health of the animals.” Such close interbreeding is done to ‘fix’ certain desirable traits in the line, but it also makes the dogs more disease-prone.

Because there is no regulation against breeding dogs which are known to carry a genetic disease like syringomyelia, dogs with conditions like this, if they are popular studs, can go on to sire dozens of litters. This spreads the genetic disease throughout the breed.

All these factors together have made modern breeds very genetically impoverished—in some breeds, only 10% of the genetic variety that was in the breed 40 years ago has been passed down to the current descendants of the breed. For instance, the Pug breed in the UK, although it has 10,000 dogs, has the genetic information equivalent to that of 50 distinct individuals. In 2004, Dr Jeff Sampson wrote:

“Unfortunately, the restrictive breeding patterns that have been developed as part and parcel of the purebred dog scene have not been without collateral damage to all breeds … Increasingly, inherited diseases are imposing a serious disease burden on many, if not all, breeds of dog.”

How artificial selection depletes information.

In the example on the right (simplified for illustration), a single gene pair is shown under each dog as coming in two possible forms. One form of the gene (S) carries instructions for large size, the other (s) for small size.

In row 1, we start with medium-sized animals (Ss) interbreeding. Each of the offspring of these dogs can get one of either gene from each parent to make up their two genes.

In row 2, we see that the resultant offspring can have either large (SS), medium (Ss) or small (ss) size. But let’s suppose that breeders want large dogs. They would select the largest dogs in the next generation to breed. Thus only the big dogs pass on genes to the next generation (line 3). So from then on, all the dogs will be a new, large variety. This is artificial selection, but natural selection would work on the same principle, if large dogs would do better in their environment. Note that:

  1. They are now adapted to their environment, in this case breeders who want big dogs.
  2. They are now more specialized than their ancestors on row 1.
  3. This has occurred through artificial selection, and could have occurred through natural selection.
  4. There have been no new genes added
  5. In fact, genes have been lost from the population—i.e. there has been a loss of genetic information, the opposite of what microbe-to-man evolution needs in order to be credible.
  6. Not only genes for smallness were lost, but any other genes these small dogs carried. They may have had genes for endurance, strong sense of smell, and other things, but they are lost from the population. Genes on their own are not selected; it’s the whole creature and all the genes they carried.
  7. Now the population is less able to adapt to future environmental changes—if small dogs became fashionable, or would perform better in some environment, they could not be bred from this population. They are also genetically impoverished since they lack the good genes that happened to be carried by the small dogs. (Source)

The list of problem goes on, now, in the agriculture, another area facing the problems with the “bottle-necking”, depletion of gene variety. Example, in Ireland, during the 1840’s, a terrible famine took place (Irish Potato Famine), causing over 1.5 million people deaths, due to a plague (potato blight) that did lead to a total crop failure.

Why did the potatoes succumb to the disease? Potatoes came from the Andes mountains of South America, where many different varieties were grown, including some which could resist potato blight disease. When potatoes were introduced to Europe in the 1500s, this did not include varieties with resistance to this disease.

Therefore the crops in Europe were all susceptible to the disease when it arrived. (Ireland suffered the most because of its very high dependence on potatoes for the complex carbohydrate portion of their diet, whereas others had more grain crops). They succumbed because of the lack of genetic variety, which included the genes for resistance to blight.

The pattern has been repeated many times since. In 1970 in the U.S., genetic uniformity resulted in loss of almost a billion dollars worth of maize because 80% of the varieties being grown were susceptible to a virulent disease known as ‘southern leaf blight.’ (FAO)

Plant breeders have been very successful in increasing the yields of all sorts of crop plants—so successful that farmers have been replacing the local, traditional varieties with the new varieties. For example, in China, at least 9,000 varieties of wheat have been lost since 1949.

The ‘Green Revolution’ saw the development of high-yielding rice and wheat varieties and their rapid replacement of traditional, community-bred varieties (‘landraces’). For example, by 1984 in Bangladesh, 96% of the wheat grown consisted of Green Revolution varieties.

A single variety of the ‘miracle wheat’ accounted for 67% of all the wheat planted. This has contributed to the feeding of many millions of people. However, the loss of the traditional varieties, and the reliance on relatively few new varieties, poses problems.

Large areas of a uniform variety are susceptible to new strains of pests and disease for which the variety lacks resistance. These new pest or disease strains can be introduced from overseas, or new varieties can occur through normal reproduction which results in new combinations of existing genes. Just as with antibiotic resistance, these new disease strains do not arise through the development of new, functional genes,3 so this has nothing to do with particles-to-people evolution.

To try to keep ahead of new strains of pests and diseases, plant breeders introduce new genes from wild plants of the crop species, or from ‘landraces,’ into new varieties. New varieties generally last only five to seven years before they are replaced.

However, with loss of the wild types and landraces, plant breeders could lack the sources of genes for the further breeding needed to increase yields, decrease dependence on fertilizers and pesticides, improve quality, breed for drought resistance, cold/heat tolerance, salt tolerance, and many other things. So the loss of the genetic information needed to achieve these objectives is a serious problem. The U.N.’s Food and Agriculture Organisation (FAO) estimates that about 75% of genetic diversity in agricultural crops has been lost this century—largely by the replacement of landraces with the new varieties.

A term was coined due to this increasingly troubling question: The genetic vulnerability, used to indicate the condition that results when a crop is uniformly susceptible to a pest, pathogen, or environment hazard as a result of its genetic constitution, thereby creating a potential for disaster. Two important factors interact to increase the potential for crop failure: (1) the degree of uniformity for the trait controlling susceptibility to the hazardous agent or environmental stress, and (2) the extent of culture (often monoculture) of the susceptible variety. The greater the uniformity for a susceptible trait and the more extensive the area of cultivation, the greater the risk of disaster.

There is cause for concern when extensively planted cultivars of major crops are derived from limited gene pools and, hence, are uniform for a high percentage of traits with narrow based resistances to common pathogens or other agents. These concerns have prompted surveys of plant breeders on their perceptions of the gravity of the problem and a reevaluation of trends in international varietal development and distribution.

Although some breeders and scientist are encouraged by the wider availability of crop gene pools into which exotic plant genes have been introduced, others are worried that genetic uniformity may be increasing on a global scale because of the widespread adoption of modern varieties with similar genetic backgrounds across continents where large numbers and mixtures of landraces were formerly grown.

Breeders can strengthen plant resistance against epidemics by broadening the diversity of resistance genes and “pyramiding” multiple genes from different sources and genes controlling other mechanisms of resistance. (source)

If random copying mistakes (mutations) originally generated all the information, surely it should not be too hard for highly intelligent scientists to create the required genes for breeding new improved varieties? However, with all that we now know about genes, no one can yet create a gene—for example, for rust resistance—from scratch. Plant breeders recognize that the information in the genes of plants is irreplaceable.

The evolutionist E.O. Wilson wrote: ‘Each species is the repository of an immense amount of genetic information. The number of genes range from about 1,000 in bacteria and 10,000 in some fungi to 700,000 or more in many flowering plants and a few animals … . If stretched out fully, the DNA [in one cell] would be roughly a meter long. But this molecule is invisible to the naked eye. … The full information contained therein, if translated into ordinary-size letter of printed text, would just about fill all 15 editions of the Encyclopædia Britannica published since 1768.’ Biologist David Janzen, University of Pennsylvania, said that destroying tropical forests for paper manufacture would be ‘like pulping the Library of Congress to get newsprint.’

Banking on genes

In recognition of the problem with crop plants, ‘gene banks’ for various crops have been set up around the world. For example, more than 80,000 rice varieties are maintained at the International Rice Research Institute (IRRI) in the Philippines. The gene bank provides rice seed samples on request. When Cambodia got through the notorious evolution-inspired Pol Pot upheavals, the rice farmers could resume growing their lost varieties from seed supplied from the rice seed collection.

However, seeds held in gene banks are vulnerable because of the need to grow the seed periodically to produce fresh seed. Gene banks are labour intensive, costly to maintain, and not easy to raise funds for. Storage at –20°C enables some seed to remain viable for up to 100 years, but this depends on continuous maintenance of refrigeration facilities. From a survey, FAO estimated that almost half of all stored seeds need to be regenerated—that is, these strains are liable to be lost.

Also, only major crop plants are covered by such gene banks. Non-cereal plants which are an important source of food in subsistence agriculture in the tropics tend to be neglected in gene banks. For example, wheat accounts for 14% of all gene banks, whereas cassava, a major poor people’s crop, accounts for only 0.5%.

In addition to the large gene banks, there are ‘Seed Saver’ groups who voluntarily collect and grow traditional varieties no longer grown commercially by farmers. Folk involved in such seed saving actions network with one another to share rare varieties.

Organizations concerned with conserving genetic resources, such as The International Plant Genetic Resources Institute (IPGRI) in Rome, Italy, now recognize the importance of getting farmers themselves to maintain their traditional varieties. Non-government organizations (NGOs) have been leading the way with this approach.

The greatest project with this desperately necessary purpose is the Svalbard Global Seed Vault, as we read in the Wikipedia page:

Svalbard Global Seed Vault is located in Svalbard

Svalbard Global Seed Vault is located in Svalbard, Norway

“The Svalbard Global Seed Vault(Norwegian:Svalbard globale frøhvelv) is a secure seedbank located on the Norwegian island of Spitsbergen near the town of Longyearbyen in the remote Arctic Svalbard archipelago, about 1,300 kilometres (810 mi) from the North Pole.[4] It was started by conservationist Cary Fowler in association with the Consultative Group on International Agricultural Research (CGIAR),[5] and functions to preserve a wide variety of plant seeds in an underground cavern. The seeds are duplicate samples, or “spare” copies, of seeds held in gene banks worldwide. The seed vault is an attempt to provide insurance against the loss of seeds in genebanks, as well as a refuge for seeds in the case of large-scale regional or global crises.”

Remember that Gene banks are a type of biorepository which preserves genetic material (again, it’s a funny thing that we may need to build these banks, if evolution/natural selection/miraculous mutations are around to create new genetic variations out of thin air, as it allegedly did during the Earth’s history).

What’s the mission of this Global Seed Vault?

“The Svalbard Global Seed Vault’s mission is to provide a safety net against accidental loss of diversity in traditional genebanks. While the popular press has emphasized its possible utility in the event of a major regional or global catastrophe, it will certainly be more frequently accessed when genebanks lose samples due to mismanagement, accident, equipment failures, funding cuts and natural disasters. Such events occur with some regularity. In recent years, some national genebanks have also been destroyed by war and civil strife. There are some 1,400 “crop diversity collections” around the world, but many are in politically unstable or environmentally threatened nations.”


It’s seems (again) that the proposed premises of the “factual” Theory of Evolution insists on failing the tests and observations, despite that it “works” flawlessly in the computer simulations, papers and evolutionist’s mind. We can’t expect that either natural and artificial selections may cause the origin of new genetic varieties and content, by logic and fact this is only possible when caused by an intelligence acting behind it, which points to A Creator God over again.


God bless you!

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