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11. Degeneration Exists
11. DEGENERATION EXISTS
(Not evolution)
11. DEGENERATION EXIST
11.1 There is degeneration
1. mutations
2. hereditary diseases
3. old age
4. cancer
5. deadly genes
6. internal viruses
7. pseudo genes
8. asexual reproduction in female lizards
9. rudimentary organs
10. blind animals in the Movile cave
11. the flightless cormorant
12. jury-rigged design
11.1.2 Conclusion
11.2 The natural lower boundary of degeneration.
11.3 The degeneration law
11.4 The beneficial degeneration
Degeneration FAQ
One aspect of the nature around us that is completely disregarded on a large scale is that there is degeneration!: pure genetic impoverishment of populations and species, and absolutely no genetic enrichment as is necessary for an evolution from unicellular organisms.
11.1 Degeneration exists
There are examples of this impoverishment and degeneration, and I will lay some of them out for you.
1.mutations
In the first place, there are mutations. Mutations are damage done to existing genes. And everyone agrees that 99% of mutations are such that absolutely nothing functional can come out of it anymore.
The evolution theory says that that remaining one percent, in combination with natural selection, leads to ‘better’ adaptation, and therefore to ‘better’ genes with ‘better’ proteins, or proteins with new functions, which in the end then leads to macro-evolution. The degeneration theory says simply that all mutations are damage to or even elimination of existing good genes, but in a number of cases could conceivably result in something which gives a ‘survival advantage’. I will come back to this with an example at the end of this chapter.
Anyhow, degeneration (99%) is a better word to characterize the work of mutations than evolution (1%).
In Figure 1, a number of examples can be seen of what mutating degeneration can do to fruit flies: all sorts of twisted wing shapes, strange abdomens and tiny eyes. These are cases where, in nature, the fly would not be able to survive.
Figure 1. Mutation=degeneration, Genetic Analysis pp. 185
2. hereditary diseases
Humanity is burdened with an incredible amount of hereditary diseases. This happens not because Evolution still has some items on its list of things to do, but because mutations cause defects in genes that used to be all right. Most people have the ‘good’ genes. However, if someone has such a defective gene, that person has a hereditary disease, or is a ‘carrier’ of that disease. If this defective gene spreads throughout the human community, then that is a form of degeneration, not of evolution.
Figure 2.The 23 chromosomes of a human with the places of the genes which a number of the better-known hereditary diseases cause if they are defective, Genetic Analysis pp.5
Since hereditary diseases originate by mutations of good functional genes, when we go back in time, we will find less and less of these damages in the human genome. It is estimated that every human being has 4 - 5 hidden lethal defects in its DNA. When we go back in time, the human population would have been much smaller then nowadays. Once there would have been only 10.000 people, or even 100. We all originated from this small group. But this small group would NEVER have all the genetic defects we have today in our 6 billion poeple. That would not even be possible. But on the other hand, they would have had ALL the good functional genes, that most of us still have. The first (group of) human ancestors must have been genetically perfect!
There was a time when certain geneticists thought that they could create or get an Übermensch, a human who would be perfect in every way, by combining all the good genes of different people in one new human race. In the light of the degeneration theory, we can now say that our earliest ancestors must have been those Übermenschen! Genetically perfect! There was not a single hereditary disease in their genes.
And who can determine all of what we have lost along the way of degeneration? What will thus never return, because no one has it any more? What did the dead genes in our DNA do before? Were our earliest ancestors, besides being undisturbed by all sorts of genetic defects and therefore hereditary diseases, also much more beautiful? Or more intelligent? Did they all have a photographic memory? Did they have a longer life span? Who will tell?
3. old age
Growing older is a fight against degeneration. More and more functions of life decrease, are damaged, cease to work. Quite a lot can be ‘patched up’ with medicines, but in the end, it is by definition a losing battle: everyone dies.Still, growing older has a genetic basis. If ‘young’ chromosomes are placed in ‘old’ cells, these old cells act like young cells (which indicates a genetic cause):
An interesting insight into this issue has emerged from studies in which nuclei .obtained from young cultured cells were fused with old cells which nuclei had been removed. Such cells, with their”young” nuclei and “old” cytoplasm, continue to divide like young cells
Cell and Molecular Biology, pp. 711
Another remarkable piece of data can be found in the syndrome of ‘progéria’, in which young children age extremely rapidly (see Figure 13). The ability to divide cells may have some relation with this:
The possibility that the process of cell aging and death is under genetic control was first suggested in 1961 when Leonard Hayflick reported that normal human fibroblasts. have a built-in limit to the number of times they can proliferate. His experiments revealed that fibroblasts taken from an embryo and grown in culture divide about 50 times before they deteriorate and die.In contrast, fibroblasts taken from adults multiply only 15-30- times before dying. And fibroblasts isolated from young children suffering from Werner’s syndrome, a rare disease that causes youngsters to age prematurely, divide only 2-10 times in culture.Further evidence for a relationship between aging and a cell’s proliferative capacity came with the discovery that the number of times a cell can divide in culture is related to the life span of an organism. Thus cells of the Galápagos tortoise, whose maximum life span is about 175 years, divide more than a 100 times in culture before dying, whereas cells obtained from mice, whose life expectancy is only a few years, divide fewer than 30 times.
Cell and Molecular Biology, pp. 709
Figure 3. a boy of twelve years old with progéria or werners syndrom ( picture archive EO)
Another piece of data concerns DNA duplication during cell division. The proteins that arrange the duplication need a piece of the DNA to hold on to. With each duplication, a small piece of the DNA at the end is lost, and the chromosome becomes a little bit shorter. Now this is not a big problem, since the ends of human chromosomes have between 250 and 1500 copies of the same piece of DNA, with the code TTAGGG, also known as the TEL sequence. But once the pieces are gone, the chromosome itself and the genes thereupon are affected, which eventually leads to the death of the cell.
It is noticeable that in the line of cells from fertilized egg cell to sex cells, this ‘shortening’ does not happen. That ‘line of sex cells’ has eternal life! If that were not the case, only a few generations could come into existence, or perhaps even only one. It appears that there is a special enzyme, called telomerase, which can add the TEL sequence to the ends of chromosomes!
Since the somatic cells[1] of multicellular organisms, in fact, lack telomerase activity, this suggests that the loss of telomerase function in somatic cells is a basis for aging in multicellular organisms.
Biochemistry, pp. 1044
All these facts show that ‘growing older’ is programmed into the DNA. In the case of progéria, you see that it is possible for aging to happen much faster than normal. Would the opposite then be possible? That people once lived much longer than they do now? Or that our earliest ancestors maybe did have the telomerase function for somatic cells and therefore had some form of ‘eternal life’? Did they lose that ‘on the way to us’? Has the human race been exposed to a very serious form of degeneration?
4.cancer
Cancer is a form of degeneration of somatic cells (non-sex cells).That is the reason that mutations can happen in these cells without those mutations being passed on to the offspring. Cancer has a genetic basis. There are all sorts of proteins which arrange cell division. There are also proteins which keep an eye on the process to see if it goes well. Such a protein, called P53, checks if the DNA is all right, and if it is not, it allows the cell to die. P53 is sometimes called ‘The Guardian of the Genome’. It is a kind of gatekeeper: if all the other mechanisms to preserve the DNA have failed, P53 initiates the self-destruction of the cell, so that the damaged DNA is prevented from spreading to many more cells.
But what if P53 itself is damaged by a mutation? Then cells can have ‘eternal life’: the programmed limited number of cell divisions no longer applies, self-destruction no longer kicks in in the case of damage, in short, the cells continue to multiply unlimitedly and uncontrolledly, without end, it becomes a cancerous tumor.[2]
When such damage occurs in sex cells and is passed on to the offspring, it is then a matter of a hereditary increased chance of cancer.
5.deadly genes
Under normal circumstances, mice have a dark gray-brown pelt. There are also mice with a yellow pelt. If these are crossed with normal mice, half will be yellow and half normal. That means that the yellow mouse was a heterozygote (two different alleles for a certain gene) and that the characteristic yellow (AY) is dominant to normal (A). However, if a yellow mouse is crossed with a yellow mouse, twice as many yellow mice as normal mice result, whereas the expectation would be that there would be three times as many yellow mice. The reason for this turned out to be that when a mouse became homozygotic (AYAY) for that yellow color, it is no longer viable. In the uterus of pregnant females, one quarter of the embryos was found dead.
Figure 4: A nest of 'yellow' mouses,Genetic analysis pp.97
The explanation for this must be that it concerns an essential protein, which, when it only occurs once, it (among other things) causes the pelt to be yellow, but its complete absence is lethal.
It turns out that there are a lot of these sort of lethal genes. Depending on what kind of gene it affects, it can result in death during the embryonic development, or later in life. Some cause death in heterozygosis, other only in homozygosis. There is a term for the complete collection of lethal genes that resides in a population or population group: genetic load. This is a clear form of degeneration. That this degeneration does not get out of hand and take over is simply because, again and again, they literally die out. However, due to new mutations in the same gene, they also come back again and again.
6.internal viruses
In chapter 7, we discussed the P-elements in fruit flies.That is DNA from another species which copies and shifts itself, and is responsible for a lot of mutation in the fruit flies’ genome. We have seen that these ‘internal viruses’ can spread throughout a population in living nature (not just by human influence). At the present time, somewhere between 3% (Biochemistry, pp. 1064) and 10% (Genetic analysis, p. 650) of the DNA of fruit flies consists of this kind of ‘rubbish’! It makes you wonder why the fruit flies are still alive! The reason is probably because the fruit flies have a lot of offspring, and all the offspring in which the genome is too messed up simply never grows. Only the fruit flies in which the transposons are located in places where they cannot do much damage can reproduce.
If you realize that the fruit flies did not have this muddying of their genome at first, you can see clearly that this is a form of degeneration. Is it possible that the extinction of an entire species could be caused by degeneration in this way?
In the 24 January '97 issue of Intermediair, there was an alarming article about these ‘retrotransposons’ with the title “The jumping brother of HIV.” A few quotes:
The retrotransposons or ‘jumping genes’ have existed for a long time and seem to do their carriers more harm than good.
Some have been active for an eternity. Others appear for a while, display increasing amounts of mutations and then die, leaving the DNA of their host full of molecular debris.
Michael Tristen and his colleagues found indications of retroviruses (active and degenerated) in reptiles, amphibians and fish.
If the retrovirus genealogies of for example fish and mammals are hardly distinguishable from each other, that could mean that their parasites are closely related and therefore can transfer from one group to another without too much difficulty. And that would have worrying implications for the evolution of new diseases.
prediction: In the DNA of fossils, very few to absolutely no transposons are present.
7. pseudo genes
The phenomenon of dead genes or pseudo genes has already been extensively covered. To show that it is not made up, the next quote says:
There are other sites in the genome where nucleotide differences do not effect protein sequences. The genome of eukaryotes is loaded with 'dead genes' called pseudogenes. Pseudogenes are copies of working genes that have been inactivated by mutation. Most pseudogenes do not produce full proteins. They may be transcribed (There is maken a matrix of, PMS), but not translated '(There is maken no protein of, PMS). Or, they may be translated, but only a truncated protein is produced.
Chris Colby, The Talk.Origin Archive, Introduction to Evolutionary Biology.
Chris Colby suggests that dead genes are copied genes that have lost their function, but it seems to me that in many cases they could have been simply (for the viability) neutral genesthat had been damaged!
Dead genes are a clear form of impoverishment and degeneration. The more dead genes in a species, the more ‘degenerated’ (the DNA of) that species is.
8. asexual reproduction in female lizards
There are about fifteen known species of lizards (of the genus Cnemidophorus) that only have females. They reproduce asexually (called parthogenesis). The offspring is therefore also all genetically identical. Still, the females imitate sexual reproduction with each other during mating season. Feminine and masculine behavior alternates synchronous with the periods of ovulation. The sexual behavior stimulates ovulation. Isolated lizards reproduce less easily than those that simulate the sexual act. The lizards originated from species in which males were involved in reproduction
Figure 5, Biology Campbell, pp. 938; two mating female lizards
These lizards that reproduce asexually are often used as 'perfect' examples of evolution. However, it is clear that this is a serious form of degeneration. During meiosis – that is the cell division which ensures that sex cells come out of a cell with a single set of chromosomes each – something goes wrong and egg cells are produced which each have a double set of chromosomes, and therefore can develop into full-fledged lizards. Defects in the genes that arrange meiosis probably cause this. It is clear that the advantages of sexual reproduction, namely variation and therefore greater chances of survival, are lost in this process.
9.rudimentary organs
Rudimentary organs are actually ‘reduced’ organs. For instance, the lynx no longer has a tail and blindworms have subcutaneous vestigial legs, but are actually lizard-like.
Figure 6, the tailless lynx
Some snakes also have vestigial hind legs, as can be seen in Figure 7. Did snakes once walk? Without legs, they must now crawl on their bellies, but they have been able to deal with it (or adapt, if you like), and have survived.
Figure 7 snake ‘legs’
Rudimentary organs have always been presented as strong evidence for evolution, and for a common ancestry. In the light of our findings, however, only one conclusion is justified: Rudimentary organs are a form of degeneration, definitely not evolution.
10. blind animals in the Movile cave
In 1986, in western Romania, a cave was discovered without a natural entrance. Construction workers stumbled across one of the rooms. In the spaces, shut off from the outside world, forty-eight species of invertebrates were discovered, including spiders, leeches and scorpions. Because there is no light in that cave, these organisms have no eyes. A clear form of degeneration! A mutation that damages or limits sight would not be a disadvantage in that cave and can spread without problems. In the end, this resulted in a total loss of sight for the whole population.
Someone could say that this was a form of adaptation. And the advantage is that the organisms now do not need to develop eyes. However, even if that were so, it is still a form of genetic degeneration, of descent, of loss of functionality and of loss of genes.
Figure 8, a blind water scorpion
11. the flightless cormorant
The flightless cormorant of the Galapagos islands is the only member of its family which cannot fly. On the islands, it has no natural predators and there is an abundance of fish right by the coast, so that the necessity of flight is no longer present. Mutations that affect the ability of flight therefore had a chance to spread within the population, where they would normally result in the death of the individual. This phenomenon often occurs in birds on remote ocean islands.
In the Dutch book De Evolutie van het Leven [The Evolution of Life] by Philip Whitfield, a Natuur & Techniek publication, this is brought up as an example of evolution, natural selection and adaptation, because it is to the benefit of the cormorant no longer to need to keep up the energy-consuming flight activity. However, it is actually clearly a form of degenerative adaptation.
Figure 9, Left: the Everglades Cormorant.Right: The cormorant that 'forgot how to fly'.
12.jury-rigged design
In The Talk.Origins Archive, there is an article about ‘jury-rigged design’, which means something along the lines of: emergency solutions, emergency constructions, matters which, if they were designed, would indicate more an obtuse design than an intelligent designer. And because there are supposedly so many examples of jury-rigged design, it is absolutely not ‘designed’. If an intelligent Designer would had created life, he would have had to approach a lot of things differently. And apparently, this is not the case, goes the logic; the imperfection of living nature indicates that it was not designed but that it had evolved.
Some of the examples used are the nerve in humans under the elbow (which hurts a lot when bumped, and is called the ‘funny bone’), the wisdom teeth (some people get them, some do not) and the extremely small forelegs of Tyrannosaurus Rex.
These and many[3] of the other examples named can be easily understood in the light of degeneration and thus have nothing to do with design nor with evolution!
What we thus see in living nature is not all the result of design. What we now see is both design and deterioration. First there is creation, then comes degeneration, as with ALL things that are designed.
11.1.2 Conclusion
If you take a look at the above examples, there is no way of avoiding it! The evolution theory has an ENORMOUS problem with this. It has to explain why there is degeneration all around us! Exactly all those examples which are used to show that evolution exists turn out to be examples of degeneration. No one up to now has used this word (in this context), but it is so very clear, so obvious, so simple to recognize, that no one can deny it:
DEGENERATION DOES EXIST
and
MOST EXAMPLES GIVEN TO PROVE THAT THERE IS EVOLUTION ARE INSTEAD CLEAR EXAMPLES OF THE OPPOSITE: DEGENERATION
Degeneration exists. Degeneration is something we observe in the living nature that surrounds us. Why has no one seen this phenomenon for what it is? Are the spectacles through which we look at the world so colored that we have totally missed this? Have we been blinded? Did we not want to see it? These matters are always seen in the light of a slowly-progressing upward climb, whereas an objective, or perhaps a fresh view of the matter shows that there is a slow, steady downwards trend. And it should be clear to everyone that degeneration is much simpler than evolution. It is easier for a winged cormorant to lose its ability to fly, than for an flightless cormorant to gain that ability, even if it already has half of what it needs (namely degenerated wings). In other words: evolution is not just some random process in which natural selection choosing something. No, if evolution exists,then it has to rise against the cliffs of degeneration.It has to go against the wild flow of the degeneration-river. An impossibility, therefore!
From today onwards, 24 November 1997, the date of publication for this book, the same day that Darwin’s book The Origin of Species was brought out, no one can wriggle out from underneath it anymore: there is no evolution from unicellular organisms to humans; in complete contrast to that, we have degeneration..!
11.2 The natural lower boundary of degeneration
Where does the boundary lie? How far can this degeneration still continue? What lies in store for us? It is not unthinkable that a species could become extinct because of pure degeneration and genetic impoverishment. Even more convincing, that is the case with the cheetah. In a documentary on the Discovery Channel, it was said that it was feared that the cheetahs would become extinct due to genetic impoverishment. The Cheetah Conservation Foundation in Namibia writes on its Internet site, in an article called called;"Why does the cheetah lack genetic diversity?"
In most species, related individuals share about 80 percent of the same genes. With the cheetah, this figure rises to approximately 99 percent. The genetic inbreeding in cheetahs has led to low survivorship (a large number of animals dying), poor sperm quality, and greater susceptibility to disease. Inbred animals suffer from a lack of genetic diversity. This means cheetahs lack the ability to adjust to sudden changes in the environment, such as disease epidemics, and have unusually high susceptibility to certain viruses.
On the other hand, there is normally also a natural lower boundary to degeneration, and that is the age at which an individual can still reproduce. If degeneration progresses so far that the organism no longer gets a chance to reproduce itself, that form of degeneration also dies out along with that degenerated organism, simply because it does not reproduce. The most serious form of degeneration is therefore when a species is just barely capable of reproducing and then dies, if it balances on the edge of survival, one surviving, another just not quite.
One example of this is the day-fly or ephemera. This creature spends most of its life as a larva under water. At some point in time, the larva climbs upward along a stalk and sheds its skin, like a dragonfly. During that one day, it sheds its skin once more and then mating and fertilization takes place. The fertilized female falls into the water, where she drowns. But before she is definitively dead, she releases the eggs, which slowly sink to the bottom of the water. It is noteworthy that the day-flies do not have mouths, because they do not have to eat in that one day.[4]
How was this able to come into existence? It seems to me that (comparable with what is also happening in the case of progéria) the process of maturing is accelerated here in some way, by one or more genetic defects. That same day, they shed their skins a second time and the flies are also fertile. Perhaps these flies had a mouth in the beginning and could eat. A new mutation caused the flies to be unable to eat. Still, they were not at a disadvantage, because they could also reproduce already on the first day. Maybe they even had the advantage, because while the other flies were eating, they were attempting to reproduce. In this way, the mutation could spread throughout the whole population. Finally, with the passing of time, the mouth-sections disappeared completely, because that was no longer selected for. The females drown from exhaustion (having eaten nothing all day) as they expel their eggs at the last moment. This is a very definitive form of degeneration. It can't go further than that.
All this would mean that species that live much longer than is absolutely necessary to produce independent offspring, are less degenerated. I do not say this because that is what the data shows. There is no data on this matter. I say this as a logical consequence of a number of observations. This is so new that no one has as yet done research in this area, so I cannot check it. It seems to me that it would offer an extremely interesting field of research for biologists though. That is why I will risk making another prediction:
prediction
The genome of organisms which live (much) longer than is necessary to reproduce is (probably) less degenerated than that of comparable organisms which reproduce and die soon afterwards.
I came across a confirmation of this in EOS Magazine, April ’97 issue, in the article “Aging, is there a way out” by Mayke Visser, when it talked about the phenomenon that osseous fish, turtles, sea anemones and other organisms appear not to age:
It is obvious that we ask ourselves what these youthful organisms have found to avoid getting old and decrepit. Still, this is not a good question. It turns out after closer scrutiny that the species that stay young so long typically belong to the oldest and most primitive groups on earth. It seems as though staying young was standard then and that aging is a relatively new process.
natural selection
All this also offers a whole different perspective on natural selection. It is not the ‘driving force of the evolutionary motor’, but a tough judge, a master of healing with a passionate hatred of festering wounds, an angel of death which battles against degeneration: if your genome is too severely damaged, if you have too many bad genes, you are not allowed to pass them on, you are not allowed to reproduce, in many cases you even have to die at once. Natural selection is an automatic mechanism that keeps degeneration in check, ensures that species do not fall under the lower boundary of reproductivity. (see figure below)
Figure 10, Natural selection guards against too serious degeneration, if it means that the carrier cannot no longer reproduce
11.3 The degeneration law
The examples named above, especially the blind water scorpion, the flightless cormorant, and the day-fly, show a simple and logical, but as far as I know not yet formulated, biological law. It goes as follows:
A species or population has a tendency in the long run to lose those characteristics that it does not absolutely need to survive.
For clarification: that is ‘tendency’ and ‘in the long run’. That means in practice, in terms of a human life span, that it can take a very long time before it is done. Furthermore: the time it takes, depends on the largeness of the population. The larger a population, the slower degeneration occurs. The smaller a population, the quicker it will impoverish and degenerate over time.
The reason for this ‘law’ is mutation and that is called genetic drift. If a certain characteristic (flight, sight, or whatever) is no longer a determining factor for the survival of the species, a mutation which damages that characteristic will not be selected out. The carrier of this mutant characteristic can therefore reproduce in peace and by sheer coincidence; the lost characteristic can spread throughout the entire population. This coincidental spreading of genes, which does not particularly take place due to selection, is a familiar concept, called genetic drift. Genetic drift is sheer coincidence: who mates with who and how many offspring do they have, which can reproduce again, etc. But other factors such as this also play a part: can a mutant gene ‘hitch a ride’ with a very beneficial gene, because it is very close to this beneficial gene on the chromosome?. This makes the chance that the two become separated by recombination very small. Because the beneficial gene is selected for, the mutant ‘hitches a ride’ and also spreads itself throughout the population. This arbitrary aspect of genetic drift can just as easily mean that a mutant characteristic disappears again by pure coincidence! But in the long run, a mutation will damage that characteristic again, so that it can once more spread itself by genetic drift. However, if at a certain point in time every individual of the population has become homozygous for that damaged characteristic, there is no way back, because the original undamaged gene has been lost. And that means that a population in the end has a tendency to lose that characteristic.It can be clear that the degeneration law is an appropriate name for this law.[5]
11.4 beneficial degeneration
Now that we have seen that degeneration exists, we need to come to a noteworthy conclusion: sometimes a certain form of degeneration can be beneficial! we could call that beneficial degeneration. It is then (overall) beneficial to the carrier, but surely degeneration at the DNA-level.An example will make it clear.
Sickle-cell anemia is caused by one change in the gene for hemoglobin, in which one amino acid (Glutamine) is exchanged for another (Valine). Hemoglobin is a robot-protein that resides in red blood cells and fastens onto an oxygen molecule and transports it throughout the body. As you may understand, this is a very essential protein. This one mistake causes a lot of problems, and has a very distinctive feature, namely that the red blood cells are no longer round, but sickle-shaped, as in Figure11.
Figure 11.normal and ‘sickle’-shaped red blood cells. Genetic Analysis pp. 93
People who are homozygous (both parts of the gene are for the wrong hemoglobin) suffer from serious ailments that can even end in death. People who are heterozygous (one right and one wrong allele) have mild ailments because both kinds of hemoglobin are produced and both kinds of red blood cells also occur. The deviation appears as it were at half strength and is therefore not as serious. However, carriers have one very great benefit: they are resistant to malaria! Ordinarily speaking, such a deviation conveys so much disadvantage (read: death) that they have little chance to spread. But because they are resistant to malaria, in areas where a lot of malaria is around, the gene does get the chance to spread, because there are many people with the right hemoglobin who die of malaria. So although sickle-cell anemia is a clear form of degeneration – damage to an essential gene– yet it bestows a survival benefit. And with that, it is a form of beneficial degeneration.
In the same line, for example, mutations can arise in bacteria that are resistant to an antibiotic or mould. If that mould or antibiotic is not around, that mutation may be detrimental (or neutral). If the mould or antibiotic is present, the mutation is beneficial.
One detrimental effect can thus be surpassed by another benefit. The benefit under certain circumstances can be so great (for instance sheer survival) that the detriment (a somewhat weaker individual) is insignificant. For those circumstances, ‘better adapted’ individuals are obtained, but genetically, disorder has still been introduced, degeneration has taken place.
In this way, a juiced-up motorcycle can be faster than the normal variant from which it originated, and thieves with such a fast motorcycle may have better chances of survival because they are able to escape from the police. A (much more complex) motor will never be able to arise from an accumulation of those kinds of changes through.
In living creatures this kind of damage can also appear, which is dependent on the circumstances and thus is beneficial. The fact that it is beneficial under the circumstances, however, may not seduce us into denying the true nature of the genetic change: that it is still just degeneration. Under those specific circumstances, it is then beneficial degeneration.
DEGENERATION FAQ
frequently-asked questions about degeneration
the rate of degeneration
:Does degeneration still occur today and, if so, at what rate?
:Yes, there certainly is. Degeneration still goes on, but the rate is not that fast. In humans, on average one mutation per individual appears, which does not always have to have a noticeable effect. Only when such a mutation spreads itself throughout a large part of a population can you call it degeneration. In the plant and animal worlds, degeneration is swiftly punished by the death of the individual.
The rate of degeneration is faster in smaller populations than in large one, because it takes much longer in a large population before every individual has lost the original ‘good’ genes,
everything was good in the past
:Was everything better in the past than it is now
:If everything was better is difficult to say, but genetically, plants and animals would have been less degenerated, more original and therefore indeed ‘better’ or healthier.
Degeneration is not in conflict with evolution
:Degeneration is not in conflict with evolution but is the flip side of evolution! ‘Survival of the fittest’ already indicates that there are those less than fit, which is degeneration.
:Of course the ‘fittest’ or ‘most qualified’ individuals of degenerating species will survive. But even these ‘fittest’ individuals do not climb upwards in relation to their ancestors (i.e. evolution), but remain equal to them or descend slowly (i.e. degeneration). Those individuals that descend rapidly down the ladder of degeneration will lose the struggle for existence to those individuals who remain ‘healthier’. But even if that is taken into account,one still cannot say that the latter evolved, that is increase in complexity. The surviving ‘fit’ individuals are also subject to degeneration. The least-degenerated individuals are the ones who survive the longest. Natural selection is the medicine for degeneration, not the engine for evolution. The moment that natural selection lapses, as with the flightless cormorant because there were no predators on the remote islands, you see that degeneration strikes.
In other words, all life on earth is subject to degeneration, no species climbs 'upwards'. If a species has a tendency to lose that genetic information which it does not necessarily need to survive, within periods of hundreds of years, then over periods of millions of years, no new information will be added, which it apparently couldn't even use in a short period of time. If a snail crawls one centimeter upward during the day and falls ten centimeter downwards during the night, it will never get higher. And, to bring it back to the matter at hand, it is precisely the examples of degeneration that are often used as examples of evolution! However, there are no examples at all of evolution going across the borders of types and increasing in complexity (unless the chaos created in the DNA by degeneration will be called 'an increase in complexity').
[1] Somatic cells include almost all the cells of the body, except for the ones which make up the ‘line of sex cells’. The line of sex cells consists of those cells which, from the fertilised egg cell to the mature individual, make the organs and cells from which the sex cells come.
[2] Actually, three or four genes must be damaged by mutations before cells receive eternal life, because the mechanisms are much more complex. But the idea stays the same.
[3] Not all the examples are forms of degeneration. In their enthusiasm, they dragged in a lot of things which have nothing to do with ‘bad design’, such as plaice that have two eyes on one side. That does not indicate a bad design at all (those fish swim on one side, after all) but it does indicate a designer with a sense of humor!
[4] source: Discovery, Wild Things, broadcast 20-5-97
[5] By the way, there is also a biological law, called the law if Dollo, which is about the irreversibility of evolution. It says that ‘in the phylogenetic development, features, once lost, do not return. (Winkler Prins Encyclopedia)! The degeneration law and the law of Dollo make a nice pair...