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An impossible conundrum for evolution


Published: 30 August 2007 (GMT+10)

Image by John Schmidt,

Cell division

Cell division, once thought of as a fairly simple thing, is now known to be an incredibly complex, orchestrated affair that shouts ‘intelligent design’.
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New genetic information?

Evolutionists have never been able to give a satisfactory answer to the problem of where the new information comes from that evolution requires for turning a microbe into a myxomycete or a maze-mastering mammal. Their best guess is gene duplication (which gives them an extra length of DNA, but it contains no new information) followed by random mutations that are supposed to turn the duplicated information into something new and useful.

They have no direct experimental evidence for this claim (and there is much against it1), so they have to rely on indirect evidence such as the so-called ‘gene families’. Some genes are similar in both structure and function to other genes, and evolutionists point to these and say they originated by chance copying and mutation from some common ancestral gene. But this is just evolutionary speculation; it is not experimental evidence.

The globin gene family is a favourite example. Hemoglobin carries oxygen in our blood and can be made up of different combinations of different kinds of globin proteins. For example, hemoglobin in human fetal blood contains a different combination of globins to that in post-natal blood. Evolutionists claim this resulted from an original globin molecule that duplicated in an early blood-using animal and mutated to form a family of different kinds of globins, which then allowed the diversification of complexity in oxygen-using processes that we see in the animal world today.2

But this example is far better explained by intelligent design.3 The human baby in his or her mother’s womb has to compete for the oxygen in its mother’s blood supply with the demand for oxygen from two other sources: the placenta that feeds it, and from the mother’s womb that surrounds it. So the fetal hemoglobin has to have, amongst other things, a higher affinity for oxygen than the mother’s hemoglobin. In contrast, when the baby is born and can draw oxygen from the air in its own lungs, it no longer has any competition so it requires a different kind of oxygen-uptake system. A wise Creator would ensure that the hemoglobin could change its form and function to cater for these very different conditions, and integrate this change into the other vast complexities of the almost miraculous reproductive process. The idea that such complex interactive changes could all occur by chance is rather hard to accept.

Information about Information

But the problem of information origin in biology is far bigger than most people realize. Information by itself is useless unless the cell knows how to use it. Evolution not only requires new information, it also requires extra new information about how to use that new information.

Information about information is called meta-information. We can see how it works in making a cake. If you want to make a cake, you need a recipe that contains: (a) a list of ingredients, and (b) instructions on how to mix and cook the ingredients to produce the desired outcome. The list of ingredients is the primary information, and the instructions on what to do with the ingredients is the meta-information.

The human genome contains an enormous amount of information, far more than we ever (until recently) imagined.4 But we now know that most of it is not primary information (protein-coding genes) but meta-information—the information that cells need to have in order to turn those protein-coding genes into a functional human being and maintain and reproduce that functional being. This meta-information is stored and used in a variety of ways:

Evolution not only requires new information, it also requires extra new information about how to use that new information
  • DNA consists of a double-helix—two long-chain molecules twisted around one another. Each strand consists of a chain of four different kinds of nucleotide molecules (the shorthand symbols are T, A, G and C). About 3% of this in humans consists of protein-coding genes and the other 97% appears to be regulatory meta-information.
  • DNA is an information-storage molecule, like a closed book. This stored information is put to use by being copied onto RNA molecules, and the RNA molecules put the DNA information into action in the cell. For every molecule of protein-producing RNA (primary information), there are about 50 molecules of regulatory RNA (meta-information).
  • Down the sides of the DNA double-helix, several different kinds of chemical chains are attached in patterns that code meta-information for turning unspecialized embryonic stem cells into the specialized cells that are needed in fingers, feet, toenails and tail-bones etc.
  • DNA is a very long thin molecule. If we unwound one set of human chromosomes, the DNA would be about 2 metres long. To pack it up into the very tiny nucleus inside the very tiny human cell, it is coiled up in four different levels of chromatin structure into 46 chromosomes. This coiling chromatin structure also contains yet further levels of meta-information . The first level (the histone code) codes information about the cell’s history (i.e. it is a cell memory).5,6 The three further levels of coiling code further information, some of which is described below, and there is no doubt more that we have yet to unravel.

The amount of meta-information in the human genome is thus truly enormous compared with the amount of primary gene-coding information.

Self-replicating molecules?

In his monumental work, The Ancestor’s Tale,7 Richard Dawkins traced the supposed ancestry of humanity back through all the evolutionary ages to the very first supposed common ancestor of all life. He supposed this original ancestor to have been an RNA-type of life form, although he admitted ignorance of the precise details.8 His choice of an original RNA life form is well-founded because RNA is the only known molecule that can do all of the three basic functions of life: (a) store coded information, (b) combine with itself and other RNAs to create molecular machines, and (c) self-replicate (but only in a very limited manner under very special circumstances).

However, recent studies showing how living cells actually replicate have made this ‘RNA world’ concept ludicrously unrealistic.

A central problem in cell division (that is, what living cells actually do, as opposed to Dawkins’ imagined self-replication) is that a large proportion of the whole genome is required for the normal operation of the cell—probably at least 50% in unspecialized body cells and up to 70–80% in complex liver and brain cells. When it comes time for a cell to divide, not only does the DNA have to continue to sustain normal cell operations, it also has to sustain the extra activity associated with cell division.

This creates a huge logistic problem—how to avoid clashes between the transcription machinery (which needs to continually copy information for ongoing use in the cell) and the replication machinery (which needs to unzip the whole of the DNA double-helix and replicate a ‘zipped’ copy back onto each of the separated strands).

The cell’s solution to this logistics nightmare is truly astonishing.9 Replication does not begin at any one point, but at thousands of different points. But of these thousands of potential start points, only a subset are used in any one cell cycle—different subsets are used at different times and places. Can you see how this might solve the logistics problem?

A full understanding is yet to emerge because the system is so complex; however, some progress has been made:

  • The large set of potential replication start sites is not essential, but optional. In early embryogenesis, for example, before any transcription begins, the whole genome replicates numerous times without any reference to the special set of potential start sites.
  • The pattern of replication in the late embryo and adult is tissue-specific. This suggests that cells in a particular tissue cooperate by coordinating replication so that while part of the DNA in one cell is being replicated, the corresponding part in a neighbouring cell is being transcribed. Transcripts can thus be shared so that normal functions can be maintained throughout the tissue while different parts of the DNA are being replicated.
  • DNA that is transcribed early in the cell division cycle is also replicated in the early stage (but the transcription and replication machines are carefully kept apart). The early transcribed DNA is that which is needed most often in cell function. The correlation between transcription and replication in this early phase allows the cell to minimize the ‘downtime’ in transcription of the most urgent supplies while replication takes place.
  • There is a ‘pecking order’ of control. Preparation for replication may take place at thousands of different locations, but once replication does begin at a particular site, it suppresses replication at nearby sites so that only one copy of the DNA is made. If transcription happens to occur nearby, replication is suppressed until transcription is completed. This clearly demonstrates that keeping the cell alive and functioning properly takes precedence over cell division.
  • There is a built-in error correction system called the ‘cell-cycle checkpoints’. If replication proceeds without any problems, correction is not needed. However, if too many replication events occur at once the potential for conflict between transcription and regulation increases, and/or it may indicate that some replicators have stalled because of errors. Once the threshold number is exceeded, the checkpoint system is activated, the whole process is slowed down, and errors are corrected. If too much damage occurs, the daughter cells will be mutant, or the cell’s self-destruct mechanism (the apoptosome) will be activated to dismantle the cell and recycle its components.
  • An obvious benefit of the pattern of replication initiation being never the same from one cell division to the next is that it minimizes the effect of any errors that are not corrected.
Such a magnificent solution to such a monster logistics problem could only come from a Master Designer

Such a magnificent solution to such a monster logistics problem could only come from a Master Designer.

The impossible conundrum

Now comes the impossible conundrum. Keeping in mind the cake analogy, lets recall that the vast majority of information in humans is not ingredient-level information (code for proteins) but meta-information—instructions for using the ingredients to make, maintain and reproduce functional human beings.

Evolutionists say that all this information arose by random mutations, but this is not possible. Random events are, by definition, independent of one another. But meta-information is, by definition, totally dependent upon the information to which it relates. It would be quite non-sensical to take the cooking instructions for making a cake and apply them to the assembly of, say, a child’s plastic toy (if nothing else, the baking stage would reduce the toy to a mangled mess). Cake-cooking instructions only have meaning when applied to cake-making ingredients. So too, the logistics solution to the cell division problem is only relevant to the problem of cell division. If we applied the logistics solution to the problem of mate attraction via pheromones (scent) in moths it would not work. All the vast amount of meta-information in human beings only has meaning when applied to the gene content of the human genome.

Even if we granted that the first biological information came into existence by a random process, the meta-information needed to use that information could not come into existence by the same random (independent) process because meta-information is inextricably dependent upon the information that it relates to.

There is thus no possible random (mutation) solution to this conundrum. Can natural selection save the day? No. There are at least 100 (and probably many more) bits of meta-information in the human genome for every bit of primary (protein-coding gene) information. An organism that has to manufacture, maintain, and drag around with it a mountain of useless information while waiting for a chance correlation of relevance to occur so that something useful can happen, is an organism that natural selection is going to select against, not favour! Moreover, an organism that can survive long enough to accumulate a mountain of useless information is an organism that does not need useless information—it must already have all the information it needs to survive!

What kind of organism already has all the information it needs to survive? There is only one answer—an organism that was designed in the beginning with all that it needs to survive.


  1. Bergman, J., Does gene duplication provide the engine for evolution? Journal of Creation 20(1):99–104, 2006. Return to Text.
  2. There is a problem that the expression of the globin genes must be precisely controlled, otherwise diseases such as thalassemia can result. See Argument: Some mutations are beneficial, chapter. 5, Refuting Evolution 2. Return to Text.
  3. So are the different hemoglobin types in different animals. Biochemist Dr Bob Hosken says: ‘in a study of the relation between the structure and function of hemoglobin in various marsupial and monotreme species, I found it more meaningful to interpret hemoglobin structure in relation to the unique physiological demands of each species. A marsupial mouse has a greater rate of metabolism than a large kangaroo, so small marsupials need a hemoglobin with a structure designed to deliver oxygen to the tissues more efficiently than that required in large animals, and I found this to be actually the case. I also investigated the relation of hemoglobin structure and oxygen transport in the echidna and platypus, and again found the oxygen delivery system of the platypus was well suited to diving, while in the echidna it was suited to burrowing.’ Return to Text.
  4. Williams, A., Astonishing DNA complexity uncovered, 20 June 2007; Astonishing DNA complexity update, 3 July 2007. Return to Text.
  5. Segal, E., Fondufe-Mittendorf, Y., Chen, L., Thåström, A, Field, Y., Moore, I.K., Wang, J.-P. Z. and Widom, J., A genomic code for nucleosome positioning, Nature 442(7104):772–778, 17 August 2006; DOI: 10.1038/nature04979. Return to Text.
  6. Latent memory of cells comes to life,, 17 May 2007. Return to Text.
  7. Dawkins, R., The Ancestor’s Tale: A pilgrimage to the dawn of evolution, Houghton Miflin, Boston, 2004. Return to Text.
  8. RNA is an unstable molecule and cannot survive naturally outside the special conditions of a cell or a protein-stabilized virus. In the experiments quoted by Dawkins, high-purity ingredients and special, entirely un-lifelike, conditions were maintained; otherwise, the RNA would have quickly broken down. See also See also Mills, G.C. and Kenyon, D.H., The RNA World: A Critique, Origins and Design 17(1): 9–16, 1996; Evolutionist criticisms of the RNA World conjecture from Cairns-Smith, A.G., Genetic Takeover and the Mineral Origins of Life, Cambridge University Press, New York, 1982. Return to Text.
  9. Aladjem, M.I., Replication in context: dynamic regulation of DNA replication patterns in metazoans, Nature Reviews Genetics 8(8):588–600, August 2007. Return to Text.

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