Archive for the ‘ADM-DM’ Category


Anne Dambricourt MalasséADM DM #0ADM DM #1ADM DM #2 – ADM DM #3

I’ll keep the same here as for parts ADM-DM-01 and ADM-DM-02, Specs in Isle, velo, the gene determining Specs’ velocity, and the same clonal population at time T0.

Let’s consider now three particular mutations of velo gene: velo-d1, velo-d2, which are the same as in ADM-DM-02, and velo-d3.
The genotype d1-d2 is always at the origin of a velo-jump of x%; the genotype d1-d2-d3 produce a velo-jump of n*x%, where n>1. Genotypes d1-d3 and d2-d3 are neutral for velocity.

For equal probabilities of occurrence of the three mutations, p, the probability to observe the triple mutant d1-d2-d3 is p1/2/3 = p3. An event less probable then the double mutant d1-d2, p1/2 = p2.

Statistically the double mutant d1-d2 appears before the triple mutant d1-d2-d3. And the double mutant is necessary to observe a phenotypic impact from the mutation d3.

Once the double mutant d1-d2 present in Specs population it will be fixed as it represents an advantage for the carriers and thus the probability to obtain the triple mutant will increase to p1•2/3 = p !

The step from the initial genotype/phenotype (T0) to the d1-d2 ones (Ts) is expected to be longer then the step from d1-d2 to d1-d2-d3, statistically mean.

The following figure illustrates six runs of the model, with x%, the velo-jump du to d1-d2, equal to 25%, and n = 2, so the velo-jump associated with d1-d2-d3 is of 50%.


Only the mean velocity of the Specs population is represented. There is a story line where d1-d2 wasn’t observed. The rectangular ROI highlights the two velo-jumps. The circular ROI highlights overflows, where the velocity is above the optimal one, and show that the model is still reversible.

Let’s take a look at a particular line story:


Arrows point to the apparition of d1-d2 and d1-d2-d3 and the corresponding velo-jumps. And in this particular example the time lapsed between the wild type and the double mutant is longer then the time lapsed between the double and the triple mutants. This graph represents what one expect to observe as a statistical result.

The graph below was obtained with x% = 25% and n = 2, just for better visualization of the velo-jumps.


We have here a typical situation of overflow. The pic of velocity (red arrow) is du to the effect of d1-d2-d3. The phenotype will reverse as a higher then the optimal velocity isn’t selected, and the optimal velocity will be reached.

Let’s summarize:

  • A population of Specs, a species with three main activities: sleep, food and sex; duration of sleep is constant so Specs existence may be considered as part alimentation and part sexual activity.
  • At the beginning of the stories lines T0 all Specs share the same genotype and present the same phenotype.
  • At the T0 Specs aren’t perfectly adapted to their environment. There is a selection pressure favoring those able to move faster and thus feed in shorter times; those dispose of larger periods for sexual activity and their genetic variants of velo will be transmitted to descendants. Foods density on Isle determine the Vmax, which is the speed of movement of Specs, making meals so sort that they don’t interfere with sexual activity.
  • During the observation period a single gene is able to mutate, velo, which is the only one modulating velocity, which is the phenotypic trait describing Specs maximal speed; variations on genotype produce equivalent variations on phenotype, directly.
  • From the many variants of velo three are remarkable, d1, d2, and d3. The probability to observe these three mutations is equal and expressed by p, which satisfy to the condition 0velocity, what I called a velo-jump. The same is for genotype d1-d2-d3, which have a more important effect. Genotypes d1-d3 and d2-d3 don’t produce a velo-jump.

What could we get from such a simple model:

  • Directional evolution of the phenotypic trait velocity, under selection pressure which is related to the actual Specs characteristics and the optimal value of velocity. The selection factor is a combination of Specs characteristics, velocity and available food resources density. Inversely proportional to velocity, it is difficulty observable when the population reach a mean velocity value equal to the optimal. The directionality of evolution of the phenotypic trait is reversible; if the population reach a mean velocity value higher then Vmax, it will tend to decrease, stabilizing around Vmax.
  • Sudden increases of the value of the phenotypic trait, velo-jumps, are possible, when d1-d2 and d1-d2-d3 genotypes are produced by random mutations. If one can evaluate the probability to see those genotypes, it’s impossible to predict when they will occur. It is also impossible to predict the time laps between d1-d2 and d1-d2-d3, but one can calculate probabilities:
    The probability to obtain d1-d2-d3 is p1/2/3 = p3
  • before the apparition of genotype d1-d2,
    the probability to obtain d1-d2 is p1/2 = p2, and
    the probability to obtain d1-d2-d3 becomes p1•2/3 = p after the apparition of genotype d1-d2.
    Thus, p1•2/3 > p1/2 > p1/2/3, which means that the more probable path is to get d1-d2 first, then after a relatively short period d1-d2-d3 (which may be considered as an acceleration of the evolution of velocity).

  1. Directionality of evolution of velocity is respected, at the phenotype level.
  2. Discontinuity of evolution of velocity is respected, at the phenotype level.
  3. Reversibility of evolution of velocity is respected, even at the phenotype level.
  4. Randomness, as builded in the model, is respected, at the genetic level.
  5. The selection factor is a combination of physiological and environmental characteristics, inversely proportional to the phenotypic trait, and it would be quite difficult to determine once the optimal value reached or by fossils examination.

The model is darwinian, the observations similar to those reported by ADM.

Maybe she could spend some time considering this option before the evocation of Unknown Factors, Internal Plans or any thing else.

To do so, it is necessary to dispose of molecular (genetic) data. A first step would be the determination of genes expressed during the cranium build at the sphenoid region; gene arrays to determine which ones then in situ hybridization, to validate and dispose of a spatial repartition overview. And this for both Homo sapiens and a closely related species, which genome is known, say Pan troglodytes.
If that fails, then something else may be considered.

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Anne Dambricourt MalasséADM DM #0ADM DM #1 – ADM DM #2 – ADM DM #3

I’ll keep the same here as for example #01, Specs in Isle, and velo, the gene determining Specs’ velocity, and the same clonal population at time T0.

Let’s consider a particularity of gene velo. If two specific mutations are present on the same molecule, velo-d1 and velo-d2, they act synergistically and the velocity of the individual is Vmax. velo-d1 and velo-d2 independently don’t affect the velocity trait, thus they aren’t selected, and they aren’t punctual mutations.
Say that this occurs at time Td1-d2, and this is in a stage of Specs history that gives it a clear advantage, substantially increasing the movements of carrier Specs, this particular combination will spread rapidly in Specs population, as the carriers have plenty of time available for sex.

The history of Specs will be determined from the occurrence of this particular random event. It represents a jump in the evolution of the particular phenotypic trait, velocity.
A jump which amplitude will be inversely proportional to Td1/d2-T0.

If you observe the increase of velocity of the Specs and don’t know anything about their genetics, you may have the feeling that there is some Unknown Factor making them faster and faster. And that at time Td1/d2 another Unknown Factor changed the rules and produced the jump of the velocity’s increace. Then you have two solutions: considering some Mysterious Internal Blueprint due to Supernatural Causation being the cause of the velocity’s increase and some Mysterious Change of the Internal Blueprint at time Td1/d2, or inventing genetics and understand how Specs evolved from Spec SlowMotion (those Specs present at T0) to Spec AsFastAsPossible (those Specs living at time Ts, including the velocity’s sudden increase at Td1/d2.

And this is a third observation: Phenotypical traits may evolve in a directional way and by jumps, while mutations are still perfectly random.

But a jump at Vmax isn’t very probable. Let’s say that this is a smaller jump, an increase of x% of the initial velocity, V0, and this particular event I’ll call a velo-jump from now on; the plot of velocity versus time (generations) will be something like that :


Concommitant to the velocity’s increase there is a drop of the selection pressure (they are correlated) and then the evolution of the phenotype will follow the same path as in example 1, reaching a plateau.

The coexistence of the two mutations in a single velo molecule is a random phenomenon. So it’s impossible to say « when » and « if » it will happen during the Specs history. I run a few simulations, and I had a very pleasant surprise; a velo-jump above Vmax. I wasn’t expecting to talk here about the reversibility of the model, but here is what I got at the second run of the model:


There are two graphs in fig above. Both represent the same data, the one at the right isn’t versus time, but log(time), this is useful to see more clearly early events. The blue curve represent velocity and the red ones selection pressure. The genotype d1-d2 appears relatively late and the velocity gain set Vs above Vmax. This phenotype isn’t privileged, as in the case where food’s density increased, I presented in example 1. So it will be progressively lost, either by reversion or by apparition of new mutations. I was glad to see that « happen », the model used for simulations seems to be well constructed.

Reversibility is conserved.

I gave it a few more runs and I overlaid a series of graphs to show alternative Specs histories:


There are three series presented here, a, b and c, corresponding to velo-jumps of 10, 20 and 40% of V0 respectively. For each series I show graphs with the x axis as time or log(time). The red arrows at « series c », points to a story where the d1-d2 genotype didn’t appeared. The duration of Specs history is normalized here. I’ll come back to this.

While Vmax is reached for every run, which mean that the Specs will be optimized for their environment, the path, trough which this is achieved, is as random as the occurrence of the d1-d2 genotype; it may even not contain this particular event.
Now, why did I normalized the histories lengths? It’s only a matter of better visualisation. Let’s see at what generation d1-d2 appeared for a set of 1000 runs :


Quite random, ranging from 5 to 53777. To make it visible, without making a particular choice, the simplest way was to normalize the duration of the stories.

One may evaluate odds that d1-d2 appears during the Specs history; this is a simple probability calculation, predicting that d1-d2 may appear. If the probabilities are equal for both mutations, and p is the probability for each one, then the probability to get both simultaneously is pd1-d2 = p2.
It doesn’t say when.
On the other hand, you may evaluate what is the probability for d1-d2 to appear after n generation and that will be n * pd1-d2 = n* p2.

Randomness is preserved at the mutations level, and thus at the genotype level, the phenotype evolves directionally as long as it doesn’t exceed the optimal value (otherwise the direction change), and a particular genetic event may produce jumps of the phenotypic trait.
One couldn’t predict the history of the Specs otherwise then in terms of probabilities; the single predetermined element is Vmax, and this is only to facilitate calculations, the real value being a function of the Specs physiology and foods density.
The probability to have two identical histories (runs of the simulations) is low. Some cases are present (difficult to see on the graph, but there are 42 repetitions! Now, that the genotype d1-d2 occurs at generation g twice (or more) that doesn’t mean that the paths where identical!

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Anne Dambricourt MalasséADM DM #0 – ADM DM #1 – ADM DM #2ADM DM #3

To start the series let’s consider something quite simple. The species I will talk about is an imaginary one, I call it Spec. It lives in an isolated island, Isle, and Specs is the only animal present on it. Isle is a paradisiac island for Specs; virtually infinite surface and unlimited food, constant whether, and the Specs are almost perfectly adapted.

Specs’ life is divided in three main parts: food, sleep and sex.

They all sleep strictly the same time. And that’s invariable through the story I’m presenting here.

So, they eat and have sex. The first priority is food; a hungry Spec is unable to have sex, it can’t quite concentrate. Food is unlimited but it’s concentration isn’t optimal and Specs have to go around to gather what they need.

At time T0 all Specs are genetically identical, a perfect clone, as those you only may find in imaginary stories, and so they present exactly the same phenotype. From time T0 and further, mutations appears, but, to keep the story simple, they are possible in a single gene, velo. Velo is the gene which determines the maximal velocity of Specs.

It’s a quite important gene, because the faster a Spec is, the faster it can go around and find food and calm his hunger, thus increasing the time devoted to sex. So, mutations in velo gene, increasing velocity, are favored as they allow for longer sex periods and increase this way the probability to be inherited by the next generation.

Such mutations tends to accumulate and Specs become faster and faster over generations, up to the point Ts where the time spend for eating becomes insignificant compared to the time spend for sex. From now on, further mutation in velo gene don’t provide evolutionary advantage and thus they wouldn’t be favored. The velocity reached is Vmax.

From time T0 to time Ts there was a progressive and continuous increase of Specs’s velocity without any external factor acting; natural selection occurs, but driven by the probability of inheritance of the faster alleles of velo.

We have here a situation where random mutations on velo will be reflected over the generations as an increase of velocity of the individuals. One may expect that the process may be progressive at both the genetic and the phenotypic levels.

If you observe the increase of velocity of the Specs and don’t know anything about their genetics, you may have to postulate that there is some « Unknown Factor » making them faster and faster. Then you have two solutions: (a) considering some « Mysterious Internal Blueprint », due to « Supernatural Causation » or anything else one could imagine, or (b) inventing genetics and understand how Specs evolved from Spec SlowMotion (those Specs present at T0) to Spec AsFastAsPossible (those Specs living at time Ts.

Now, we know that even in the absence of directly involved, external, natural selection factors, Specs evolved following a strictly darwinian model, with completely random mutations at the genetic level, leading to a directional evolution of a phenotypical trait, velocity.

The selection factor in this case is the time available for sex. It exists without any external intervention, natural or supernatural, and will progressively vanish as the velocity of Specs increase to reach a plateau. In fact, the selection pressure will decrease proportionally to the increase of Specs’ ability to move fast.

And this is the first observation: phenotypical traits may evolve in a directional way, while mutations are perfectly random. The species is progressively adapting.

And there is a second observation: selection factors may be neither internal or external and their intensity may be directly dependent from the degree of evolution of a phenotypic trait. And selection factors may be invisible once the species is adapted. Here the selection factor is closely related to food’s density, which is an external factor. The schema proposed make the assumption that during Specs history food’s density don’t change.

Fig 1 :


Blue line corresponds to the mean velocity of the Specs; red line to the selection pressure. Top graph : increase of velocity and consequent dicrease of the selection pressure; no changes of foods density. Lower graph : Food’s density change during the period observed, reducing the selection pressure, which in a first time appears to be « negative« , then reach zero. The mean velocity of the Specs population drops in the absence of selective pressure (see below).

What if food’s density increase? Say to the point that feeding time is short enough to not hinder sex time. The selection pressure will drop, and the mutations accumulated will no more represent an evolutionary advantage. They will tend to disappear, simply, replaced by any other random mutations. The mean velocity of the Specs population will decrease and eventually reach the basal level again

No speciation observable here, just a succession of races of Specs.

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Anne Dambricourt MalasséADM DM #0ADM DM #1ADM DM #2ADM DM #3

ADM presents a set of observations showing that a phenotypical character evolved following a particular direction, and done show in a discontinuous manner, with several steps becoming shorter over time. And as reversion isn’t observed, she conclude to irreversibility of the process.

Those are well documented facts, and I trust ADM as paleontologist. I regret that people talked about falcification, probably without taking enough time to think about such a severe accusation.

The central point, which wasn’t considered as far as I know about this case, is that ADM presented data about a phenotypical variation, and that’s all. No genetic data. Of course fossils can’t provide this information, and this is maybe the reason why she didn’t considered the genetic aspect of the problem. But she make an interest parallel with embryogenesis, and this is probably the source of genetic data one would like to consider, as embryos are available from several species of primates, including humans.

I will present, and try do do it in the simplest manner, a quite simple model presenting all the characteristics that leaded ADM, and other, to consider that these observations where incompatible with darwinism. This isn’t the model I would start with to explain ADM findings; a more elaborated one must be constructed, taking in account all information available about the development of the skull, including genes’ expression variations which determine at the molecular level the steps of the process.
What is the interest of the model I’m presenting? Showcase that random alterations at the genome’s level, associated with natural selection factors (at least one) may lead to the directional, discontinuous evolution of a phenotypical trait.

I kept the model as simple as possible: one gene, one selection factor; thus it will be accessible to everybody with a basic knowledge of biology. I present it in three steps:
One to showcase directional evolution of a phenotypic trait, and it’s reversibility if external conditions change, due to randomly occurring mutations.
One to show how phenotypic jumps may be observed, corresponding to particular, randomly occurring, genetic events.
One to make evident that the succession of such phenotypical jumps may be accelerated while mutations are kept random.

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Anne Dambricourt Malassé • ADM DM #0ADM DM #1ADM DM #2ADM DM #3

My recent interest on Intelligent Design and non-darwinian evolution hypothesis was triggered by the buzz made around a documentary presented by the franco-dutch TV channel, Arte; my favorite one. Then there was the Dover episode in the struggle of american IDers trying to be labeled « scientific » to gain credibility in front of the public opinion and access to public schools science curriculum.

I think that the best attitude of scientists, including darwinists, should be to keep it strict about what science is, per definition, and let the supernatural causations for religions; after all they were first in the place and this is their only way to do when it comes to explain the world: supernatural entities, gods or God.
Imagine the results of the appropriation of supernatural by some other then religions. Religions will lose their only competence and will become useless, and all faiths to supernatural should be unified. That would be great, I mean religions fall, but it isn’t work for scientists.

I would like to focus on the initial cause of existence of this blog, the documentary directed by Thomas Johnson, « Homo Sapiens, une nouvelle histoire de l’homme » [for translations hoover over the french texts], and consider three quite distinct layers:

  1. The buzz concerning this documentary,
  2. The debate that followed it’s diffusion,
  3. The central element of the documentary.

The Buzz

If you take a look on TV channels programs you would find so much crap that, if the same kind of reactions, as the one against this particular documentary, was the rule, there should be a continuous buzz! Occasionally the introduction of a new kind of programs produce strong reactions, says, reality TV.
But this was a simple documentary, and documentaries are usual stuff, and would be happy to see them take a larger part in TV programs. Much more interesting usually then reality TV.
It was the content of the documentary that was disturbing. Why? Certainly because it presented the point of view of a Research Director, CNRS opposing darwinism. So what? One would expect that the diffusion of the documentary should be programed by demand of the darwinists! Personally I was quite interested by hearing Anne Dambricourt Malassé presenting her findings and making clear her arguments against darwinism.
It is mandatory for scientists to question the quality of their tools as often as possible, to be sure using the best and fittest available. And I expect that every single fellow darwinist do so with the theory of evolution of the species. If one have a question against darwinism, the best conduct is to hear it and answer it. As far as supernatural causation isn’t implied; in this case they may chose to hear it, but they doent’ have to answer it, at least as scientists. And if there is a possible confusion made possible due to the fact that a scientist presented a non scientific hypothesis (it isn’t forbidden as far as I know), a simple communicate, making that clear, should be sufficient.

The Debate

To calm down the buzz a debate was programmed following the diffusion of the documentary. Now, that was a really clever movement. A debate is a much more interesting stuff than a simple documentary.
As soon as the announcement was made I set up an alarm so to be sure to don’t lose this rare occasion.
But they certainly mistaken calling that a debate. It was a simple interview of two darwinists, by a journalist, . Malassé (ADM) wasn’t there, neither any other supporter of her hypothesis, to reply to or ‘s critics.
You can call that a discussion or an interview, but certainly not a debate. And it wasn’t even a focused discussion. Once I seeing that only darwinists were present I was expecting a demonstration of how darwinism could account for ADM’s findings. Or, at least, why ADM’s hypothesis couldn’t be considered as scientific. Neither came. Just generalities about how wonderful and well accepted by the biologists the darwinism is. Nothing specific to destroy ADM’s hypothesis.
The result was what one could expect: more buzz.
It is probable that the two darwinists didn’t had enough time to study the particular case, both are busy people. In this case either they should asked for a week or two before addressing the question or ask to a colleague or even to their students to give it a try. You don’t go to a debate expecting to be accepted just because you said you where right. Evidence is the key, not just talking.

The element

In the documentary, ADM present her findings, and they are quite interesting and clearly presented.
Problems appear just at the moment she is trying to explain how this could have happened.
I didn’t recorded the documentary, not expecting what followed. So to study her claims I had to search for her publications. None in PubMed and just four hits otherwise and up to now. But I hope I’ll get the complete set soon. Two important points:

  • The two papers opposing darwinism are in french. That’s important, it means that the international scientific community may not have access to these readings; usually biology is published in english.
    That means that the probability to find someone who could have opposed her point of view are low and personally I consider that unfair; both for darwinists and for her, as the findings are really interesting.
  • ADM is a paleontologist, and seem to be praised by her colleagues, as such. But she isn’t neither geneticist or evolutionist. One would expect collaboration with one or the other discipline in the process to explain her findings. This is a quite common case, to consult and collaborate with specialists. And if for one or another reason you are willing to question a theory you better take all required steps to show that your approach was exhaustive. But here we simply don’t know what darwinian models where found incompetent to explain the facts.

ADM show data clearly indicate a directional and discontinuous phenotypic variation, that may be a key element for humans’ vertical position. Great!
The hiatus is that this doesn’t seem to be compatible with random (non directional), gradual (discontinuous) genetic variations selected by the environment (natural selection).

That doesn’t seem to be a darwinian process.
« Doesn’t seem » may be interpreted either as:

  • it isn’t, or,
  • apparently it isn’t but in fact it is

Before any other interpretation is attempted one expect that a thorough exploration of darwinian models was done. And the question can be formulated as : is there a darwinian model that may explain directional discontinuous phenotypic variations? Well, the answer is simpler than I expected from all this buzz: YES. And could categorize it as a strong darwinian one, nothing incompatible with ‘s approach of darwinism.

Keywords to build such a model are: cumulative and cooperative, to account for « apparently directional » and « apparently discontinuous » respectively. And one should keep in mind that every single natural selection factor should be considered and that it would be, as usual, counter productive to focus to a single one.

As I like building models I set up a few variations around my central idea which came during the debate: cumulative mutations in a single genetic spot progressively leading to a threshold over which phenotypic variations appears suddenly due to the intervention of a second genetic element. [as I’m expecting et al to answer the question « what is it? » I’ll edit this part later to insert the known example]. It takes a little bit more complexity to make it appear discontinuous and accelerating over time, but is just a little bit more, nothing really complex.

Such models may be used as working hypothesis to unravel the mechanism explaining ADM’s findings, in association with gene expression data (GEO could be of some help here) in order to name the contributing genetic elements. That should be facilitated if the sequence of events is replicated during in utero development, because the molecular events would be directly observable.

Two questions arise spontaneously:

  • Why ADM failed to describe such models, alone or in collaboration with colleagues specialized in genetics or molecular biology, and
  • why her darwinist opponents failed to do so rather than discussing generalities?
  • Those two questions I can’t answer, otherwise than by speculating, so I’ll let them unanswered.

    On the other hand, answering the question « is there a darwinian model that may explain directional discontinuous phenotypic variations? » by the simplest of affirmations, yes, should raise the question « which one? », and that I can answer, in extenso.
    So, I’m starting here a series ADM-DM#n which will finish by the display of a darwinian model, able to explain phenotypic, directional and discontinuous variations, by random and continuous genetic alterations (mutations). This isn’t for biology agnostics, I’ll suppose that whoever wish to comment these posts have a minimal knowledge of what a gene, a mutation, an allele, molecular cooperation, and selection factors, are.

    But I will answer questions by anyone, trying to set things in the simplest manner, so even agnostics of biology should be able to understand.

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