A problem with molecular evolution?

Lets assume that indeed something like one in 10^9 mutations will give us a new function. now, if we are talking about 2 parts that depend on each other (such as hormone and its receptor or venom and venom sack), in that case we will need about 10^18 mutations to get that new function, which doesnt fit with the geological time.

Let’s assume that the moon is made of brie. In that case, the Apollo missions must have sunk into the gooey mass and disappeared without a trace.


A mutation changes one of the enzymes that produces a hormone, resulting in an altered hormone.

The new hormone binds to a different protein receptor which is beneficial.

Subsequent evolution of the protein receptor increases fitness.

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Meanwhile, back in reality:

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Here’s your error right here.

Not sure what went wrong?


Consider your immune system; in particular, antibodies.

Common to antibodies is that they have parts that are fixed, and also parts that are variant as a result of vdj recombination.

How big is a typical antibody?

How many possible functions do your antibodies have?

(Hint: Alot of possible functions!)

Let’s do a rough approximation.

Well, a typical antibody is 150kDa. Let us assume they are IgG antibodies and ignore IgA, IgM antibodies to simplify.

An average amino acid molecular weight is 110Da (let’s just round down to 100Da to simplify).

So the typical antibody comprises approximately 1500 amino acids.

1500 amino acids are coded by 4500 nucleotides.

From these 4500 nucleotides alone (actually less, because the variable part of an antibody is only a small part of the antibody), your body can become immune to coronavirus, influenza, pneumococcus, haemophilus, smallpox, polio, pertussis, diptheria, tetanus, rotavirus, measles, mumps, rubella, amongst many many more.

So. Where did your math go wrong?

It is simple. Each mutation carries with it the potential for functions in combination with other mutations. So it is an error to try to multiply them individually, as the possible function of a mutation depends on the rest of the genome and other mutations.

Second, your estimate of function affecting mutations is way off (deleterious mutations also affect function - even if it is as simple as a mutation adding the function “aggregate together” to a protein).

The human genome is 3 billion bp. I’m very sure the number of mutations that affect function in your genome is much higher than 1 in 1 billion!!

Let’s try another tack. Imagine a “peak fitness” organism having 1 billion base pairs, and no junk nucleotides.

Imagine if we mutated ALL 1 billion base pairs.

Then, for the mutated organism (well, mutated DNA sequence I suppose), there is a possible beneficial mutation at every single base pair!!

Thirdly, fitness is never independent of environment.

Imagine an alien species, Xenu, who value compactness and efficiency.

They decide that in their breeding program, they will choose the shortest genomes to breed for the next generation, until the organism’s genome is below a certain cutoff.

Then every single mutation, deletion, reducing the genome size can be beneficial in such an environment.


Mutations don’t happen in a vacuum.
The number of mutations that affect function and fitness is high.
Whether a mutation is beneficial or deleterious is environment-dependent.


can you be more specific?

how that hormone evolved in the first place without its receptor?

how it will be beneficial?

Sure. I meant a very runny and soft brie, probably not very aged, of the sort produced in France. Was that specific enough?


I prefer an aged Vermont cheddar, myself. As sharp as possible.


No, we won’t. 10^18 mutations would give us 10^9 new functions - and hence 10^18 possible combinations of pairs those new functions. There’s no reason whatsoever to think that only one of those pairs of combinations would be useful, and lots of reasons to think otherwise.

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A hormone doesn’t require a receptor in order to evolve. Modifications of existing hormones will work just fine.

Why couldn’t it be?

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Promiscous, moonlighting side-reaction of another enzyme.

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I already provided a layperson level article to @scd explaining this. He just carries on like nothing happened. Then asks John to specify what kind of brie he is talking about.

That @scd continues to think he deserves to be treated by us with anything other than derision, scorn and mockery is laughable.


When you are attacking the person and not his argument it is evidence he is over the target.

Another one.

I don’t really think that anybody posting on a message board deserves to be treated that way. That said, I think scd’s ideas certainly deserve to be ignored completely.

Why? There are mathematical problems with molecular evolution. Should we just ignore them?

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Texas sharpshooter fallacy in 3 . . . 2 . . . 1 . . .



Should we ignore nonsensical and uninformed objections like those found in the OP? Absolutely.


They are not nonsensical at all. They are fundamental reasons there is no viable model for the origin of novel genes and proteins.

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That data is equally well explained as evidence that people are tired of explaining how he’s wrong over and over again.

No there isn’t.

There are multiple viable models for de novo gene birth: