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You are making the same mistakes as the author regarding the use of the word "random". If a bird that has a long beak can reach the bugs, while a bird with a short beak cannot, the short beaked birds die out. This is not random. Selection pressures, while unpredictable, are not random. The bugs that could bore deep survived, which caused the birds with the short beaks to die out. Those are natural selective pressures, and they are not random.

Just what percentage of the 3 billion base pairs in the genome do you think affect the anemia ? You seem to call that building up a genome informationally....I can't see how.

I don't personally know, but it has been identified in the area that has to do with hemoglobin production. A single transcription error can affect that, and produce sickle-cell anemia. I have different alleles for hemoglobin production than somebody from sub-saharan Africa. I do not understand how anybody could not "see how" that is building up a genome informationally. We have different information in our genomes.

If you think the DNA repair machinery and its coordination systematically with the cell replication process was a part of a primitive cell, I suggest you rethink this paradigm because I don't think it makes sense at all.

What are you calling a primitive cell? Do you have a basic understanding of how the "DNA repair machinery" works? If you did, it would make sense. If you don't, then why are you telling me to rethink it?

Here's my point...

Deleterious mutations do accumulate. Bergman is not talking about that in his article, he is talking about BENEFICIAL MUTATIONS. DO THEY REALLY OCCUR AND IF SO, TO WHAT EXTENT ? DO THEY DO SO TO PRODUCE HUMAN LIFE ?

Sickle-cell introduces genetic disease into a population and
occurs at a natural 'background rate' and is called a
'balanced polymorphism'.

It can never move to fixation because
there would be no 'normal' alleles to confer the advantage in the heterozygous state and all members of the population would have a genetic disease that would kill them.

So, I don't think Sickle-cell can even be used to explain 'beneficial' mutations arising and moving to fixation in a population.

THIS IS THE WRONG TYPE OF MUTATION AND THAT I THINK , WAS Dr. BERGMAN's POINT.

Regarding your statement to the effect that ...

He seems to be confusing natural
selection with random mutation.

Try to understand what he is saying. Dr. Betgman was saying that non-functional DNA cannot be 'selected' and
should exhibit more randomness than is seen.

It could be that it is functional, thereby explaining the
non-randomness, but that goes back to the first problem of it arising by 'beneficial' mutation in the first place.

Regarding ....

anemia being a defense against malaria and why is sickle cell anemia not found anywhere else?

The gene is a naturally-occurring point mutation and the allele is found in areas that do not have high levels of malarian mosquitos.

Finally,

Your assumed 'primitive cell' populations would
have failed to survive because 'reproductive error catastrophe' would have resulted in extinction before the repair mechanisms could have 'evolved'.