rationalskepticism.org

GenesForLife wrote:

The problem with his scenario above is that amylase production seems to match dietary habits and there is no reason to infer that duplication of the amylase gene is a harmful mutation. So the accident occurs in just those groups that can make use of it.

Here's the source of your confusion. The mutation doesn't occur in groups that make use of it, it is fixed in populations that do. I'll let you figure out what the difference is between a mutation occurring for a certain reason and a random mutation getting fixed in a population for a particular reason.

You essentially look at what mutations were fixed and go "Ooh, the mutation occurred to give us an advantage" but as your very own source points out, you would be well advised to read and assimilate this.

. If we consider all the mutations that led to these pivotal point in our evolution, human origins begin to look like a trail of unfeasible coincidences. But that is only because we do not see the harmful mutatios that were weeded out, points out John Hawks at the University of Wisconsin-Madison. "What we're left with is the ones that were advantageous." It is only from today's viewpoint that the mutations that give us our current physical form appear to be the "right" ones to have. "

You are assuming that these duplications are accidental mutations that became fixed in various human populations at an unspecified time in the past 100 000 years. But as P.Z.Myers says:

(The amylase gene) seems to be in a hotspot for duplication, and different people have different numbers of copies of the gene. If you just had one copy of the gene per chromosome, your cells would each have a grand total of two copies…but instead, we more typically have 5 to 7, with some people having only 2, and others having 15 or more.

So it is difficult to figure out in what way they are fixed. We are talking here of salivary amylase gene copy number variation. Copy number variation has been shown to occur between monozygotic twins who presumably started out with identical genomes. In other words if they can't be shown to be fixed even in an individual how can they be shown to be fixed in an unobserved population?

Ellison Medical Foundation

We have recently shown that monozygotic twins frequently differ in their genes by changes in so called copy number variation (CNV), which represent one type of genetic differences that can be frequently seen between any two unrelated people.

So in what way are they fixed?

GenesForLife wrote:
I suggest you find some of Susu.exp's posts on the distribution of mutations and you will know exactly where your idea of organisms developing mutations to meet future needs goes awry. I will search for some of them later and will post them here.

I am not talking about an organism meeting future needs. I'm talking about organisms responding to a high intake of starch.

I'd be interested to know if any research has been carried out in order to determine if amylase copy numbers vary within one individual. For example between DNA extracted from an individual's saliva and say stem cells from the same individual.

I did find this but they don't mention amylase and I haven't had time to read through it yet.

The exploration of copy-number variation (CNV), notably of somatic cells, is an understudied aspect of genome biology. Any differences in the genetic makeup between twins derived from the same zygote represent an irrefutable example of somatic mosaicism. We studied 19 pairs of monozygotic twins with either concordant or discordant phenotype by using two platforms for genome-wide CNV analyses and showed that CNVs exist within pairs in both groups.