Increases in Genetic Information

Perhaps you can explain how students produced doctoral theses in 1908 about a discovery that wasn't made until 1912?

By the way, lactase persistence spread through populations that had dairy skills because it provided a selective advantage. The mutation is absent in those parts of the world with no dairy background in their history.

That is all that mutations do, is they destroy. They are not a process of creation. Sometimes those genes that they destroy happen to aid the organism in surviving or digesting milk sugar but over all they do not make the organism more fit. Mutations do not create anything.

Ref: Nature, vol 414, pp 305-308 (2001) - "Haemoglobin C protects against clinical Plasmodium falciparum malaria" , by D Modiano et al. It's not online, to my knowledge, except by paid subscription - but I could email you a pdf.
Normal human hemoglobin ("HbA") is coded for by DNA which reads, as the 16th through 18th positions of a certain gene, GAA. This codon tells a cell's protein factory to put the amino acid glutamate at the sixth spot along the peptide that will become the beta chain of your or my hemoglobin. However, in a large number of West Africans, particularly the Mossi of Burkina Faso, this speck of DNA reads AAA. The distribution of folks with this variant looks like a bull's-eye: lots of the gene in one area of Burkina Faso, and fewer and fewer people with it as you move away from that center. The distribution is consistent with the idea that one person had the mutation about a thousand years ago, and that it spread through his or her descendants since. (Most people weren't terribly mobile in that area until nearly modern times - at least until the slave trade started.)Now this DNA change alters that sixth amino acid on the beta chain of hemoglobin to lysine, making HbC. Most people with hemoglobin C never know it - some have mild anemia, gallstones, or spleen problems. But Modiano's paper documents that Mossi children that have both genes for HbC are 7% as likely to develop malaria as their classmates who have boring old HbA. 7% as likely to get the disease that kills a million kids in West Africa every year. And that's because their genome has the information to make a protein that has one amino acid that's different from the one in their neighbors, and in their ancestors, too, if you go back a ways. New information. Useful new information. (You will agree that being able to make two different proteins is "more information" than being able to make only one, won't you? Kids in the study that had the AC genotype - that had both HbA and HbC in their blood - had a 29% reduction in their chance of getting malaria.) New, useful, "information" from a mutation.Now a footnote: if your DNA reads GUA instead of GAA in this position, you get a valine in position 6 and have sickle-cell trait - the result of a different mutated hemoglobin called HbS. This protects against malaria, too, but the side effects can be severe, including fatal, especially if you have both genes for HbS. This, too, is "new information" - a different protein is being made.

Besides, for an animal like a dog that almost never gets vitamin c, a mutation like that would kill it.

If they moved away to a place where the threat of Malaria was not so rampant they would be less fit because they would have Anemia. The mutation made the blood cells less susceptible to the Malaria virus but, at the same time made the blood cells less able to pick up oxygen.

If all the HbA people died off and only HbC lived when Malaria disappeared then the people would be alive but with slower metabolisms, slower brains, not progressive evolution but regressive.