All mammals are born with the ability to drink their mother's milk. It's simple survival. Mammals who couldn't drink mother's milk died.
Humans have managed to change this deadly equation slightly. It's reasonably certain that after herding and milking started, babies who had lost their mother were given animal milk as a desperate substitute. That often worked for older infants.
A few, a very few, infants could not drink any mammal's milk at all. That's because their bodies completely lacked the ability to manufacture the lactase enzyme that would digest the lactose sugar in milk. Lactose is identical and in nearly the same percentage in all milkable animals. Substituting a different animal's milk wouldn't be any use. They had to wait until soy milk and other non-milk based formulas were invented.
Fortunately, this condition, known as congenital lactose intolerance (Congenital LI) was thought to be extremely rare. When I wrote my book, Milk Is Not for Every Body, I came across a medical journal article that stated that only 40 cases were known, total, worldwide, ever.
That estimate was probably low even at the time. Now a new report has appeared in that lively journal BMC Gastroenterology. Four novel mutations in the lactase gene (LCT) underlying congenital lactase deficiency (CLD) by Suvi Torniainen et al. (BMC Gastroenterology 2009, 9:8doi:10.1186/1471-230X-9-8) looked at the DNA in patients from several countries.
They discovered that a variety of small mutations could cause similar changes resulting in Congenital LI. Their conclusion was that:
The figures presented here suggest that CLD may be more common than previously estimated. CLD should be suspected in neonates with severe diarrhoea which starts after introduction of milk feeding. A high concentration of lactose is present in liquid faeces and may easily be identified.