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COMMENTS HAVE BEEN DISABLED

Because of spam, I personally moderate all comments left on my blog. However, because of health issues, I will not be able to do so in the future.

If you have a personal question about LI or any related topic you can send me an email at stevecarper@cs.com. I will try to respond.

Otherwise, this blog is now a legacy site, meaning that I am not updating it any longer. The basic information about LI is still sound. However, product information and weblinks may be out of date.

In addition, my old website, Planet Lactose, has been taken down because of the age of the information. Unfortunately, that means links to the site on this blog will no longer work.

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Friday, January 30, 2009

Congenital LI May Occur More Frequently Than Thought

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.

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