The inability of some poeple to absorb milk sugar (hypolactasia) was studied by the authors. Hypolactasia causes many gastrointestinal complaints. Of the 1902 people studied, 18% showed genetically caused adult-type hypolactasia. These people have a down regulation of the lactase enzyme during development (around the age of five.) These people have symptoms of gas, bloating and diarrhea because of undigested lactose sugar in the intestine.
Consumption of milk products and milk-related symptoms were studied in patients genotyped as having adult-type hypolactasia compared to those had normal genotype. The patients were studied by questionnaires regarding dairy consumption and gastrointestinal symptoms. DNA testing was done on each patient.
The study patients were Finnish. Those with the adult-type hypolactasia genotype reported that they drank less milk than those without symptoms. Nineteen percent of the patients reported gastrointestinal symptoms. Of the adult-type hypolactasia patients, 24% reported gastrointestinal symptoms. This was significantly higher than for the entire study group. Nine percent of adult-type hypolactasia subjects drank milk daily. Of the people with lactase persistence, 46% drank milk, regularly. (Celiac disease can cause hypolactasia without the presence of the genotype for hypolactasia.)
CONCLUSION: People with the genotype for adult-type hypolactasia had more milk related symptoms than those with the genotype for lactase persistence into adulthood. Genotyping is a useful way to diagnose adult-type hypolactasia versus other causes of lactose intolerance.
NOTE: Recent studies of the genome of ancient humans indicate the adult-type hypolactasia was normal at one time in the ancient past. Lactase persistence developed as the result of a mutation, probably in northern Europe. Dairy products have been used by adults in Europe for at least 5,000 years. Read about the difference between milk intolerance from lactose deficiency and milk allergy.
To read the author’s abstract of the article click on the link to the author’s title of the article above.
PMID: 17451204.
Summary #309.

