Adult-type hypolactasia (low lactic acid tolerance), an evolutionary phenomenon, is known as lactase non-persistence and primary lactose malabsorption. The lactase enzyme helps metabolize lactose (milk sugar.) Historically, a mutation occurred which prevents that down-regulation of lactase at weaning and lactose digestion persists into adulthood.
Not all humans have this mutation. Over 50% of the adult population of the world doesn’t tolerate milk products due to insufficient lactase enzyme. The symptoms of hypolactasia are abdominal pain, bloating, gas and diarrhea with milk use. Some people with low lactase enzyme are asymptomatic.
Poor lactose tolerance can be due to gastrointestinal infections, celiac disease and irritable bowel disease. Lactase activity is necessary for infants to breast feed and gradually declines after weaning. Congenital lactase deficiency (CLD) causes diarrhea, dehydration and weight loss when the infant is breast fed.
A mutation which allows adults to tolerate milk may have occurred about 10,000 years ago when humans developed agriculture. Adult-type hypolactasia is autosomal recessive and is common in Asia and Africa. It is normal. The mutation allows adults to digest lactose and is more common in northern Europe.
Studies of the connection of lactose tolerance to diabetes, osteoporosis, bone mineral densities, colon cancer and ovarian cancer are inconclusive. A study in Sardinia (with high diabetes rates) theorized that lactose absorption might cause diabetes. Galactose (a product of lactose metabolism) is toxic to ovarian cells and could increase the risk of ovarian cancer.
CONCLUSION: Adult-type hypolactasia with milk intolerance is a common cause of abdominal symptoms and is normal. Tolerance of milk is a mutation. Lactase enzyme aids lactose absorption; but, milk products may have unknown negative health effects in humans.
NOTE: Cow milk residue has been found in the remains of ceramic pottery from about 7,000 years ago in Europe.
Read about milk intolerance among working people.
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PMID: 16019716.
Summary #279.
