Soy & Lactose Intolerance

Lactose (β galactose 1,4 glucose) is the unique sugar in the milk of most mammals and serves as the most important source of energy for the breast-fed infant. Lactose intolerance was first described by Hippocrates but only within the past 50 years has the condition been recognized and diagnosed medically.

Lactose is hydrolyzed in the small intestine, primarily in the jejunum, by the enzyme lactase. Nearly all infants digest lactose with ease. Despite what the average consumer thinks, congenital lactase deficiency is an extremely rare condition.1

This said, 75-90 percent of lactase activity is lost within a few years after weaning among most U.S. adults, with the exception of white Northern Europeans and some African dairying tribes.2

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Ethnic Variation of Lactose Maldigestion

Researchers believe that hypolactasia (low lactase) was the norm among all adult humans prior to the establishment of agricultural-based societies. However, in certain populations, milk consumption continued beyond childhood and lactase persistence had a selective advantage which led to genetic adaptation.

Between 30 and 50 million Americans are lactose intolerant, with certain ethnic and racial populations being more widely affected than others. As many as 75 percent of all African Americans and American Indians and 90 percent of Asian Americans are lactose intolerant. Chinese and Japanese lose 80-90 percent within three to four years of weaning, but Ashkenazi Jews can retain 20-30 percent of lactase activity for many years.2-4

According to Murray5 and Sahi,2 the prevalence of lactose maldigestion is more than 50 percent in South America, Africa and Asia. In Europe it varies from about 2 percent in Scandinavia to about 70 percent in Sicily. In general it can be said that about two-thirds of the world is lactase non-persistent.

There is some disagreement about whether intestinal lactase activity continues to decline with age.6

Symptoms of lactose intolerance following consumption of dairy foods include:

  • Gut pain and distension
  • Flatus
  • Diarrhea

These symptoms begin about 30 minutes to 2 hours after the person eats or drinks foods containing lactose. The severity of symptoms varies depending on the amount of lactose an individual can tolerate.

For the extremely sensitive, even exposure to small amounts may cause serious problems.7

Because this sugar has many applications in the food industry, it can be difficult for lactose intolerant individuals to identify and avoid all sources of lactose. The estimated annual production of lactose as a food additive is 330,000 tons.7

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Testing Lactose Digestion

Lactose digestion can be studied in several ways. The most common measures the amount of hydrogen in the breath after the consumption of lactose. The amount of hydrogen correlates well with maldigested lactose.8

However, the extent to which people categorized as lactose intolerant can actually tolerate some lactose is unclear since the standard laboratory test involves the ingestion of 50 grams of lactose, which causes symptoms in 80-100 percent of lactose maldigesters.9

In contrast, 1 cup of dairy milk contains only about 9 to 14 grams. Plus, the lactose content of some dairy foods, such as hard cheese, is low.

Several studies have been unable to document differences between digesters and maldigesters of lactose in response to milk with and without lactose.10, 11 Conversely, some people will experience symptoms in response to just 2 to 3 grams of lactose in a chocolate bar. There is some evidence of colonic adaptation to a high-lactose diet so that classic symptoms of lactose maldigestion diminish over time.12

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References

  1. Savilahti E, Launiala K, Kuitunen P. Congenital lactase deficiency. A clinical study on 16 patients. Arch Dis Child 1983;58(4):246-52.
  2. Sahi T. Genetics and epidemiology of adult-type hypolactasia. Scand J Gastroenterol Suppl 1994;202:7-20.
  3. Flatz G. Genetics of lactose digestion in humans. Adv Hum Genet 1987;16:1-77.
  4. Swallow DM. Genetics of lactase persistence and lactose intolerance. Annu Rev Genet 2003;37:197-219.
  5. Scrimshaw NS, Murray EB. The acceptability of milk and milk products in populations with a high prevalence of lactose intolerance. Am J Clin Nutr 1988;48(4 Suppl):1079-159.
  6. Vesa TH, Marteau P, Korpela R. Lactose intolerance. J Am Coll Nutr 2000;19(2 Suppl):165S-75S.
  7. Matthews SB, Waud JP, Roberts AG, Campbell AK. Systemic lactose intolerance: a new perspective on an old problem. Postgrad Med J 2005;81(953):167-73.
  8. Bond JH, Levitt MD. Quantitative measurement of lactose absorption. Gastroenterology 1976;70(6):1058-62.
  9. Bayless TM, Rothfeld B, Massa C, Wise L, Paige D, Bedine MS. Lactose and milk intolerance: clinical implications. N Engl J Med 1975;292(22):1156-9.
  10. Suarez FL, Savaiano DA, Levitt MD. A comparison of symptoms after the consumption of milk or lactose- hydrolyzed milk by people with self-reported severe lactose intolerance. N Engl J Med 1995;333(1):1-4.
  11. Suarez FL, Savaiano D, Arbisi P, Levitt MD. Tolerance to the daily ingestion of two cups of milk by individuals claiming lactose intolerance. Am J Clin Nutr 1997;65(5):1502-6.
  12. Pribila BA, Hertzler SR, Martin BR, Weaver CM, Savaiano DA. Improved lactose digestion and intolerance among African-American adolescent girls fed a dairy-rich diet. J Am Diet Assoc 2000;100(5):524-8; quiz 9-30.
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1. Savilahti E, Launiala K, Kuitunen P. Congenital lactase deficiency. A clinical study on 16 patients. Arch Dis Child 1983;58(4):246-52.
2. Sahi T. Genetics and epidemiology of adult-type hypolactasia. Scand J Gastroenterol Suppl 1994;202:7-20.
3. Flatz G. Genetics of lactose digestion in humans. Adv Hum Genet 1987;16:1-77.
4. Swallow DM. Genetics of lactase persistence and lactose intolerance. Annu Rev Genet 2003;37:197-219.
5. Scrimshaw NS, Murray EB. The acceptability of milk and milk products in populations with a high prevalence of lactose intolerance. Am J Clin Nutr 1988;48(4 Suppl):1079-159.
6. Vesa TH, Marteau P, Korpela R. Lactose intolerance. J Am Coll Nutr 2000;19(2 Suppl):165S-75S.
7. Matthews SB, Waud JP, Roberts AG, Campbell AK. Systemic lactose intolerance: a new perspective on an old problem. Postgrad Med J 2005;81(953):167-73.
8. Bond JH, Levitt MD. Quantitative measurement of lactose absorption. Gastroenterology 1976;70(6):1058-62.
9. Bayless TM, Rothfeld B, Massa C, Wise L, Paige D, Bedine MS. Lactose and milk intolerance: clinical implications. N Engl J Med 1975;292(22):1156-9.
10. Suarez FL, Savaiano DA, Levitt MD. A comparison of symptoms after the consumption of milk or lactose- hydrolyzed milk by people with self-reported severe lactose intolerance. N Engl J Med 1995;333(1):1-4.
11. Suarez FL, Savaiano D, Arbisi P, Levitt MD. Tolerance to the daily ingestion of two cups of milk by individuals claiming lactose intolerance. Am J Clin Nutr 1997;65(5):1502-6.
12. Pribila BA, Hertzler SR, Martin BR, Weaver CM, Savaiano DA. Improved lactose digestion and intolerance among African-American adolescent girls fed a dairy-rich diet. J Am Diet Assoc 2000;100(5):524-8; quiz 9-30.
2. Sahi T. Genetics and epidemiology of adult-type hypolactasia. Scand J Gastroenterol Suppl 1994;202:7-20.

3. Flatz G. Genetics of lactose digestion in humans. Adv Hum Genet 1987;16:1-77.

4. Swallow DM. Genetics of lactase persistence and lactose intolerance. Annu Rev Genet 2003;37:197-219.

Soy Fact

Approximately 30 million Americans are lactose intolerant.

National Institutes of Health