Prevalence, Age & Genetics of Lactose Intolerance

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People of all races.

Prevalence, Age, Gender & Genetics:

Late onset lactase deficiency is the most common type of lactoe intolerance (LI). It is estimated to affect around 75% of the world population. Lactose intolerance varies from human group to another one. Moreover, onset of lactose intolerance varies from children of a group to another.

Prevalence of Lactose Intolerance

The prevalence of primary lactose deficiency varies according to race. In a review by Gudmand-Hoyer E in published on The American Journal of Clinical Nutrition (1994), it is lowest in Scandinavia and Northwest Europe (3-8%) and close to 100% in most of Southeast Asia. In Europe the frequency increases in the southern and eastern directions, reaching 70% in southern Italy and Turkey. There is also a high prevalence of lactose maldigestion in the people of Africa with the exception of cattle-raising nomads. Moreover, studies conducted by Scrimshaw and Murray and Sahi review the prevalence of lactose maldigestion globally. The prevalence is above 50% in South America, Africa, and Asia, reaching almost 100% in some Asian countries. In the United States, the prevalence is 15% among whites, 53% among Mexican-Americans and 80% in the Black population. In Europe it varies from around 2% in Scandinavia to about 70% in Sicily (see map below). Australia and New Zealand have prevalence of 6% and 9% respectively. In general, it can be stated that about two thirds of the world adult population is lactase non-persistent.

Click on map to enlarge.

Click on map to enlarge image. Explanation of Map: Prevalence of adult-type hypolactasia in different European countries and populations (small number = prevalence of a population, large number = average prevalence of the country) and hypothetical isograms for the frequencies of the lactase non-persistence gene. Reprinted with permission from Sahi.

Data from NIDDH

The National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) of the NIH (USA) estimates that between 30 and 50 million Americans are lactose intolerant. This includes an estimate of lactose intolerance affecting 75% of African-Americans and 90% of Asian and Native Americans. By the way, the US Census estimates the US population at 261,638,000 as of January 1, 1996 and is made up of 72% white; 13% African-American; 11% Hispanic; 4% Asian and Pacific Island; and 1% Native American, Eskimo, and Aleutian

 

Human Group Individuals Examined Percent Intolerant Allele Frequency
Swedish   2% 0.14
Europeans in Australia 160 4% 0.20
Swiss   10% 0.316
American Caucasians 315 12% 0.346
Finns 134 18% 0.424
African Tussi   20% 0.447
African Fulani   23% 0.48
American Blacks 20 75% 0.87
Australian Aborigines 44 85% 0.922
African Bantu 59 89% 0.943
Chinese 71 93% 0.964
Thais 134 98% 0.99
American Indians 24 100% 1.0
Data obtained (in part) from "Lactose and Lactase", Scientific American, October, 1972, by Norman Kretchmer

Age

The age at which lactase deficiency presents varies from one race to another. In Blacks and Asians, hypolactasia usually manifests itself in early childhood (1-2 years in Thai), whereas in whites, it seems to occur later in childhood or in adolescence (10-20 in Finns). Lactose intolerance is not common in young white children. However, rotavirus infections may be an important cause of secondary lactose maldigestion in children, and, as the infection is cured, lactose maldigestion disappears as well.

There might be differences in hydrogen production after ingestion of lactose according to age, but the findings are not entirely consistent. The amount of breath hydrogen was shown to increase with age up to the age of 64 to 70 years and after lactulose challenge in a group of elderly subjects whose mean age was 76 years compared with a group of younger adults with a mean age of 32 years. However, in the study of Rao et al., hydrogen excretion was lower in the age group over 70 years than in the group between 60 and 69 years. It is not known whether these variations are due to differences in lactose digestion or in the colonic microflora.

Gender

Hardly any studies have compared lactose tolerance between the genders. According to some studies in a randomly selected population, gender did not have any effect on the prevalence of hypolactasia.  In a study by Jussila it was reported that, among 504 hospital patients, women experienced gastrointestinal symptoms and nausea after milk ingestion more often than men. In a study by Krause et al., women marked higher symptom scores than men despite lower hydrogen excretion. Their results respecting differences in hydrogen excretion are not consistent with those of an other study by Saltzberg et al., who found no difference in hydrogen excretion between men and women after lactulose ingestion. Based on the results of the above studies, women seem to experience stronger gastrointestinal complaints than men, but it is not possible to draw any conclusion on the possible differences in hydrogen production between the genders.

Genetics

Selective adult-type hypolactasia is inherited through a single autosomal recessive gene. Both pretranscriptional and posttranscriptional mechanisms seem to be involved in the expression of the low enzyme activity. A Finnish group has recently reported assignment of the CLD gene. Their analyses indicate that one major mutation in a novel gene causes CLD in the Finnish population.

A culture-historical hypothesis has been proposed for lactase persistence: After the beginning of dairy farming, when there were periods of dietary stress, there would have been an advantage for those individuals who had high levels of intestinal lactase. As a result of increased survival, high intestinal lactase activity would have become typical of such a group. Lactase persistence is, indeed, more common in the areas with long traditions of dairy farming. However, production of the enzyme does not seem to be induced by lactose consumption.

This information is adapted from Lactose Intolerance, Journal of the American College of Nutrition, Vol. 19, No. 90002, 165S-175S (2000) by Tuula et al. and from other medical journals.

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