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Objective To determine whether African-American adolescent girls who were fed a dairy-rich diet for 21 days could adapt to lactose, experiencing an overall improvement in lactose tolerance as well as a decrease in hydrogen gas production.
Design Twenty-one--day dietary intervention study.
Subjects/setting Seventeen of 21 African-American girls (aged 11 to 15 years) enrolled in a calcium metabolism study chose to participate in the lactose tolerance study. Subjects were screened for any diseases, conditions, or medications that might alter calcium metabolism or colonic fermentation. Subjects were housed in a fraternity on the Purdue University, West Lafayette, Ind, campus, and were supervised 24 hours a day.
Intervention Subjects consumed a dairy-based diet averaging 1,200 mg calcium and 33 g lactose per day for 21 days. Lactose digestion was assessed by an 8-hour breath hydrogen test on days 1 and 21, and symptoms of intolerance (abdominal pain, bloating, flatulence, and diarrhea) were evaluated hourly on a ranked scale during the breath hydrogen tests and once each evening during the 21-day feeding period.
Main outcome measures A comparison of breath hydrogen production and gastrointestinal symptoms at the beginning and end of the study.
Statistical analyses performed The Wilcoxon signed ranks test was used to compare the area under the curve for the 2 breath hydrogen tests. Spearman's p test for trend was used to determine whether there was a change in symptoms. All statistical analyses were 2-tailed and significance was set at P=.05
Results Fourteen of the 17 subjects had lactose maldigestion. Breath hydrogen excretion decreased significantly (P[less than].03) from the beginning (148.3[pm]27.0 ppmxhours) to the end (100.7[pm]19.3 ppmxhours) of the 21-day period. Gastrointestinal symptoms were negligible during both the breath hydrogen tests as were symptoms during the 21-day period.
Applications/conclusions The diet was well tolerated by the subjects. Furthermore, the decrease in breath hydrogen suggests colonic adaptation to the high-lactose diet. The results indicate that lactose maldigestion should not be a restricting factor in developing adequate calcium diets for this population. The existence of lactose maldigestion does not result in lactose intolerance in this population when it is fed a dairy-rich diet. J Am Diet Assoc. 2000; 100:524-528.
Lactose maldigestion is the inability to completely digest lactose, the major carbohydrate found in milk . Intestinal digestion of lactose involves the breakdown of lactose into glucose and galactose by a membrane-bound lactase, located on the brush border of the small intestine [1,2]. The resulting monosaccharides are rapidly absorbed into the portal circulation. In people with lactose maldigestion, a portion of the lactose load is not digested in the small intestine; it passes into the large intestine, where it is fermented by the colonic microflora. The fermentation produces short-chain fatty acids and gases, including hydrogen, carbon dioxide, and sometimes methane [1-3].
Approximately 75% of the world's population loses the ability to completely digest a physiological dose of lactose after infancy [1,4]. When lactose maldigestion occurs in the absence of a gastrointestinal disease, it is known as primary lactase nonpersistence [4-6] and is directly related to the loss of the majority of intestinal lactase activity. It is estimated that 70% of adult African-Americans are lactose maldigesters . Lactose maldigestion may be evident in this …