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Information On Lactose Intolerance
Lactase Enzyme
Mounting evidence indicates that milk- ''nature’s most perfect food,'' as many a child can attest – contains in its unaltered or unfermented state a substance which is indigestible by a large majority of the world’s population. Lactose, the natural sweetener in milk, requires the presence of lactase, an enzyme produced in the small intestine, in order to be reduced to the usable form of sugar, glucose (Simoons, 1973). In the absence of lactase, ''sweet'' milk may, though it doesn’t always, precipitate symptoms of digestive tract distress, cramps, flatulence, and/or diarrhea (Bayless et al., 1976).
Anthropologists, geographers, and other scientists have documented in the past 20+ years the prevalence of lactase deficiency in various ethnic population groups (Simoons, 1973; 1978’ Harrison, 1975; McCracken, 1971).
Definitions
Distinctions among the terms used in conjunction with this condition are not always made in the literature. For the sake of clarity, definitions for lactase deficiency, lactase malabsorption, and lactose intolerance follow.
Primary adult lactase deficiency, considered ''normal'' for most of the earth’s population, is the condition resulting when the brush border of the small intestine has nearly ceased production of lactase. This severe reduction in intestinal lactase, thought to be genetic in nature (McCracken, 1971), apparently occurs at different ages. Investigators have reported its onset from shortly after weaning through young adulthood (Simoons, 1980). Another condition, secondary lactase deficiency, usually results from nutritional deficiency or disease of the digestive tract rather than being generically induced.
Primary adult lactase deficiency (hereafter referred to as lactase deficiency) leads to lactose malabsorption, which is simply the body’s inability to metabolize some or all of the lactose as a result of the absence or deficiency of lactase (Simoons, 1980). Diagnosis can be made by blood glucose tests or breath hydrogen tests subsequent to lactose ingestion. Blood sugar levels will not increase appropriately and breath hydrogen will be excessive if the lactose is not hydrolyzed sufficiently. Some persons, but not all, who are diagnosed as malabsorbers develop the uncomfortable symptoms associated with lactose intolerance. Some of the possible symptoms are bloating, cramping, gassiness, and diarrhea. Generally, 80-95% of malabsorbers experience the discomfort of lactose intolerance following ingestion of the amount of lactose equivalent to that in an 8oz. glass of milk.
Studies which have attempted to determine if lactose malabsorption adversely affects absorption of other nutrients in milk, primarily calcium and nitrogen, have shown inconclusive results.
Asymptomatic lactose malabsorption conceivably can be a hidden source of malnourishment, if the absorption of other nutrients is prevented. This underscores the impotence of continued research in this area.
Lactose intolerance is symptomatic lactose malabsorption, which often causes the person to quit drinking milk and eating other offending dairy products entirely, although there are other options for the lactose-intolerant person.
Lactose malabsorption and lactose intolerance are to be distinguished from milk allergies. The digestion difficulties arising from lactose intolerance are not allergic conditions. Some people will often refer to these problems as allergies. Allergies are usually associated with milk – protein hypersensitivity (Paige and Bayless, 1981).
Prevalence in the U.S.
With the reigning theory explaining these conditions being one of genetic origin, a summary of the ethic differences, as they relate to lactose intolerance, is necessary to understand the prevalence of lactose malabsorption and intolerance in the United States.
The genetic theory is thought to offer the most potential for explaining the regional population distributions of lactose absorbers and malabsorbers. Research shows that among populations with a low percentage of lactose malabsorption (0-30%), a preponderance originate in Northwest European countries or in some pockets on the Mediterranean and Near East, Africa, and the Indian subcontinent. These people all share the longest known tradition of dairying. Consequently, milk has been abundant for usage by adults, as well as by small children. In addition, it is posited, those who had genetically adapted to adult lactose absorption had survival advantages in times of shortages of other foodstuffs; this resulted, over thousands of years, in the dominance of that particular gene in those particular groups.
On the other hand, population groups displaying high proportions of lactose malabsorption (80-100%) are generally found in geographic areas in which dairying or adult milk usage has never, until perhaps recently, been a part of the culture. In the absence of genetic challenge, no evolution has occurred. These areas include the majority of the world’s populations: all American Indians and Eskimos; most Mediterranean and Near Eastern groups; all Southeastern and East Asians; the Pacific groups which have been studied-Fijians, New Guineans, and Australian aborigines; and the remainder of African and Indian subcontinent peoples (Simoons, 1978).
Finally, a small group in the mid-range of lactose malabsorption prevalence (30-60%) is found to be dominated by populations whose ancestry is mixed-absorbers (milk users) and malabsorbers. These include: some American Blacks, African-Arab mixes, Eskimo-Finnish people, and Mexican-Americans, among others (Simoons, 1978).
In light of the hypothesis of genetic causation and corroborative findings, lactose malabsorption rates among the U.S. population are easily understood. Studies specific to U.S. population groups have found American whites (assumed to be predominantly of Northwest European ancestry) to have lactose malabsorption incidence rates of 6-25%, while American blacks show rates of 45-81% (Simoons, 1978). Mexican-Americans have been found to have 47-74% incidence (Simoons, 1978), and the few studies on American Indians, Aleuts, and Eskimos show rates of 75% among the genetically purest and 50 % among those of mixed European ancestry (Johnson et al, 1978; Simoons, 1978). Lastly, among American Orientals, studies show a lactose malabsorption incidence of 95%, and Simoons (1978) reported an incidence of 65-100%.
Questions to be answered
Do persons beyond the young-adult age become genetic malabsorbers? If the answer is yes, lactose malabsorption will become more prevalent, since the median age in the U.S. is increasing. Milk may therefore not longer be a reliable source of nutrition for relatively large number of the population, and a new public health concern may need to be addressed.
Also briefly discussed above, is the question of malabsorption of other nutrients if people are lactase deficient-i.e. is lactose absorption necessary for utilization of other nutrients in milk? This is particularly important with respect to calcium, since calcium deficiencies not only are now implicated in the occurrence of osteoporosis, but also may contribute to the occurrence of hypertension. Should this be a concern only for those who are lactose intolerant?
We need to be able to predict the rate of lactose intolerance from known rates of lactose malabsorption. It’s possible that with better public education regarding these conditions and the greater availability of modified products, a larger number of the malablsorbers would realize that they are lactose intolerant.
Another potential problem, which is not addressed, concerns the economically disadvantaged. Since poverty rates are also high among those groups with a higher prevalence of lactose malabsorption in the U.S., is there greater risk within these groups of malnourishment, whether from insufficient calories (if diarrhea is present as a result of lactose intolerance, or if milk is not used) or malabsorption of nutrients?
Finally, over time, assuming that the above genetic and geographic hypotheses hold and that intermarriage continues to dilute genetic fields, will the rate of lactose malabsorption remain in the mid-range or continue to drop to the range of Northwest European lactose absorbers. The fact that the population groups with the higher incidences of lactose malabsorption are also some of the groups with the highest growth rates in the U.S. indicates that further study of these disparate human conditions is needed.
What Can Be Done
Meanwhile, since dairy products are highly visible, popular foods in our culture, not to mention highly invisible popular additives in processed foods lactose in unaltered forms is difficult to avoid, even if one eliminates or limits consumption of fresh dairy products. Cooking the milk does not necessarily convert the lactose to glucose or lactic acid, the digestible breakdown products of lactose; cream soups, puddings, cream pies, and custards are not usually lactose-free foods. What, then, can the lactose-intolerant individual do to obtain a discomfort-free, yet nutritious diet?
Since most persons who are lactose intolerant are able to tolerate varying amounts of lactose, they have several options regarding consumption of dairy products. One option is to determine one’s threshold for the occurrence of symptoms associated with lactose intolerance and to consume less than that amount of lactose. The threshold ought to be ascertained by using the milk product normally consumed and under the same conditions that it is normally consumed. Researchers have found that the thresholds for lactose tolerance may vary, depending on whether solid food is ingested along with the milk and on the variety of milk product. Whole milk is tolerated better than low-fat varieties, and sweetened, flavored milk is less troublesome than whole milk.
Another option is to restrict milk usage to its fermented forms, such as yogurt (yogurt) and some natural cheeses. Though unpasteurised yogurt may contain lactose at percentages approaching those in milk, digestion of the yogurt is enhanced, due to the inherent lactase activity in yogurt. Naturally aged Cheddar and Swiss cheeses, on the other hand, are very low in lactose because the lactose-rich whey is separated and removed from the cheese curd and most of any remaining lactose is hydrolyzed during the fermentation process. However, ingestion of other fermented microbe-containing milk forms such as acidophilus milk and buttermilk (or cultured milk) are more frequently associated with symptoms of lactose intolerance.
A third option is to ingest ''Lactzyme'' lactase enzyme with your dairy food meal. This enzyme ''predigests'' some of the lactose, rendering the dairy food product more digestible for the lactase-deficient person.
References:
Alpets, D.H. 1981. Carbohydrate digestion: Effects of monosacehardie inhibition and enzyme degradation an lactase activity.
Chpt. 5 in Paige and Bayless (1981).
Bayless, T.M., Rothfeld, 8,. Masse, C., Wise, L. Paige, D., and Bedine, M. 1975. Lactose and milk intolerance: Clinical implications. New Eng. J. Med. 292:1156.
Harrison, G.G. 1975, Primary adult Lactase deficiency: A problem in anthropological genetics. Am. Anthropol. 77:812
McCracken, R. D. 1971. Lactase deficiency: An example of dietary evolution. Current Anthropol 12:479.
Paige, D. M. and Bayless, T. M. 1981. ''Lactosa Digestion.'' Johns Hopkins Univ. Press, Baltimore, Md.
Simmons, F.J. 1978. The geographic hypothesis and lactose malabsorption: A weighing of the evidence Digestion 23:953 |
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