Yogurt anyone?

SELECTED

demonstrates that the most important UGI malignancy in Japanese polyposis patients is gastric cancer. This may in part be related to the high overall gastric cancer incidence in Japan. This study reemphasizes that the potential of UGI tract cancer in patients with familial polyposis is a real one. and that LJGI x-rays and endoscopy should be a mandatory part of the evaluation of every patient with familial polyposis/Gardner’s syndrome. The interval for follow-up evaluations depends on what is found. If the patient has adenomatous duodenal or gastric antral polyps, annual evaluation would be in order. If only gastric fundal

hyperplastic polyps are present, a 3-5-yr follow-up interval might be more appropriate. Large, adenomatous antral or duodenal polyps Where tion.

should be treated this is not feasible,

YOGURT Martini

MC, Smith

when possible surgery should

by endoscopic means. be a strong considera-

ANYONE? DE, Savaiano

DA (Department

of Food

Science and Nutrition, University of Minnesota, St. Paul, Minnesota) Lactose digestion from flavored and frozen yogurts, ice milk, and ice cream by lactase-deficient persons. Am J Clin Nutr 1987:46:636-40. The article by Martini et al. is a helpful and enlightening guide to understanding why some popular milk products cause symptoms and others do not in lactase-deficient people. Sixteen healthy male volunteers with a diagnosis of lactase deficiency on the basis of an abnormal hydrogen breath test were divided into two groups. One group was given milk, strawberry yogurt, and unflavored yogurt, and the other was given milk, ice milk, ice cream, and three frozen yogurts specially prepared at the University of Minnesota. Each product contained the same amount of lactose (20 g). The frozen yogurts were deliberately made up to contain different P-galactosidase activity; frozen yogurt 1 contained no P-galactosidase activity, frozen yogurt 2 contained only 0.4 LJ, and frozen yogurt 3 contained a high P-galactosidase activity of 4.08 U. After an overnight fast, the volunteers had a breath hydrogen analysis and were then fed test meals in a random order on a blinded basis. Hourly breath tests were done for 8 h following the meal and all symptoms were recorded. Each test meal was analyzed for lactose concentration and fi-galactosidase activity. When test meals of milk, strawberry yogurt, and unflavored yogurt were compared, the unflavored yogurt caused significantly less hydrogen excretion in the lactase-deficient population than did the milk (p < 0.005). The strawberry yogurt resulted in more hydrogen production than the unflavored yogurt but half the hydrogen production compared with the milk, although these differences were not significant. Neither flavored nor unflavored yogurt caused symptoms. In the \.olunteer group that tested milk versus frozen milk products. frozen yogurt 3, with the high P-galactosidase activity, caused significantly less hydrogen excretion than ice milk, ice cream, and frozen yogurts 1 and 2. Gastrointestinal symptoms were noted by a varying number of the volunteers for each of the other products except for frozen yogurt 3, for which none were noted. An analysis of seven commercial unfrozen yogurts indi-

SUMMARIES

247

cated that all of them contained P-galactosidase activity. If, however, these commercial yogurts were frozen at -14°C or -707X, the p-galactosidase activity fell to 34% or 73% of the original activity, respectively. If the yogurt was frozen and then rethawed repeatedly over 1 wk. the activity fell further. When four commercial frozen yogurts that had been pasteurized after fermentation were tested for /?galactosidase activity, no activity was found. In their discussion, the authors make several points. First, although all commercial yogurts contained pgalactosidase activity, the activity varied and tended to be higher in unflavored yogurts. However, neither flavored nor unflavored yogurt led to symptoms in this study. Second, commercial frozen yogurts, in contrast to the unfrozen variety, have been pasteurized after fermentation to increase shelf life. This reduces the P-galactosidase activity to zero. Ingestion of this type of frozen yogurt leads to symptoms in some lactase-defic:ient patients, as well as to consistently elevated hydrogen breath tests. Third, the higher levels of solids in the ice milk and ice cream did not prevent gastrointestinal symptoms from developing after their ingestion in this study. Comment. Patients with lactose intolerance frequently ask which, if any, lactose products they can eat without getting the symptoms they dread. As most people obtain their daily calcium requirement from dairy products, it is important for lactoseintolerant patients to identify dairy products they can eat so they do not automatically need calcium supplementation. Yogurt is one of the products that has been problematic. Will it or won’t it cause symptoms? Are there differences among yogurts? Is frozen yogurt any better or worse than unfrozen yogurt in terms of causing symptoms? Is it better than ice milk or ice cream for lactose-intolerant patients? What answers can we derive from the results of Martini et al.? The answer to the first question is that the results of Martini et al. indicate that unfrozen yogurt does not cause symptoms in lactase-deficient patients. Yogurt, a fermented dairy product produced by the enzymatic conversion of milk sugars to lactic acid by bacteria, has been shown to be much better tolerated by lactasedeficient patients than nonfermented products (J Am Diet Assoc 1974;65:418-9). Epidemiologic data also support this finding in that Middle Eastern peoples consume yogurt frequently although there is a high degree of malabsorption of lactose among them (Paine DM. Bayless TM, eds. Lactose digestion. Baltimore: Johns Hopkins University Press. 1981:11-22, N Engl J Med 1984;310: l-3). Yogurt is made by taking concentrated milk produced by the partial evaporation of whole milk or the addition of milk solids and adding the culture organism Lactobacillus bulgaricus and Streptococcus thermophiles to it for incubation (N Engl J Med 1984;310:1-3). The incubation is stopped when an acid pH (-4.0) is reached [Am J Clin Nutr 1987;45:432-6). Both bacteria contain the enzyme p-galactosidase, a lactase (J Dairy Sci 1974;57:592) that decreases the lactose in the conc,entratud milk so that the lac.tose level in the final yogurt product. although reduced, is still on a par with unconcentrated milk (Nutr Rev 1984;42:216-8). Probably, the more important reason why yogurt is better tolerated by lactase-deficient people is the fact that the bacteria in it remain viable after their passage through the acid environment of the stomach, in part because of the good buffering capacity of yogurt (Am J Clin Nutr 1987;45:432-6). Data in both rats (J Dairy Sci 1976;59:601-6) and humans (N Engl J Med 1984;310:1-3) indicate the presence of P-galactosidase in the upper small intestine in amounts sufficient to hydrolyze significant amounts of the lactose present there. Because of this inherent enzyme property,

248

SELECTED

SUMMARIES

GASTROENTEROLOGY

yogurt has been labeled

an “autodigesting” type of milk product (N Engl J Med 1984;310:1-3). Heating or pasteurizing the yogurt to increase its shelf life markedly diminishes the lactase activity by destroying the viability of the organisms (J Dairy Sci 1984;67:1-6, Am J Clin Nutr 1987:45:570-4). It is of interest that two other cultured milk products, buttermilk, also produced by a fermentation process, and milk containing Lactobacillus acidophilus (sweet acidophilus milk], do not have the same enzyme property as yogurt and caused symptoms in some susceptible subjects (Am J Clin Nutr 1984;40:1219-23). The data of Martini et al. answer the second question concerning differences among yogurts in the affirmative, by showing for the first time that unflavored yogurt caused less of a change in breath hydrogen than did strawberry yogurt and that commercial unflavored yogurts generally had higher P-galactosidase activity than flavored ones. However, in their study, no symptoms were reported by lactose-deficient volunteers after the flavored yogurt, despite the larger change in breath hydrogen. This finding points up the fact that multiple factors are probably involved in the production or prevention of symptoms in lactase-deficient people, including the physical state of the material ingested, the effect of the foodstuff on gastric emptying, the substances produced by the cultured bacteria while in the small intestine, and the variety of gases

released

during

fermentation

in the colon

(Am J Clin Nutr

1984;40:1219-23). Because

frozen

and her group with

breath

deficient

dairy

tests

patients

their study,

products

are extremely

at the University and

of Minnesota

symptom

tolerate

them.

pasteurization

popular, decided

recording

whether

The answer

of yogurt

1, had

symptoms.

elevated

breath

Moreover,

the

tests, addition

before

and

lactose-

was generally freezing

shelf life led to zero P-galactosidase activity Lactose-intolerant people ingesting this product, gurt

Martini

to evaluate no. In

to increase

the

in the product. i.e., frozen yo-

3 of 8 volunteers

of a starter

had

culture

to the

product

so that the frozen yogurt would be labeled as having as in frozen yogurt 2, did not change the “active culture,” @-galactosidase activity sufficiently. Lactose malabsorption and symptoms

freezing with

were

seen in 2 of 8 volunteers.

process

freezing

itself

as destructive

at a lower

temperature.

Their

data identify

of /.Qalactosidase -70°C.

i.e.,

the

actilfity, preferable

to

-14°C further

for preservation of some enzyme activity. The enzyme is reduced by repeated freezing and thawing. Only frozen

yogurt

3, which

had a starter

of P-galactosidase

after

culture

pasteurization

added

to it with a high level

but

before

freezing,

had

sufficient P-galactosidase activity to prevent intestinal symptoms and produce significantly less hydrogen (p < 0.05) than the other frozen products. Unfortunately, as Martini et al. point out, a product

like this is not commercially

Finally,

the data

milk, despite their to fewer symptoms. product,

although

the results. 111summary, with dairy

of Martini

available

et al. show

that

at present. ice cream

and ice

high levels of fat and milk solids, did not lead Two of 8 volunteers had symptoms with each the portions

this article

tested

provides

lactose-intolerant patients products and their potential

were large, perhaps a rational

the various for causing

skewing

basis for discussing yogurt and frozen side effects. On the

basis of the data presented these patients will most likely tolerate flavored as well as unflavored yogurts. Unfortunately some of them will certainly have symptoms after ingesting ice cream, ice milk, or frozen yogurt. Making ice cream or ice milk from lactase-treated milk (Paine DM, Bayless TM, eds. Lactose digestion, Baltimore: Johns Hopkins University Press, 1981:252-6) may decrease symptoms. A further advance in the tolerance of frozen yogurt yogurt

could also be made if this article’s suggestion that frozen be produced by adding active culture with a high level of

P-galactosidase

after pasteurization

by the companies

but before

Vol. 95, No. 1

freezing

is heeded

making this product. t1. SHIELDS. M.D.

FURTHER INSIGHTS INTO MUCOSAL ADAPTATION Chaves M, Smith MW, Williamson RCN (Department of Surgery, University of Bristol, Bristol and AFRC, Institute of Animal Physiology, Babraham, Cambridge, U.K.) Increased activity of digestive enzymes in ileal enterocytes adapting to proximal small bowel resection. Gut 1987;28: 981-7 (August). The authors examined adaptability of two digestive enzymes in rat ileal enterocytes after 60% proximal small bowel resection. There were two control groups in which the small intestine was transected and rejoined in either ileum or jejunum without removal of tissue. Food and water were allowed ad libitum. Three weeks after resection or transection tritiated thymidine was injected intraperitoneally 2, 10, 20, 30, or 40 h before the animals were killed by cervical dislocation. A &cm intestinal segment, 2-6 cm distal to the anastomosis, was removed. Half of each segment was used for measurements of enterocyte migration rates by autoradiography. The other half was used for cytochemical determinations by scanning microdensitometry of a-glucosidase and neutral aminopeptidase activities. Changes in enzyme activities recorded along the length of the villus were computer-fitted by logistic growth curves. Comparisons were made between enzyme activities found in enterocytes at similar positions on the villus surface. Relations between enzyme activity and enterocyte age were also examined. Resection increased ileal villus height by 81”/” and crypt depth by 340/o compared with transection. Values for ileal remnants remaining after resection were also 39%41%) greater than those for jejunum from transected controls. In resected ileal remnants cu-glucosidase activity in crypts was greater than controls and increased threefold to fourfold over the first 250 pm of villus surface. There was a pronounced fall in enzyme activity as the enterocyte migrated further toward the villus tip. This rise and fall also occurred in control ileal villus enterocytes but was much less noticeable. Aminopeptidase activities in crypts of resected ileal remnants were greater than in ileal control tissues. Activities increased with enterocyte migration in both resected and control groups but at different rates, so that by 250 pm of villus surface aminopeptidase activities were the same. Enzyme activities declined during further enterocyte migration and activities at the villus tips were the same in both resected and control groups. As the villus was longer in ileal remnants from resected animals, the decline in aminopeptidase was less steep in ileal remnants than in controls. Enterocyte migration rates were linearly related with time in both control and ileal remnant tissues, but migration was faster in ileal remnants. In relating enzyme profile to enterocyte age both a-glucosidase and aminopeptidase activities appeared earlier in ileal remnants, with a fourfold increase in enzyme activities by 10 h. Over the subsequent 10 h the rate of appearance of