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Letters to the Editor |
Physicians Committee for Responsible Medicine 5100 Wisconsin Avenue, Suite 404 Washington, DC 20016 E-mail: barnard{at}pcrm.org
Dear Sir:
Suarez et al (1) suggest that lactose maldigestion should not be a major impediment to a dairy-rich diet. However, problems with the design of their study preclude such a conclusion.
First, the subject sample was skewed toward those least likely to be bothered by digestive difficulties. The lactose maldigestion group included 14 whites, 9 Asians, 5 Hispanics, and only 2 African Americans. Whites not only are much less likely than African Americans to have lactose maldigestion, but when it occurs are also much less likely to have troublesome symptoms. In a 1994 study in which 360 mL whole milk (containing 16.5 g lactose) was fed to 46 whites and 52 African Americans, lactose maldigestion was identified by breath testing in 15% of whites and 36% of African Americans aged <50 y and in 20% of whites and 71% of African Americans aged 
50 y (2). These findings are not surprising. What is noteworthy is that of those actually identified as having lactose maldigestion, only 25% of whites had symptoms compared with 73% of African Americans, who experienced abdominal cramps, flatulence, diarrhea, and bloating (2). Symptoms of lactose maldigestion are simply milder in whites.
Second, the investigators did not rule out self-selection. In a previous report by the same investigators, 15 of the original 34 subjects declined further testing after their first lactose test. The remaining subjects were presumably those least bothered by symptoms. As in the current report, most were Asian or white; only 3 were African American (3). The burden is on investigators to establish that their sample is representative of persons with lactose maldigestion; yet Suarez et al offered no description of their subject selection.
Third, a dairy-free control would have been helpful in sorting out why persons with maldigestion had more symptoms than at baseline not only from unmodified milk but also from lactose-reduced dairy products. No data support the authors' speculation that symptom reports were affected by the participants' "mind set." It may well be, as they also suggest, that components of milk other than lactose, eg, proteins, may have caused the symptoms.
Fourth, their conclusion that symptoms are not a major impediment to dairy ingestion is poorly supported. Indeed, the lactose maldigestion group reported bloating, fullness, nausea, and flatus from dairy ingestion.
Finally, although we need calcium in the diet, dairy products may not be a clinically effective source if our goal is to prevent fractures. In the Nurses' Health Study of 77761 women aged 34–59 y (98% of whom were white) followed over a 12-y period, those who obtained more calcium from dairy products had slightly, but significantly, more bone fractures than did those who drank little or no milk, even after adjustment for weight, menopausal status, smoking, and alcohol use (4). These findings confirmed those of a 1994 study of elderly men and women in Sydney, Australia (racial composition unspecified), in which higher dairy product consumption was associated with increased fracture risk (5). Those with the highest dairy product consumption had approximately double the risk of hip fracture of those with the lowest consumption.
The best available evidence does not indicate that calcium from dairy sources reduces fracture rates at all. Moreover, in part because of the exclusion of African Americans from nearly all calcium intervention trials (because of much lower rates of osteoporosis), there is no evidence that African Americans, for whom lactose intake often presents an unpleasant challenge, benefit in any way from increased dairy consumption.
REFERENCES
Research Office Minneapolis Veterans Affairs Medical Center 1 Veterans Drive Minneapolis, MN 55417
Dear Sir:
Barnard believes that faults in the design of our study (1) cast doubt on the conclusion that a dairy-rich diet produces minimal symptoms in persons with lactose maldigestion. His first criticism is that the lactose maldigestion group contained a small number of African Americans, a group Barnard believes to be relatively hypersensitive to symptoms of lactose malabsorption. The study he cites in support of this belief, however, was both unblinded and uncontrolled (2). Abundant evidence indicates that reliable conclusions concerning symptoms of food intolerance can be obtained only through double-blind studies (3). In fact, several double-blind studies have shown that, regardless of race, persons with lactose maldigestion tolerate moderate amounts of lactose (4–6). Note also that the racial composition of our study group was roughly representative of the lactase-deficient population in Minnesota (1).
Barnard's second criticism is that a study carried out in 1997 (7) showed that only 19 of 34 subjects whom we identified as having lactose maldigestion took part in a subsequent investigation of symptomatic responses to lactose. Although it is possible that some subjects declined to participate further because of the severity of their symptoms, the stated reason was that they did not want to take the Minnesota Multiphasic Personality Inventory 2 test, a requirement of that particular study.
Barnard states that our lactose maldigestion group reported symptoms of bloating, fullness, nausea, and flatus during ingestion of dairy products. The critical finding of our study, however, was that with the exception of the number of passages of flatus, these symptoms were not significantly more severe when the subjects ingested the lactose-containing products than when they ingested the nearly lactose-free products. In addition, the symptoms were usually considered to be trivial with both dietary regimens. As noted in our paper, milk components other than lactose cannot be excluded as a cause of these trivial symptoms.
We do not claim to be experts in the area of calcium intake and osteoporosis. However, evidence supporting the concept that a high calcium intake slows the progression of osteoporosis was sufficient to convince a National Institutes of Health panel to recommend that postmenopausal women consume 1500 mg Ca/d (8,9). We are unaware of any data suggesting that this beneficial effect occurs only when calcium is ingested in tablet form as opposed to dietary products. We agree with Barnard that the Harvard Nurses' Health Study (10), a study based on dietary recall, failed to support the idea that a high dietary intake of calcium reduces the incidence of fractures.
REFERENCES
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