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PEDIATRICS Vol. 110 No. 4 October 2002, pp. 826-832


COMMENTARY

Milk: Can a "Good" Food Be So Bad?

Abbreviations: NSLP, National School Lunch Program • PCRM, Physicians Committee for Responsible Medicine • PETA, People for the Ethical Treatment of Animals • AAP, American Academy of Pediatrics

Since at least the turn of the 20th century, the value of milk as a nutrient-dense food for children has been reflected in documents that call for its inclusion in public feeding programs (Table 1). In 1909, children in Cleveland who participated in summer programs were offered a meal of "bread, and jam and a hot dish" and could get milk in the mornings "on orders from the medical inspector." A year later, home economics classes in Boston prepared sandwiches and milk for elementary school children 2 days each week. By June 1940, federal funds were allocated to provide milk for children in 15 Chicago elementary schools. The price to children was 1 cent per half-pint, with subsidies from private donations available for those who could not pay. The half-pint container of milk became a lunchtime staple for millions of North American children in 1943, when the milk program was made part of the federal school lunch program. And after President Harry Truman signed the National School Lunch Program (NSLP) into law in 1946, a half-pint of milk was 1 of 5 required components in a type A lunch, which was designed to meet one third of a child’s daily nutritional requirements. Children whose schools did not participate in the NSLP could purchase milk at the subsidized price of 3 cents per half-pint.1 In the 1950s, federal milk subsidies to school milk programs served the dual purpose of promoting a healthful food and using agricultural surpluses.1


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TABLE 1. Emphasis on Milk in Early Child Feeding Programs in the United States—Selected Examples

 
US dietary guidance documents consistently have included dairy products as one component of a healthful diet. Nonetheless, milk consumption has been falling and with it, adequate intake of calcium, which is essential for bone health. The decline is associated with several factors, including the increased consumption of soft drinks and juice.2 Special interest groups have contributed to the problem as they promote research that suggests that milk consumption can cause serious and even life-threatening disease. Individual members have gone as far as to suggest that milk be eliminated from school feeding programs.

Although the primary agenda of the major interest groups is animal rights, members have found it more advantageous to focus on human health, because those arguments resonate with a far greater percentage of the population. This article presents the evidence for these arguments to provide the scientific framework against which to determine whether it is necessary to reexamine the national guidelines for dairy products as a way to insure adequate calcium consumption, with a particular focus on children. We review the studies that explore the links between milk consumption and both type 1 diabetes mellitus, and lactose intolerance. These 2 topics, more than any other myths associated with risks of milk consumption, have received major and extended coverage in the media and have raised broad concerns about the safety of milk for children. To examine these claims, we conducted Medline searches of the literature published on those topics in refereed journals. Anti-milk advocacy organizations have argued that it is quite feasible to consume the nutrients in milk from alternative foods. To address that claim, we examine the appropriateness of calcium supplements and calcium-fortified foods that are available in increasing variety as replacements for milk in the diets of children.

HOW DID MILK MAKE IT TO THE 10 O’CLOCK NEWS?

The scientific arguments concerning the prevalence of lactose intolerance and a possible link between milk and type 1 diabetes mellitus have received considerable attention from the media over the past several years. Groups like the Physicians Committee for Responsible Medicine (PCRM) and People for the Ethical Treatment of Animals (PETA) have used scientific evidence related to both of these conditions, and more recently, studies that identify a link between milk consumption and prostate cancer, to support their claims. Formed in 1985, PCRM includes nearly 5000 physicians and 100 000 laypersons and promotes preventive medicine, higher ethical standards for research, broader access to medical services, and a plant-based diet. In December 1999, PCRM filed a lawsuit against the Advisory Committee to the US Department of Agriculture/Department of Health and Human Services Dietary Guidelines for Americans, claiming that members of the committee had inappropriate ties to the meat, egg, and dairy industries that biased their ability to objectively evaluate the Dietary Guidelines. These guidelines are the basis for federally funded nutrition programs, such as the School Breakfast Program, the NSLP, the Food Stamp Program, and the Special Supplemental Nutrition Program for Women, Infants and Children. With the exception of the Food Stamp Program, milk is a component of each of these programs. PCRM requested that the Advisory Committee modify its recommendation of 2 to 3 servings of dairy foods a day to include other sources of calcium, including soy-based beverages, tofu, and fortified juices. They believe the Dietary Guidelines are insensitive to the health needs of minorities, 75% of whom worldwide experience some degree of lactose intolerance, and that the Dietary Guidelines should support plant foods, such as green leafy vegetables and legumes, as alternative sources in meeting the daily calcium requirement.

In February 2000, the Advisory Committee agreed to recommend calcium-fortified soy milk as an alternative to milk in the Dietary Guidelines that were about to be released, although absorption of calcium from fortified soy milk is reportedly not comparable with that of cow’s milk.3 PCRM then dropped the portion of its lawsuit concerning the composition of the Advisory Committee’s membership. In the final version of the Dietary Guidelines 2000, the language reads Milk, Yogurt, and Cheese Group (Milk Group), and a footnote explains that "... one cup of soy-based beverage with added calcium is an option for those who prefer a nondairy source of calcium."4

PETA, the other of the 2 anti-dairy activist groups, believes it is unethical to drink milk because of the abuse inflicted on commercial dairy cows. In March 2000, PETA parodied the America’s Dairy Farmers and Milk Processors "Got Milk?" campaign with "Got Beer?" This campaign encouraged college students to boycott milk in favor of beer. PETA supports the substitution of calcium-fortified juices, soy milk, and rice milk for regular milk and used the "Got Beer?" campaign to assert that even beer is more nutritious than milk. In response to substantial public outcry, the campaign was dropped from college campuses. It was replaced with "Dump Dairy," a campaign featuring advertisements for "missing" cows, a play on efforts to locate missing children by displaying their photographs on milk cartons.

In 1999, the question of whether milk should be the primary source of calcium in school-feeding programs became a political issue in Massachusetts. State Senator Dianne Wilkerson of Boston endorsed the efforts of PCRM and supported the replacement of milk with calcium-fortified beverages. Wilkerson argued that children with lactose intolerance who drink milk during the school day experience decreased academic performance. At that time, she proposed a bill authorizing the State Departments of Public Health and Education to appoint an advisory committee that would jointly review the federally funded programs of which milk is a component and to assess whether adequate provision is made for people with lactose intolerance. The bill was approved by the Massachusetts State Legislature. The advisory committee authorized by that bill considered the relevant evidence and concluded that both the Department of Education and the Department of Public Health have basic policies that offer an appropriate selection of calcium-rich foods, including alternatives to regular dairy products, to federally funded programs for children.

MILK CONSUMPTION AND TYPE 1 DIABETES: IS THERE A CONNECTION?

Since the hypothesis of a relationship between milk consumption and type 1 diabetes was first proposed nearly 2 decades ago, research has focused almost exclusively on feeding practices during the first year of life. The results of those studies, which include both animal experiments and observations in humans, remain inconclusive.518 The applicability of animal studies to human populations is uncertain, and observational human studies are susceptible to recall bias, selection factors, and confounding. Nonetheless, in 1994, the American Academy of Pediatrics (AAP) modified its infant feeding guidelines to include recommendations for those at risk of type 1 diabetes. Specifically, families with a strong history of type 1 diabetes were "strongly encouraged" to avoid feeding commercially available cow’s milk formula to infants. Substitution of soy-based formulas for all infants, regardless of risk category, was not recommended because of animal studies linking soy protein intake to the development of type 1 diabetes.19

In 2000, the Juvenile Diabetes Research Foundation International issued a position paper concluding that there is no compelling scientific evidence to support the claim that drinking cow’s milk increases the risk of type 1 diabetes in children or adults.20

In the past decade, 3 studies with relatively strong designs have reported data related to the cow’s milk hypothesis. The Diabetes Autoimmunity Study in the Young is a cohort study comprising siblings and offspring of persons with type 1 diabetes.14 Initially analyzed as a case-control study, at baseline participants included 18 children ranging in age from 9 months to 7 years with subclinical ß cell immunity (a condition that precedes the development of type 1 diabetes). Consumption of cow’s milk, other dairy foods, cereal, fruit, vegetable, or meat protein by either 3 months or 6 months old did not differ between cases and controls. Contrary to what the cow’s milk hypothesis would predict, children with ß-cell autoimmunity were breastfed slightly longer than controls (P < .07). As a nested case-control study, in which the investigators apply the case-control method to prospective data, this study avoids the potential for bias attributable to differential recall. However, its statistical power is limited by the small numbers of study subjects with ß-cell immunity.

The Childhood Diabetes in Finland study used a prospective design, which avoids potential recall bias.12 Investigators enrolled 725 unaffected siblings between the ages of 3 and 19 along with 801 children newly diagnosed with type 1 diabetes. Because genotyping for the HLA class II alleles thought to be involved in type 1 diabetes was available on a disproportionate number of children who progressed to clinical diabetes, the data were analyzed in a nested case control design, rather than as a classic prospective study. Controls matched on critical factors were selected from among the siblings who did not progress to type 1 diabetes during the follow-up period. Although the proportion of cases and controls who had been breastfed for at least 2 months or had received cow’s milk supplement before 2 months old did not differ between cases and controls, a larger proportion of cases had consumed 3 or more glasses of milk daily before entering the study. More than twice as many cases as controls carried the risk conferring HLA allele. In the presence of these markers, the relative risk associated with high consumption of milk in childhood exceeded fivefold. Although the broad age range of the subjects in this study is wide and the data do not permit an examination of the relationship between time of milk exposure and age at onset of the disease, these data support the hypothesis that there may be a subset of at-risk children for whom cow’s milk consumption promotes the development of type 1 diabetes.

Lastly, a second case-control study, The Finnish type 1 Diabetes Prediction and Prevention Study, identified almost 3000 infants at genetically increased risk for the development of type 1 diabetes by their HLA status.13 The interim report was based on the first 65 infants to become islet cell antibody-positive before age 4 and 390 control children who were islet cell antibody-negative. Short-term breastfeeding (<2 months) and the early introduction (<4 months) of cow’s milk or cow’s milk-based infant formula each independently predisposed genetically susceptible young children to progressive signs of ß-cell autoimmunity. These findings are entirely consistent with the current AAP infant feeding recommendations, but have no real relevance to milk consumption in school-aged children.

Although there may be a role for milk proteins in ß cell autoimmunity in a subset of high-risk children who have the HLA allele, the reaction could well be nonspecific. The autoimmune response may be a reaction to the early introduction of anything other than breast milk or infant formula. In addition to identifying persons who are genotypically at risk, Harrison and Honeyman15 argue for a role for immune mucosal function in the development of type 1 diabetes. Based on their review of the literature, they conclude that apparent heightened immunity in children with the HLA allele is not specific to cow’s milk, but reflects enhanced immunity to dietary proteins in general. They suggest it would be more fruitful to explore immune function in mucosal tissue and its relationship to the etiology of type 1 diabetes. From this perspective, the observed protective effects of breastfeeding would originate with constituents in breast milk that promote intestinal wall maturation, whereas the observed detrimental effects of cow’s milk proteins would reflect impaired mucosal function and would be nonspecific. This hypothesis would explain many of the seemingly contradictory observations, including the potent diabetogenicity of plant-based proteins found in soy and wheat.

At the time AAP released their statement, they called for a prospective, randomized trial to determine the relationship between cow’s milk consumption and diabetes. Seven years later, the only 2 prospective studies we found12,14 were not randomized.

The issue could not be put to rest entirely, however, without an intervention trial. Fortunately such a trial is getting underway. Funding for an international randomized, controlled study designed to identify any possible role of cow’s milk in the development of type 1 diabetes in children who are genetically at risk was awarded to several research groups in October 2001. That multicenter trial, which is planned to last at least 5 years, will provide the data that are necessary to more definitively address any remaining question about a relationship between cow’s milk and type 1 diabetes.

Given evidence available at the present time, it would seem that type 1 diabetes develops in only 5% of individuals at risk based on familial disease; proteins in wheat and soy seem to be more potent diabetogens than those found in milk; and that the critical timing of exposure to potential diabetogens remains unclear. There are clearly insufficient data to support the claim that milk contributes to type 1 diabetes in school-aged children.

LACTOSE INTOLERANCE: THE EXTENT AND PRACTICAL IMPLICATIONS OF THE CONDITION

It is difficult to precisely track the beginnings of the perception that milk should be eliminated from the diets of large groups of minorities, which is the argument used by groups who advocate broadening the dairy guidelines within federally funded feeding programs. In all likelihood, it was set in motion when the consumer press began to widely publish the results of studies that were based on diagnostic procedures that exaggerated the extent of lactose intolerance.21 Advertisements for lactose-free products may have further contributed to confusion about the severity of the problem.

Lactose intolerance is the inability to completely digest lactose, the sugar in milk. In the small intestine, the enzyme lactase splits lactose into 2 simple sugars, glucose and galactose. If insufficient lactase is produced and lactose is not digested, it travels to the large intestine where it is fermented by bacteria into organic acids and gas. This gas, along with the osmotic effect of unabsorbed lactose and water, is responsible for the symptoms of lactose intolerance, which can include abdominal fullness, cramps, and diarrhea.22

The prevalence varies across different ethnic groups, but ~25% of American adults experience some degree of lactose intolerance.2326 The severity of symptoms also varies, ranging from quite mild to severe. Curiously, severity of reported symptoms is not consistent with intestinal lactase activity.

Lactose intolerance is easily diagnosed by a hydrogen breath test, which is a reliable, economical, and noninvasive procedure. Patients are given a test dose of 12 g of lactose, the amount present in a single cup of milk. The breath is then measured for hydrogen, which is produced as bacteria ferment the undigested sugar. Patients may also be asked to describe their symptoms during the test. Of note is that in double-blind studies, the relationship between the existence of lactase deficiency and symptoms reported is inconsistent. Many people with low lactase levels report little discomfort, whereas others with no demonstrated deficiency report significant discomfort.27

To complicate the picture further, many individuals self-diagnose the condition without confirmation of the diagnosis by hydrogen breath test.2830 They may completely avoid milk and other dairy foods, despite the fact that clinical studies do not support such drastic measures even among those in whom a diagnosis of lactose intolerance has been confirmed. Simply anticipating the possibility of discomfort may cause individuals to experience abdominal pain and cramping after eating dairy foods. Children of parents who are lactose intolerant may learn to avoid milk and to consider it a cause of abdominal discomfort, regardless of whether they can digest lactose.31

Some individuals suffering from abdominal distress mistakenly attribute their discomfort to lactose intolerance when they are actually suffering from irritable bowel syndrome, a condition that has no known cause.27 Acute gastrointestinal illness can cause temporary lactose intolerance and may lead to continued, unnecessary avoidance of milk. The problem is compounded even further by the common perception that lactose intolerance is an "allergy." Because so many people recognize the need to avoid the offending food in the case of true food allergies, this has translated to "avoidance" as the appropriate treatment for lactose intolerance.

A large series of studies that included minorities, adults, and children found that 1 to 2 cups of milk was tolerated with few or no symptoms in most lactase-deficient subjects when the milk was spaced evenly throughout the day and consumed with food.22,23,3136 In one double-blind, randomized, crossover design trial, African American, Asian, white, and Hispanic middle-aged women with and without lactose intolerance consumed ~1300 milligrams of calcium from 2 cups of either lactose-free or regular milk, 56 g of cheese, and 1 cup of either lactose-free or regular yogurt.36 More than two thirds of the lactose-intolerant women reported that their symptoms were milder than expected between the 2 treatment periods. Half said they would be willing to continue consuming these dairy foods to meet their calcium requirement. These findings have recently been replicated in younger African American adolescents.37 These findings should not be surprising given the results of studies conducted among African tribesmen, such as the Masai >20 years ago. Among these people, the prevalence of lactose intolerance has been estimated to reach over 60%, but they routinely consume considerable quantities of milk without symptoms.38

In controlled studies, it has been demonstrated that people who have trouble digesting lactose can improve their tolerance by consuming at least some dairy products that contain lactose.39 In the study of African American adolescents,37 subjects with lactose maldigestion tolerated a diet rich in dairy foods. Subjects in that study demonstrated a decrease in breath hydrogen with increased dairy consumption. For those who associate milk consumption with symptoms, dairy alternatives exist. These include hard cheeses, yogurt, and the large variety of lactase-treated dairy products and lactase tablets.

IS IT FEASIBLE FOR CHILDREN TO ACHIEVE ADEQUATE AMOUNTS OF CALCIUM WITHOUT MILK AND MILK PRODUCTS?

Most anti-milk advocates recognize the importance of calcium in the diet of children. However, they argue that it is relatively simple for children to get adequate calcium without consuming dairy products. This approach raises several questions. First, is it feasible to provide adequate amounts of calcium from nondairy foods? Second, what is the role of calcium-fortified foods in meeting requirements for this nutrient? Third, is it appropriate to disregard the other nutrient contributions of milk, aside from calcium? And finally, are calcium supplements a viable alternative for children?

Milk and other dairy products contribute >70% of the calcium intake in the United States. The Adequate Intake for children is 1300 mg per day. Three cups of milk provide 900 mg, and the rest can be consumed in a varied diet. Achieving that level of intake without dairy products requires careful attention to selection of foods that naturally contain some calcium and others to which it is added. Unfortunately, calcium is found in significant amounts in relatively few foods. These foods are not consumed consistently in large amounts by most of the population and tend not to be popular with children (Table 2).


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TABLE 2. Alternative Nondairy Sources of Naturally Occurring Calcium and From Foods Fortified With Calcium

 
Variation in the bioavailability of calcium in foods further challenges the goal of meeting requirements without dairy foods. Bioavailability refers to the amount of calcium available for use by the body and that is dependent, in part, on both the calcium load and substances in food that bind calcium. The calcium in milk is ~30% bioavailable.40 Of the 300 mg of calcium in a glass of milk, 90 mg would expected to be absorbed. By comparison, accounting for calcium load size, to absorb that amount of calcium from broccoli, a vegetable in which calcium is highly bioavailable, it would be necessary to consume two and one fourth cups.41

Calcium binders such as oxalic acid—found in vegetables such as rhubarb, spinach, chard, and beet greens—and phytic acid, found in the outer layers of cereal grains, drastically reduce calcium’s bioavailability.40,4245 A cup of spinach, for example, provides >240 mg of calcium, but to absorb an amount of calcium equal to that in milk, it would be necessary to consume over 8 cups.41

Major brands of calcium-fortified orange juice contain the same amount of calcium per unit volume as milk, but use different calcium compounds. Published data on the bioavailability of these compounds in the juice are lacking. Since the introduction of calcium-fortified orange juice several years ago, calcium has been added to a number of juices and to other foods. Other fortified juices typically contain 100 mg of calcium per serving (Table 2). Routine dependence on these fortified foods requires careful planning to ensure that children will consume adequate amounts of the mineral.

Even if fortified orange juice was the primary source of calcium, a child would need to drink 3 cups of juice to obtain the amount in 3 cups of milk. According to the most recently available data, only 1 in 5 elementary school age children consumes any citrus juice and on average, the amount consumed is under 2 ounces.46 There are no data as to how much of the juice consumed by children is calcium-fortified. If children were to consume the 3 cups of fortified juice, it would provide 330 calories, about the same amount that would be provided in an equivalent amount of 1% fat milk. For a 10-year-old child, that represents 16.5% of total calories, but few of the other nutrients found in milk. Milk is an inexpensive source of high-quality protein and provides 31% of the riboflavin in the American diet. Fluid milk is also routinely fortified with vitamins A and vitamin D. In fact, milk is the only significant food source of Vitamin D, a nutrient critical to the utilization of calcium that is particularly important in winter months.

Fortified soy milk represents another potential alternative source of and is often recommended by anti-milk advocates. Unfortunately, these products vary in their nutrient profiles. Moreover in our experience, relatively few children readily accept them. Although fortified soy milk products represent a potential alternative, until there are standards for nutrient fortification of these foods, they should not be encouraged except in specific cases and selected with guidance from the pediatrician or nutrition professional.

A policy that promotes calcium supplements as a dietary alternative for children brings other problems, as well. For many families, it would represent an additional expense they could not afford. Moreover, we have been unable to find published studies that document the level of compliance with the use of calcium supplements, and there is no basis to suggest that calcium supplements would be a reasonable alternative for children.

SHOULD THERE BE A CHANGE IN NATIONAL FEEDING PROGRAM POLICIES REGARDING THE PROVISION OF MILK?

A rational look at the risks and benefits of consuming milk and milk products suggests that the current guidelines to insure adequate calcium intake are grounded in strong science. Calcium intake is already insufficient in the United States, where osteoporosis is a major and rapidly growing public health problem. Although it does not seem reasonable to insist that children who do not want to drink milk be required to take it anyway, milk should be available to all who choose it and efforts to promote consumption among school-aged children should continue. The argument that milk consumption in childhood "causes" type 1 diabetes is equivocal at best. The claim that milk causes children to suffer discomfort so severe that it disrupts their ability to learn is exaggerated. For those who do experience discomfort associated with milk consumption, alternatives are already available in some school systems and should be made available in others.

If we believe that youngsters should understand that a variety of foods from several basic groups of food are the foundation of a healthful diet, then we should communicate that message in the classroom, in the school feeding environment, and in the home. It is a relatively easy task to teach them that calcium is critical to the health of their skeleton and that the major source of calcium is milk and milk products. It is a far more difficult task to teach children that they can sometimes obtain calcium from such foods as breakfast bars, waffles, orange juice, and an increasingly long list of other foods where calcium is not normally found but to which it may be added. Although it is possible to consume adequate dietary calcium without dairy products, to do so requires acceptance of careful planning and monitoring by parents and caregivers and consumption of large amounts of foods that are typically not a regular part of the diets of most children in the United States. Such a major shift in food consumption patterns seems unlikely.

Jeanne P. Goldberg, PhD, RD and Sara C. Folta, MS

Center on Nutrition Communication
Gerald J. and Dorothy R. Friedman School of Nutrition Science and Policy
Tufts University
Boston, MA 02111

Aviva Must, PhD*,{ddagger}

* Department of Family Medicine and Community Health
Tufts University School of Medicine
{ddagger} Jean Mayer USDA Human Nutrition Research Center on Aging at Tufts University
Boston, MA 02111

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FOOTNOTES

Received for publication Nov 30, 2001; Accepted May 9, 2002.

Reprint requests to (J.P.G.) Center on Nutrition Communication, Gerald J. and Dorothy R. Friedman School of Nutrition Science and Policy, Tufts University, 68 Harrison Avenue, 5th Floor, Boston, MA 02111. E-mail: jeanne.goldberg{at}tufts.edu

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PEDIATRICS (ISSN 1098-4275). ©2002 by the American Academy of Pediatrics

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