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6 Nutrition Label Content Beyond the issue of the specific foods to be covered by nutrition labeling requirements is the actual information that should be provided on food labels. The current nutrition information panel contains information on calories, protein, fat, carbohydrate, sodium, and percentage of the U.S. Recommended Daily Allowances (U.S. RDA) for protein and seven vitamins and minerals (21 CFR 101.9; USDA, 1989~. Over information about the nutrient content of foods frequency may be obtained from the ingredient listing and from nutrient descriptors found on the principal display panel of food labels (see Chapter 7~. In light of the findings and recommendations in The Surgeon General's Report on Nutrition and Health (DHHS, 1988) and the National Research Council (NRC) report, Diet awl Health: Implications for Reducing Chronic Disease Risk MARC, 1989a), this information is at once incomplete and excessive. The Committee was directed to consider recommendations for food labeling reform based on the knowledge of nutrition in relation to long-term health contained in these reports. For nutrients and other food components currently included or proposed for inclusion on the nutrition information panel, this chapter describes their health relevance, dietary recommendations, current provision of labeling information, and the Committee's recommendations for nutrition labeling. Comprehensive information on dietary sources of nutrients and dietary intake patterns are provided in Chapter 4. 158

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NUTRITION LABEL COSTED 159 CALORIES Health Relevance of Calories Scientists, consumers, and food manufacturers all acknowledge that the information about calories per serving is one of the key elements of the nutrition information panel. Because of this consensus, only the highlights of current scientific evidence are provided in the discussion that follows. There is consensus among health care professionals Hat obesity (defined as excess body fat) is associated with excess morality. Nutrition and Your Health: Dietary Guidelines for Americans (IJSDAIDHHS, 1985), the Surgeon General's report (DHHS, 1988), the NRC Diet and Health report (1989a), and the Report of the Dietary Guidelines Advisory Committee on the Dietary Guidelines for Americans (USDA, 1990) emphasize the importance of maintaining a healthy or desirable weight to minimize the risk for chronic diseases such as diabetes, coronary heart disease (CHD), stroke, hypertension, and certain Apes of cancer. The causes of obesity include genetic factors, diet, and inactivity. In experimental animals, diets high in fat promote obesity (Schemmel et al., 1970~. It is not clear how caloric density and diet composition influence obesity in humans. An estimated 34 million American adults are obese (based on a standard of greater than 20 percent in excess of desirable body weight), and more than 80 million Americans are trying to control their weight (CCC, 1985~. In order to maintain a stable body weight, caloric intake must be in balance win energy expenditure. Methods used to lose weight emphasize the need to decrease caloric intake and increase energy expenditure (Kayman et al., 19903. Provision of information on the caloric content of food products may be useful not only for obese individuals trying to lose weight but also for those who are trying not to gain excess weight. The number of calories in a food is the one component of the food label that consumers seem to understand. Current Provision of Desired Information Information about calories often is found in two places on the food label: the nutrition information panel and He principal display panel. C)n the nutrition information panel, the Food and Drug Administration (FDA) and the U.S. Department of Agriculture (USDA) require the disclosure of total calories per seeing, expressed as kilocalories (21 CF~ 101.9(c)~3~. The principal display panel may include nutrient descriptors that are regu- lated by FDA and/or USDA, such as low calorie, reduced calorie, diet, sugar free, and no sugar, with some minor differences (21 CF11 105.66(c), (d), `fl; USDA, 1982a). Some descriptors may be misinterpreted by the consumer to imply that a food is low in calories. There is a need for more uniform use of the terms light and lite with respect to the caloric content of foods to avoid con-

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160 Nl~lWTION LABEl1NG sumer confusion (NRC, 1988), since four government agencies (FDA, USDA, the Federal Trade Commission ~Cl, and the Bureau of Alcohol, Tobacco, and Firearms) have jurisdiction over products Hat carry these terms. The noncaloric use of these terms is discussed in Chapter 7. For the purposes of marketing and nutrition education, some manufacturers are currently declaring calories in terms of the food's contribution to the total number of calories to be consumed in a day. One example is the increasing number of packaged foods designed to be eaten as a single meal and the use of various reference standards for total daily calories. The establishment of a single daily standard for calories for any purpose, including labeling, is difficult given the wide range of average caloric intakes for adults. However, if manufacturers are going to refer to the total number of calories to be consumed in a day, Hen a reference standard needs to be established. Committee Recommendations The Committee recommends that: FDA and USDA should continue to require the disclosure of calories expressed as ldlocalories per serving on the nutrition information panel. If the manufacturer chooses to express nutrients as a percentage of total calories, 2,000 calories should be used and stated as the reference point for the average adult who engages in light physical activity. This amount will overestimate the needs for some individuals (e.g., many women) and underestimate the needs for others (e.g., many men). A daily reference standard based on a population average of 2,350 calories has been proposed by FDA (55 ~d. Reg. 29,476-29,533, July, 19, 1990), but a 2,0(X) OCR for page 158
NUTRITION LIBEL CONTENT 161 that dietary saturated fatty acid intakes be reduced in order to reduce plasma cholesterol levels and thereby reduce the incidence of and mortality from CHD and related conditions. The specific recommendation has usually been to reduce total fat intake to 30 percent or less of total calories and saturated fatty acid intake to less than 10 percent of total calories (NRC, 1989a). Although it is widely believed that even lower total fat and saturated fatty acid intakes would be more beneficial, there has been concern about the palatability of foods with lower levels of fat content. Because no human populations that consume large proportions of polyunsaturated fatty acids (more than about 10 percent of total daily calories) have been adequately studied, and because some observations in experimental animals have suggested that polyunsaturated fatty acids might contribute to cancer, recommendations regarding fat intake usually include a limit on polyunsaturated fatty acid intake to about 10 percent of total calories. The American Heart Association (AMA, 1986), the Surgeon General's report (DHHS, 1988), and the NRC Diet and Health report (NRC, 1989a) included recommendations to limit cholesterol intake to 300 mg daily as a means of lowering plasma cholesterol concentrations and thereby preventing atherosclerotic disease. Rods of Fat and Cholesterol in the Body Fats and Oils Fats and oils are complex organic molecules that are formed by combining three fatty acid molecules with one molecule of glycerol. Generally, fatty acids are straight chains of carbon atoms with two hydrogen atoms bound to most carbon atoms, but they vary in chain length and in the number of double bonds between carbon atoms. Generally, fatty acids in animal and plant tissues range from 4 to 24 carbon atoms. Those with no double bonds are called saturated fatty acids, those with one double bond are called monounsaturated fatty acids, and those with more than one double bond are called polyunsaturated fatty acids. Fats containing predominantly saturated fatty acids are solid or viscous at room temperature; those containing predominantly monounsaturated or polyun- saturated fatty acids are liquid at room temperature. One polyunsaturated fatty acid, linoleic acid, which has 18 carbon atoms and two double bonds, is an es- sential nutrient because it is necessary for normal cellular function but the body cannot synthesize it; other fatty acids required by mammals can be synthesized by the body. The principal function of fatty acids consumed in the mammalian diet is energy. Fats stored in adipose tissue provide a long-term reserve source of energy, because they produce about twice as much energy per unit of mass as protein or carbohydrate does. Fats and oils also greatly affect the taste, consistency, stability, and palatability of foods. Humans prefer foods containing

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162 NUTRITION LABELING more than 15 percent fat (by weight, about 30 percent of calories), even though 5 percent fat in the diet (by weight, 10 percent of calories) is nutritionally adequate. The U.S. population currently consumes about 36 percent of its calories from fat (LSRO, EASES, 1989). Fats and oils in Americans' diets are derived from plant and animal sources. Generally, saturated fatty acids are derived from meat and daily products, whereas mono- and polyunsaturated fatty acids are derived from plant sources. Three exceptions are palm, palm kernel, and coconut oils, which are quite rich in saturated fatty acids. Cholesterol A quite different material than fats and oils, cholesterol is commonly classified among the lipids. It is a large molecule composed of several six-carbon rings joined together at their sides and with other structures joined to the outside rings. Cholesterol is an essential component of mammalian tissues, but it is synthesized in the body and is not an essential nutrient. Cholesterol is used to produce body hormones and cellular structures, but not for energy. It has no taste and its presence or absence does not affect the palatability of foods. Currently, U.S. intakes by men and women range between 304 and 435 mg/day (NCEP, 1990~. Health Effects of Dietary Fat and Cholesterol Coronary Heart Disease Evidence that dietary fat or cholesterol was involved in causing atherosclerosis and CHD first appeared early in the twentieth century, at about the same time that myocardial infarction was identified as a distinctive clinical syndrome and was found to be related to atherosclerosis and thrombosis of the coronary arteries. Almost no attention was directed toward diet as a possible cause of atherosclerosis or its major clinical sequela, CHD, until after World War II, when it became apparent that this disease had reached epidemic proportions in the industrialized countries. In the Scandinavian countries, heart disease rates declined ~amadcally during World War II, a period when foods rich in fat were in short supply (Keys, 1975). Retrospective case-control studies also revealed that CHD was associated with serum cholesterol concentrations and that the senile cholesterol concentration was controlled, in part, by the amount and type of fat and cholesterol in the diet. International comparisons, studies of migrant populations, and observations of vegetarians showed that saturated fatty acid and cholesterol intakes were associated with CHD rates, but these correlations were often confounded by other differences in life-style. Many controlled experiments in humans and animals have demonstrated that saturated fatty acids and cholesterol in the diet elevate serum cholesterol concentrations, and when saturated fatty acids were replaced with monounsat-

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NzrrRlTIoN LABEL conquer 163 u~a~ and polyunsaturated fatty acids, serum cholesterol concentrations were lowered (NRC, 1989a). A massive research project, the National Diet Heart Study, showed that serum cholesterol levels could be lowered in free-living populations by fat-modified diets. On the basis of early observations, AHA rec- ommended reductions in dietary saturated fatty acids in 1957 Cage et al., 1957y, and later it recommended reductions in dietary cholesterol intake (AMA, 1965~. The Surgeon General's report (DHHS, 1988) and the NRC Diet and Health report (NRC, 1989a) reaffirmed these recommendations. The concentration of cholesterol in plasma (or serum) has been considered a major risk factor for CHD. Fat and cholesterol, which are insoluble in an aqueous medium, are carried in the blood within particles stabilized by specialized proteins (apolipoproteins). There are several distinct classes of lipoproteins in plasma, each containing different proportions of cholesterol and other fats. Subsequent epidemiological studies disclosed that the concentration of low- density lipoprotein (LDL) cholesterol was positively associated with the risk of CHD (Medalie et al., 1973) and that the concentration of high-density lipoprotein (HDL3 cholesterol was inversely associated with the risk of CHD (Gordon et al., 1977; Miller et al., 1977~. These associations were confirmed in animal experiments and in postmortem human studies relating plasma lipoprotein cholesterol concentrations to atherosclerotic lesions (Solberg and Strong, 1983~. Thus, it became important to distinguish between the effects of LDL and HDL cholesterol concentrations. Evidence Regarding Saturated Fatty Acids In 1952, two independent groups of investigators- in the United States (Kinsell et al., 1952) and in Europe (Groen et al., 1952) discovered almost simultaneously that the saturation level of dietary fatty acids influenced plasma cholesterol concentrations. A large number of human and animal experiments subsequently confirmed that saturated fatty acids with chain lengths of 12 to 16 carbon atoms (lauric, myristic, and palmitic acids) were the most active in raising serum cholesterol concentrations, whereas fatty acids with chain lengths of 10 or fewer carbon atoms or 18 carbon atoms (stearic acid) had no effect. Investigators developed equations that consistently predicted (on average) the effects of changes in fatty acid intake on the plasma cholesterol concentration. Monounsaturated fatty acids, represented mainly by oleic acid, had little or no effect on plasma cholesterol concentrations compared with the effects of equivalent calories such as those from carbohydrate and, therefore, were omitted from these predictive equations. The predictive power was also increased when stearic acid was omitted from the intake of saturated fatty acids. Recent exper- iments have reconfirmed the observation that, although stearic acid contributes calories, it does not raise plasma LDL or HDL cholesterol levels (Bonanome and Grundy, 1988~. When saturated fatty acids are replaced by polyunsaturated fatty acids,

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164 NUTRITION LABELING represented in the diet mainly by linoleic acid, serum cholesterol concentrations are reduced to as low as and possibly lower than the levels produced by equivalent calories such as those from carbohydrate (NRC, 1989a). Recent experiments have also reconfirmed that oleic acid maintains LDL cholesterol concentrations at about the same level that polyunsaturated fatty acids do and showed that it does not lower HDL cholesterol levels (Grundy, 1987~. Thus, monounsaturated fatty acids might be included with polyunsamra~ fate acids in a computation of fatty acids that would be expected to produce more desirable plasma lipoprotein profiles. Several epidemiological comparisons found a strong association between average intakes of saturated fatty acids and mortality from CHD (Keys, 1975~. A low samurai fatty acid intalce (less than 10 percent of total calories) is common to all populations with low CHD rates. The results of correlations based on individual intakes within a population have been less consistent and conclusive. This discrepancy is attributed to the low range of intakes within each population and to the misclassification of dietary intakes and endpoints. The effects of dietary fatty acids on plasma lipoproteins and atherosclerosis have generally been confirmed in animal experiments. Another issue concerns the health effects of stearic acid, a samurai fatty acid. Unlike the other saturated fatty acids, it has been found that stearic acid does not elevate serum cholesterol levels. The results of early studies have been confirmed by recent experiments in humans; however, the controversy continues. Evidence Regarding Omega-3 Farm Acids In early research on the effects of polyunsaturated fatty acids on lipoprotein metabolism, investigators noticed that some of the highly unsaturated oils from marine sources were as effective as vegetable oils in lowering serum cholesterol levels. Years later, it was reported that Eskimos who consumed large quantities of fish had low rates of atherosclerotic heart disease. Renewed investigations showed that the effects on lipoprotein metabolism were due to the high proportions of omega-3 polyunsaturated fatty acids in oils from marine mammals. When these fatty acids are included in the diet, they dramatically reduce plasma triglyceride levels but do not seem to reduce LDL cholesterol levels unless they are substituted for saturated fatty acids (Woodward and Carroll, 1988~. They also affect the hemostatic system by altering platelet function and prostaglandin metabolism In ways that may reduce the risk of thrombosis (Herold and Kinsella, 1986~. The potential beneficial effects of omega-3 fatty acids have led to some recommendations that individuals should increase their consumption of fish oils that contain these substances in order to prevent atherosclerosis and thrombosis. However, many studies have also found some adverse effects for example, an increase in LDL cholesterol levels~nd neither the beneficial effects nor the safety of high intakes of omega-3 fatty acids have been thoroughly documented. The Surgeon General's report (DHHS, 1988) and the NRC Diet and Health

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NUTRITION LABEL CONTENT 165 report (NRC, 1989a) did not recommend increased intakes of fish oils as a means of preventing CHD. Fish oils and omega-3 fatty acids must be differentiated from fish as a food. Fish is widely recommended as an excellent source of protein Hat is low in fat, and in some epidemiological studies, fish consumption is inversely associated with cardiovascular disease (Kromhout et al., 1985~. Evidence Regarding Trams Fatty Acids When vegetable oils are hy- drogenated to make them more palatable as substitutes for animal fats, geomet- ric isomers of the unsaturated fatty acids called bans fatty acids are farmed. Because these isomers are not present in natural foods in the proportions Hat occur in hydrogenated fats, their effects on lipid and lipoprotein metabolism, plasma lipid levels, and atherosclerosis have been investigated intensively (NRC, 1989a). Although bans fatty acids lack any activity as essential fate acids, no deleterious effects have been demonstrated in humans, and no deleterious ef- fects have been found in animal experiments with levels of intake comparable to customary human intakes. There remains some possibility of a long-term effect of bans fatty acids on lipid metabolism, and this question should be reconsid- ered periodically as knowledge of lipid metabolism and the changes underlying chronic disease increases, but present knowledge provides no basis for limiting or reducing the current usual intake of bans fatty acids. Evidence Regarding Dietary Cholesterol Although the first evidence linking a dietary lipid with atherosclerosis came from experiments with rabbits in 1913, the discovery of the effects of saturated fatty acids on plasma cholesterol levels in 1952 overshadowed the potential effects of dietary cholesterol. Most animal species, including guinea pigs, swine, and several nonhuman primates (notable exceptions are dogs and rats), have been found to be sus- ceptible to the cholesterolemic effects of dietary cholesterol. Indeed, in animal models of diet-induced atherosclerosis, cholesterol seems to be more important than the type or amount of dietary fat. Epidemiological studies have almost invariably found strong correlations between dietary cholesterol intake, plasma cholesterol concentrations, and CHD (McGill, 1979~. However, there were also strong correlations of saturated fatty acid intakes with CHD, and multivariate analyses of the data usually resulted in nonsignificant correlations of dietary cholesterol intake with CHD rates. Cross-sectional dietary studies, designed to test individuals within a popu- lation for the association between dietary intakes and plasma cholesterol levels, usually found no association between dietary intakes of cholesterol and plasma cholesterol or lipoprotein concentrations. These negative results were considered inconclusive based on the limited range of dietary intakes found within popula- tion groups (in contrast to the wide ranges of mean intakes between population

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166 NUTRITION LABELING groups), and also because measurement error seriously degraded correlations based on individual values. The independent effect of dietary cholesterol is an important issue, because one widely produced and consumed food, the egg, is rich in cholesterol but contains only moderate amounts of saturated fatty acids. Beginning in about 1960, a number of carefully controlled experiments in humans measured plasma cholesterol levels (and later, LDL and HDL cholesterol concentrations) in individuals fed diets containing varying amounts of cholesterol. Eventually, a consensus indicated that dietary cholesterol did affect plasma cholesterol levels, particularly LDL cholesterol levels, independent of total fat intake and type of fat. Furthermore, several long-term cohort studies of humans have recently reported that reliable estimates of dietary cholesterol intake, when expressed as milligrams per 1,000 kcal, were positively correlated with the incidence of CHD during subsequent years of follow-up (Shekelle et al., 1981; Stamler and Shekelle, 1988~. The correlations were independent of the plasma cholesterol levels. These results suggest the possibility that dietary cholesterol might influence atherosclerosis or its clinical manifestations by some mechanism other than elevation of LDL cholesterol levels. Cancer There is less evidence linking total dietary fat and saturated fatty acids to cancer than to heart disease, but the accumulated epidemiological evidence does suggest that dietary fat intake is associated win the risk of colon, prostate, and ovarian cancers and, possibly, with breast cancer (NRC, 1982, 1989a). Animals fed high-fat diets are more likely to develop cancers of the breast, intestinal tract, and pancreas than are those fed low-fat diets. In animals, polyunsaturated fatty acids promote cancers more effectively than do saturated fatty acids, but high samurai fatty acid intakes also increase the probability of cancer in animals if the minimum requirement for polyunsaturated fatty acid intake is satisfied. Although dietary cholesterol intake is highly correlated with saturated fatty acid intake in humans, there is no evidence that either high or low cholesterol intakes are associated with cancer at any site. Some reports that low plasma cholesterol levels were associated with a higher risk of cancer led to concern about the potential adverse effects of plasma cholesterol-lowering diets, but these associations were thought to be due, in part, to low plasma cholesterol levels in early cancers that is, a result of the cancer rather than a precursor. Galibladder Disease Most gallstones occurring in the U.S. population are the result of the presence of excess secretion of cholesterol into the bile by the liver. Because

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NUTRITION LAME CONTENT 167 both dietary cholesterol and polyunsaturated fatty acids increase secretion of cholesterol by the liver, it has been hypothesized that these dietary components may be responsible for gallstones. Coding of cholesterol to some species of rodents causes gallstones. Obesity predisposes an individual to gallstone formation, presumably be- cause it is associated with increased secretion of cholesterol into the bile. How- ever, no epidemiological or experimental evidence In humans has directly im- plicated either dietary cholesterol or fat as a cause of gallstones. It is likely that some individuals who are genetically predisposed may be susceptible to He lithogenic effects of dietary fat or cholesterol, but these individuals cannot yet be identified (NRC, 1989a). Current Provision of Desired Information There are three locations on food labels that may provide useful information about fat and cholesterol, including the ingredient listing, He nutrition inforrna- tion panel, or descriptors of specific levels or Apes of fats and cholesterol on the principal display panel. Ingredient Listing Ingredients are required to be listed on a majority of packaged foods; this would provide information on food components that are fats and oils, whether derived from animal or plant sources (21 CFR 101.4(b)~14~; USDA, 1989~. The common or usual names of fats and oils would reveal fat sources; however, the current ingredient listing rarely provides information about the salivated fatty acid or cholesterol content for consumers seeWng this information. Ike use of weight as the criterion for listing ingredients may cause the consumer to overlook a more important measure, that is, the relative contribution of fats and oils to available calories in a food. For example, fats and oils provide more than twice the amount of calories per gram compared with protein and carbohydrate, but fats might not be listed first on the ingredient label because of their weight. However, the actual fats and oils present in a product can be difficult to determine. Until 1971, all fats were allowed to be listed generically on ingredient labels as '~vegetable shortening" by FDA and as "shortening" by USDA. When regulations that required listing of specific fats and oils by weight were proposed, a convincing case was made that product sources often change, depending on their availability and price. An individual listing was judged to be costly for manufacturers and, ultimately, for consumers, if labels had to be changed every time the source changed. The resulting compromise allows manufacturers to list fats and oils as they are contained in the product (by weight) or to list all those that might be used from time to time. Under this so-called "andJor" provision, any specific product would likely contain one or two of the oils listed

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168 NUTRITION LABELING The great disadvantage of "and/or" labeling of fats and oils is Mat many of the commonly used oils vary widely in fatty acid content. If coconut oil is the only oil used, over 80 percent of the fatty acid content of the product might be saturated; if rapeseed oil were chosen, the same product might have a fatty acid content that was less than 7 percent saturated fatty acids. Although fatty acid content varies among many of the commercial oils, functionality of the oil in many products such as baked goods limits the range of fatty acid content of oil that can be used. Nevertheless, the information that is clearly relevant to the product's composition and that many consumers consider important in planning their diets teas often been unavailable. Nutrition Information Pane] If a manufacturer chooses to or must provide nutrition labeling, the label must declare the amount of fat per serving in grams (21 CFR 101.9(c)~6~. Only if a claim about the fatty acid content is made must the content of saturated and unsaturated fatty acids be declared on the nutrition information panel, using the terms saturated fat and unsaturated fat. In this case, the percentage of total calories contributed by fats is required; however, the cholesterol content is not (21 CFR 101.25(c)~. If a claim regarding cholesterol is made, the amount per serving must be given on the label, but no specific information about the fatty acids need be listed (21 CF~ 101.25(b)~. As a result, foods rich in cholesterol but containing certain vegetable oils may describe their relatively low percentage of saturated fat without revealing the cholesterol content. For foods with a significant amount of vegetable fats, the fatty acid content may not be reported if there is a claim of the absence of cholesterol on the label. For food labels that provide either fatty acid or cholesterol content, FDA requires that the label indicate that such information is given for individuals who, on the advice of a physician, are modifying their dietary intake of fat andfor cholesterol (21 CFR 101.25(d)~. Since the 1986 proposal to regulate cholesterol-related terms, this requirement has not been enforced but is an indication of the specific subpopulation on which the concept of a low-saturated- fat, low-cholesterol eating pattern was originally focused Within the past 5 years, a national consensus on the efficacy of plasma cholesterol reduction in the prevention of CHD in the entire population has been reached that favors dietary modification as the first step in achieving a reduction in the risk of CHD. In July 1990, FDA issued a tentative final rule that included revised quantitative fat declaration and definitions with criteria for their use (55 Fed. Reg. 29,45~29,473, July 19, 1990~. The agency continued to use its existing rules on total fat content When fatty acid or cholesterol content is declared, both are to be declared immediately following the statement of fat content and

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192 N~r~TlON LABELING of white rice and white flour has not been implemented or low levels of dietary thiamin are associated with consumption of raw fish, whose intestinal microbes contain thiaminase. In the United States, thiamin deficiency is unlikely in healthy individuals but has been observed in individuals whose heals is otherwise compromised by such conditions as alcoholism, renal disease, chronic febrile infections, chronic intravenous feeding, or inborn errors in metabolism. Deficiency is associated with abnormalities of carbohydrate metabolism related to decreased oxidative deca~oxylations. The clinical condition associated with a prolonged deficient intake is beriberi, which is characterized by mental confusion, anorexia, muscle weakness, ataxia, peripheral paralysis, edema or muscle wasting (depending on the type of beriberi), tachycardia, and enlarged heart. The average thiamin daily intake is reported to be 1.75 mg by adult men, 1.05 mg by adult women, and 1.12 mg by children aged 1 to 5 (NRC, 1989b). A minimum of 1.0 mg/day is the recommended level for all adults (NRC, 1989b). An additional 0.4 mg/day is recommended throughout pregnancy for maternal and fetal growth as well as increased maternal caloric intake. An increment of 0.5 mg/day is recommended throughout lactation. The 1989 RDA allowance for infants is 0.4 mg/1,000 kcal; this increases to 0.5 mg/1,000 kcal for children and adolescents. Riboflavin In Nutrition Monitoring in the United States (LSRO, FASEB, 1989), n- boflavin was not considered to be a current public health issue. No specific recommendation concerning riboflavin was given in either the Surgeon Gen- eral's or NRC reports. This B vitamin functions primarily as a part of two Gavin coenzymes (flavin mononucleotide and Gavin adenine dinucleotide) that catalyze many oxidation- reduction reactions. Riboflavin is essential in the function of vitamin B6 and niacin. Riboflavin is readily absorbed in the small intestine. Deficiency is rare in the United States, but symptoms include oral-buccal cavity lesions, a generalized seborrheic dermatitis, and normocytic anemia Average reported intakes are 2.08 mg/day by men, 1.34 mg/day by women, and 1.57 mg/day by children ages 1 to 5 ARC, 1989b). A minimum intake of 1.2 mg/day is recommended for adults (NRC, 1989b). An additional intake of 0.3 mgiday is recommended during pregnancy; and 0.5 mg and 0.4 mg/day are recommended for the first 6 months and thereafter, respectively, for lactation. Because of the possibility of growth inhibition with inadequate intakes by children, the allowance is set at 0.6 mg/100 kcal for infants and approximately 1 mg/day for children.

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NlJTRITION lABF1 CONTENT Niacin 193 In Nutrition Monitoring in the United States (LSRO, FASEB, 1989), niacin was not considered to be a current public health issue. No specific recommen- dation concerning niacin was given in either the Surgeon General's or NRC reports. This nutrient functions in the body as part of two coenzymesnicotinamide adenine dinucleotide and nicotinamide adenine dinucleotide phosphate. These coenzymes are present in all cells and function as part of the metabolic processes of glycolysis, fatty acid metabolism, and tissue respiration. Pellagra is a deficiency disease characterized by dermatitis, diarrhea, inflammation of the mucous membranes, and ultimately, dementia. Pellagra was once a common nutritional disease in the United States but it is no longer a public health issue. Niacin occurs in the diet in high concentrations in meats. Conversion of tryptophan to niacin contributes to the dietary source pool for niacin. The conversion factor is 60:1 ~yptophan to niacin. As a result, mink and eggs are considerable sources of Iryptophan because it is converted to niacin. Niacin in processed cereal grains is biologically unavailable. However, fully synthetic niacin is added to fortified milled grain products, making them good sources. The calculated daily intakes of total niacin equivalents are 27 mg by women and 41 mg by men (NRC, 1989b3. The RDA for niacin is 15 mg/day for adult women and 19 mg/day for adult men. Dunng pregnancy and lactation, the increments are 2 mg/day and 3 mg/day, respectively. For infants under age 6 months, the RDA for niacin is 5 mg/day and increases to 6 mg/day until age 1. For children the niacin RDA climbs gradually to the adult levels. Vitamin B6 In Nutrition Monitoring in the United States (LSRO, FASEB, 1989), vitamin B6 was considered to be a potential public health issue. No specific recommen- dation concerning vitamin B6 was given in either the Surgeon General's or NRC reports. Vitamin B6 is comprised of various dielary compounds pyridoxine, pyri- doxal, pyridoxamine, their phosphate esters, and glycosylated forms of pyridox- ine. The various dietary forms are all absorbed by intestinal mucosal cells. In the liver, erythrocytes, and other tissues, these forms are conver~d to pyridoxal phosphate and pyridoxamine phosphate, which serve as coenzymes in transam- ination and numerous other reactions. Deficiency rarely occurs alone, but rather is seen in individuals who are deficient in several B-complex vitamins. Charac- teristics of severe deficiency include epileptiform convulsions, dermatitis, and anemia. Infants experience a variety of neurological symptoms and abdominal distress. Biochemically detected marginal vitamin B6 nutriture has been observed in certain subgroups of ~e U.S. population.

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194 NurRITIoN LABELING Although present in a number of foods, considerable losses of the vitamin occur during processing. Bioavailability varies widely and is influenced by food composition and certain drug interactions. The requirement for vitamin B6 increases as the intake of protein increases. Average vitamin B6 intake was 1.87 mg/day by adult males, 1.16 mg/day by adult females, and 1.22 mg/day for children aged 1 to 5 (NRC, 1989b). The RDA for vitamin B6 is 2.0 mg/day for men and 1.6 mg/day for women, win an average protein intake of 100 g/day and 60 gm/day, respectively (NRC, 1989b). However, the RDA would not be sufficient for individuals whose habitual protein intake is above the 90th percentile. During pregnancy an increase of 0.6 mg/day is needed, and during lactation an additional allowance of 0.5 mg/day is needed to compensate for additional protein requirements. During Be first 6 months of life, 0.3 mg/day is recommended and 0.6 mg/day is recommended for older infants. The recommendation is 1.0 mg/day for children aged 1 to 3, 1.1 mg/day for children aged 4 to 6, and 1.4 mg/day for children aged 7 to 10. Toxicity of vitamin B6 supplements has been reported at doses greater than 100 mg/day. Folate In Nutrition Monitoring in the Muted States (LSRO, FASEB, 1989), folate was considered to be a potential public health issue. No specific recommendation concerning folate was given in either the Surgeon General's or NRC reports. Folate functions metabolically as a coenzyme in the transport of single- carbon fragments from one compound to another in amino acid metabolism and nucleic acid synthesis. Deficiency of folate leads to impaired cell division and altered protein synthesis. Late consequences lead to overt megaloblastic bone marrow and macrocytic anemia. Folate is widely distributed in the food supply, being particularly rich in liver, yeast, leafy vegetables, legumes, and some fruits. However, up to 50 percent of food folate can be destroyed during food preparation, processing, and storage. Bioavailability is variable, depending on the physical form, and the presence of inhibitors, binders, or other factors in foods. The average daily intake is generally from 280 to 300 ,ug in the United States. The RDA for folate is 200 Mg/day for adult males and 180 ,ug/day for adult females (NRC, 1989b). These levels appear to provide normal tissue stores and other indicators of folate status. Due to the problems of adsorbability, the RDA during pregnancy is set at 400 Mg/day to accommodate increased requirements. During lactation the RDA is set at 280 Mg/day for the first 6 months of pregnancy and 260 Mg/day up to 1 year. For the first 6 months of life, the RDA is set at 25 ,ug/day and at 35 Mg/day up to age 1. For children, the RDA increases incrementally to the adult level.

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NurRrTloN labs collard Fluoride 195 The Surgeon General's report (1988) recommended that community water systems should provide fluoride at optimal levels for the prevention of dental canes. Diet and Health ARC, 1989a) advised that it is necessary to maintain an optimal fluoride intake, primarily during the years of tooth formation and growth. In Nutrition Monitoring in the United States (LSRO, FASEB, 1989), fluoride was considered to be a potential public health issue. This mineral is incorporated into bone and tooth enamel in the human body and is believed to be beneficial, if not essential, to dental health. The negative correlation between tooth decay in children and fluoride concentrations in Ming water was demonstrated nearly 50 years ago. Subsequent studies have confirmed that fluoridation of public water supplies is an effective and practical means of reducing dental canes. The protective effect against caries is greatest during ma~cunal tooth formation in the first 8 years of life. Evidence sugggests, however, Rat adults can benefit from continued consumption of fluoridated water. The richest dietary sources of fluoride are tea and marine fish consumed with their bones. Much of the fluoride intake depends on the effects of the water supply on beverages and food preparation where fluoridation is used. Absorption of fluoride is variable, creating difficulties in establishing dietary recommendations. Although no RDA has been established for fluoride, the estimated safe and adequate daily dietary intake ranges from 1.5 to 4 mg/day for adults (NRC, 1989b). For those in younger age groups, the range is set to a maximum level of 2.5 mg/day. Ranges of 0.1 to 1 mg/day are set for birth to 12 months, and 0.5 to 1.5 mg/day for ages 12 to 36 months. Z. In Nutrition Monitoring in the United States (LSRO, FASEB, 1989), zinc was considered to be a potential public health issue. No specific recommendation concerning zinc was given in either the Surgeon General's or NRC reports. Zinc is an essential mineral and is a constituent of several hundred enzymes that are involved in numerous metabolic pathways. Zinc status is subject to strong homeostatic regulation. Although large amounts are deposited in bone and muscle, the body pool of readily available zinc is small and has a rapid turnover rate. As a result, there is evidence that zinc deficiency has a rapid effect on cell growth and repair. The general signs of dietary zinc deficiency include loss of appetite, growth retardation, skin changes, and immunological abnormalities. Pronounced deficiency results in hypogonadism and dwarfism. Signs of marginal deficiency are manifested as slowed wound healing, hair loss, and impaired taste and smell acuity.

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196 NUTRITION LABELING The bioavailability of zinc from foods varies widely; animal products are good sources, whereas whole-grain products contain less available forms of the mineral. The interaction of zinc with dietary protein, physic acid, and copper may have practical significance in Americans' diets. The zinc content of typical diets of adults furnishes 10 to 15 mg/day (NRC, 1989b). Dietary intakes are lower than recommended levels in some groups DISCO, EASED, 1989~. Infants and young children consume diets containing about 5.5 to 8.5 mg of zinc per day. Elderly individuals generally consume from 7 to 10 mg of zinc per day. The RDAs for zinc for adult men and women are 15 mg/day and 12 mg/day, respectively (NRC, 1989b). A zinc intake of 15 mg/day is recommended during pregnancy; during lactation, an additional zinc intake of 7 mg/day is recommended for the first 6 months and an additional 4 mg/day is recommended for the second 6 months. A recommendation of 5 mg/day is set for formula-fed babies. For adolescent children, the recommendation is set at 10 mg/day. Current Provision of Desired Information Current food labels provide information on the vitamin and mineral content in the ingredient listing, the nutrition information panel, and the principal display panel. The ingredient listing provides information about any individual vit~nins and minerals that have been added to foods during the manufacturing process (21 CF1( 101.41. No information is available about the micronutrient composition of other ingredients of foods in the ingredient listing. The nutrition information panel lists the micronutrients currently required when nutrition labeling is used in the following order: vitamins A and C, thiamin, riboflavin, niacin, calcium, and iron (21 CFR 101.9(c)~7~. Other optional vitamins and minerals, when they are added or naturally occurring, must be listed following the required micronutrients. Each micronutrient is listed as a percentage of the U.S. RDA contained in the food. The U.S. RDAs are standards based on the 1968 RDA, and a more extensive discussion is provided in Chapter 7. The percentages are expressed in 2 percent increments up to the 10 percent level, in 5 percent increments up to the 50 percent level, and in 10 percent increments above the 50 percent level. Nutrients present in amounts less Man 2 percent of the U.S. RDA may be indicated by a zero or an asterisk referring to a footnote at the bottom of the table: "contains less than 2 percent of the U.S. RDA of this (these) nutrient (nutrients)" (21 CFR 101.9(c)~7~(i)~. When a product contains less than 2 percent of the U.S. RDA for at least five of the required nutrients, the manufacturer may choose to declare no more than three of those nutrients, with an appropriate accompanying statement. The principal display panel frequently carries terms describing the content of vitamins and minerals that manufacturers wish to highlight in promoting a food. FDA regulations provide that a claim may be made that a food is a significant

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NUTRITION lABEL COMET 197 source of a vitamin or mineral if that micronutrient is present in a food at a level equal to or in excess of 10 percent of the U.S. RDA in a serving (21 Con 101.9(c)~7~(v)~. Other examples of micronutrient descriptors include high in vitamin C, iron fortified, or high in calcium. However, currently there are no official definitions for such terms for specific micronutrients. Committee Recommendations On the basis of recent dietary recommendations, current public health is- sues, and the consumption patterns of Americans, the Committee considered the current requirements for and potential changes in He listing of micronutrients on the nutrition information panel and acknowledges that the current selection of micronutrients required to be listed is dated. The Committee's recommendations for change are based on current consumer interest, scientific evidence to support consensus on health benefit, conclusions drawn by reports of expert panels, and knowledge of essential nutrients. Although a more comprehensive listing could be recommended, the limitation of space on labels for nutrition information and He lack of scientific evidence demonstrating general public health problems led the Committee to focus its attention on micronutrients reported to be current public heals issues (see Table 6-1~. The Committee based its decision primarily TABLE ~l Priority Status as a Public Heals Issue of Fbod Components Current Potential Public NoeCurrendy Public Health Health Issue, Public Health Issue Further Study Needed Issue Food energy Fat Saturated fat Cholesterol Alcohol Iron Calcium Sodium Dietary fiber Vitamin A Carotenes Folacin Vitamin B6 Vitamin C Potassium Zinc Pluande Protein Carbohydrates Vitamin E Thiamin Riboflavin Niacin Vitamin B12 Magnesium Copper Phosphorus SOURCE: Adapted from LSRO, FASEB (Life Sciences Re- search Office, Federation of American Societies for Experimental Biology). 1989. Nutrition Monitoring in the United States: An Update Report on Nutrition Monitoring. Prepared for the U.S. Department of Agriculture and U.S. Department of Health and Human Services. Government Printing Office, Washington, D.C. 408 pp.

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198 NUTRITION LABELING on the attention given to them by reports from the Surgeon General, the Expert Panel on Nutrition Monitoring, and NBC (DHHS, 1988; LSRO, FASEB, 1989; NBC, 1989a). As indicated several times in this report, the Committee put primary emphasis on the importance of consuming a diet consisting of a variety of foods. The decision to limit the number of micronutrients to be listed engendered concern, and therefore led the Committee to add the following words of caution on important dietary sources of nutrients. Labeling dairy products as particularly good sources of calcium might lead to the consumption of foods also rich in animal protein, which has been shown to enhance urinary calcium excretion, thereby compromising calcium status and perhaps even exacerbating the risk of osteoporosis ARC, 1989b3. Emphasizing iron richness may bring particular attention to foods for which the bioavailability of iron is said to be high, such as meats that contain the heme forms of iron, whereas recent reports (such as the Surgeon General's, Diet and Health, and the Dietary Guidelines) have urged moderation in the consumption of these foods (DHHS, 1988; NRC, 1989; USDA/DHHS, 1985~. On balance, however, the Committee acknowledges the considerable consumer interest generated in these nutrients, in part, by these recent reports and recognizes that there are other sources of calcium and iron that possess considerable nutritional benefit and that need to be identified for the consumer. For vitamins A and C, there is little evidence of a public health problem in the U.S. population. If food sources rich in vitamin A were to be listed, it is unlikely that the nutritional value of provitamin A-Wpe compounds (carotenoids) would be distinguished from preformed vitamin A (retinoids). Not only are there likely to be important biological differences in the ability of these compounds to inhibit chronic degenerative diseases but also carotenoids are found in foods (plants) whose consumption is encouraged, and retinoids are found in foods (animal products such as liver) whose consumption is not encouraged. Listing of vitamin C would provide information on good sources of this nutrient (e.g., fruits and vegetables), but those sources also provide a variety of other important micronutrients. For zinc and folate, there was even less evidence demonstrating the need to emphasize consumption of foods rich in these nutrients. Consumers should likewise assess their intake of vitamins and minerals in terms of total diet rather than the contribution of individual foods. The current listing on the food label of micronutrients as a percentage of the U.S. RDA encourages manufacturers of some food products to fortify each micronutrient to 100 percent. Treatment of vitamins and minerals in qualitative rather than quantitative terms would help to reduce the incentives for overfortification of foods. Furthermore, the current listing implies more precision and accuracy than really exists due to the inaccuracy in measuring at least some of the nutrients in this group.

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NUTRITION L4BF1 CONTENT 199 The Committee recommends that: FDA and USDA should continue to require disclosure of calcium and iron content per serving, but use He source definitions described in Chapter 7 (i.e., very good source of, source of, and contains). FDA and USDA should allow, as an option, disclosure of Be content of all other micronu~ients for which RDAs exist. FDA and USDA should establish standardized definitions for the terms used to describe the micronutrient content of foods on Me principal display panel and these definitions should be the same as those used on the nutrition information panel (see Chapter 7~. REFERENCES ADA (American Diabetes Association), Task Force on Nutrition and Exchange Lists. 1987. Nutritional recommendations and principles for individuals with diabetes mellitus. Diabetes Care 10:126-132. AHA (American Heart Association), Committee on Nutrition. 1965. Diet and Heart Disease. American Heart Association, New York. AHA (American Heart Association), Committee on Nutrition. 1986. Dietary guidelines for healthy American adults. Circulation 74:1465A-1468A. Bonanome, A., and S.M. Grundy. 1988. Effect of dietary steanc acid on plasma cholesterol and lipoprotein levels. N. Engl. J. Med. 318:124~1248. Butrum, R.R., C.K. Clifford, and E. Lanza. 1988. NCI dietary guidelines. Rationale. Am. J. Clin. Nutr. 48:Suppl. CCC (Calorie Control Council). 1985. Sweet Choices~uestions and answers about sweeteners in low-calorie foods and beverages. CCC, Atlanta. 6 pp. Crapo, P. A. 1984. Theory vs. fact: The glycemic response to foods. Nutr. Today 19:6-11. DHHS (U.S. Department of Health and Human Services). 1988. The Surgeon General's Report on Nutntion and Health. Gove~ntnent Printing Office, Washington, D.C. 727 PP Glinsmann, W.H., H. Irausquin, and Y.K. Park. 1986. Evaluation of health aspects of sugars contained in carbohydrate sweeteners: Report of Sugars Task Force. J. Nutr. 116:S1-S216. Gordon, T., W}3. Castelli, M.C. Hjortland, W.B. KanneL and T.R. Dawber. 1977. High density lipoprotein as a protective factor against coronary heart disease. The Framingham Study. Am. J. Med. 62:707-714. Groen, J., B.K. Tjiong, C.E. Kamminga, and A.F. Willebrands. 1952. The influence of nutrition, individuality and some other factors, including venous forms of stress, on the serum cholesterol; an experiment of nine months duration in 60 normal human volunteers. Voeding 13:556-587. Grundy, S.M. 1987. Monounsaturated fatty acids, plasma cholesterol and coronary heart disease. Am. J. Clin. Nutr. 45:1168-1175. Heird, W.C., J.F. Nicholson, J.M. DriscolL Jr., NJ. Schullinger, and R.W. Winters.

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200 NUTRITION LABELING 1972. Hyperammonemia resulting from intravenous alimentation using a mixture of synthetic 1-amino acids: A preliminary report J. Pediatr. 81:162-165. Herold, P.M., and J.E. Kinsella 1986. Fish oil consumption and decreased risk of cardiovascular disease: A comparison of findings from animal and human feeding trials. Am. J. Clin. Nutr. 43:566-598. HPI`RG (Hypertension Prevention Trial Research Group). 1990. The hypertension pre- vention trial: Three-year effects of dietary changes on blood pressure. Arch. Intern. Med. 150:153-162. Kayman S., W. Bruvold, and J.S. Stem. 1990. Maintenance and relapse after weight loss in women: Behavioral aspects. Am. J. Clin. Nutr. In press. Keys, A. 1975. Coronary heart disease_the global picture. Atherosclerosis 22:149-192. Kinsell, L.W., J. Partridge, L. Baling, S. Margen, and G. Michaels. 1952. Dietary modification of serum cholesterol and phospholipid levels. J. Clin. Endocrinol. 12:909-913. Kromhout, D., E.B. Bosschieter, and C. de Lezenne Coulander. 1985. The inverse relation between fish consumption and 20-year mortality from coronary heart disease. N. Engl. J. Med. 312:i205-1209. Lanza' E., D.Y. Jones, G. Block, and L. Kessler. 1987. Dietary fiber intake in the U.S. population. Am. J. Clin. Nutr. 46:790 797. LSRO, FASEB (Life Sciences Research Office, Federation of American Societies for Experimental Biology). 1989. Nutrition Monitoring in the United States: An Update Report on Nutrition Monitoring. Prepared for the U.S. Department of Agriculture and the U.S. Department of Health and Human Services. Govemment Printing Office, Washington, D.C. 408 pp. Massachusetts Medical Society, Committee on Nutrition. 1989. Fast Food Fare: Consumer Guidelines. Prepared by Connie Roberts. N. Engl. J. Med. 321:752-756. McGill, H.C., Jr. 1979. The relationship of dietary cholesterol to serum cholesterol concentration and to atherosclerosis in man. Am. J. Clin. Nutr. 32:2664-2702. Medalie, J.H., H.A. Kahn, H.N. Neuteld, E. Riss, and U. Goldbourt. 1973. Five- year myocardial infarction incidence. II. Association of single variables to age and birthplace. J. Chronic Dis. 26:32~349. Miller, N.E., D.S. Thelle, O.H. Forde, and O.D. Mjos. 1977. The Tromso Heart Study. High-density lipoprotein and coronary heart-disease: A prospective case-control study. Lancet 1:96~968. NCEP (National Cholesterol Education Program). 1990. Report of the Expert Panel on Population Strategies for Blood Cholesterol Reduction, National Institutes of Health. Government Printing Office, Washington, D.C. 140 pp. NRC (National Research Council). 1982. Diet, Nutrition, and Cancer. Committee on Diet, Nutrition and Cancer, Food and Nutrition Board, Commission on Life Sciences. National Academy Press, Washington, D.C. 478 pp. NRC (National Research Council). 1988. Designing Foods: Animal Product Options in the Marketplace. Report of the Committee on Technological Options to Improve the Nutritional Attributes of Animal Products, Board on Agriculture. National Academy Press, Washington, D.C. 367 pp. NRC (National Research Council). 1989a. Diet and Health: Implications for Reducing Chronic Disease Risk. Report of the Committee on Diet and Health, Food and Nu-

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NUTRrTlON LABEL CONTENT 2~)1 trition Board, Commission on Life Sciences. National Academy Press, Washington, D.C. 749 pp. NRC (National Research Council). 1989b. Recommended Dietary Allowances, 10th ed. Committee on the 10th Edition of the Recommended Dietary Allowances, Food and Nutrition Board, Commission on Life Sciences. National Academy Press, Washington, D.C. 285 pp. Page, I.H., F.J. Stare, A.C. Corcoran, H. Pollack and C.F. Wilkinson. 1957. Atheroscle- rosis and the fat content of the diet. Circulation 16:163-178. Prosky, L., N.G. Asp, I. Furda, J.W. DeVnes, T.F. Schweizer, and B.F. Harland. 1985. Determination of total dietary fiber in foods and food products: Collaborative study. J. Assoc. Off. Anal. Chem. 68:677-679. Rock, RJ. 1986. Policy letter of June 24, 1986, to Giant Food, Inc., Washington, D.C. Center for Food Safety and Applied Nutrition, Food and Drug Administration, Washington, D.C. Rank, RJ. 1988. Policy letter of August 26, 1988, to J.S. Kahan and B.L. Rubin, Hogan and Hartson, Washington, D.C. Center for Food Safety and Applied Nutrition, Food and Drug Administration, Washington, D.C. Schemmel, R., O. Mickelson, and J.L. Gill. 1970. Dietary obesity in rats: Body weight and body fat accretion in seven strains of rats. J. Nutr. 100:1041-1048. Shank F.R., L. Larsen, F.E. Scarbrough, J.E. Vanderveen, and A.L. Forbes. 1983. FDA perspective on sodium. Food Technol. 37:73-77. Shekelle, R.B., A.M. Shtyock, O. Paul, M. Lepper, J. Stamler, S. Liu, and WJ. Raynor, Jr. 1981. Diet, serum cholesterol, and death from coronary heart disease. The Western Electric Study. N. Engl. J. Med. 304:6~70. Solberg, L.A., and J.P. Strong. 1983. Risk factors and atherosclerotic lesions. A review of autopsy studies. Arteriosclerosis 3:187-198. Stamler, J., and R. Shekelle. 1988. Dietary cholesterol and human coronary heart disease: The epidemiologic evidence. Arch. Pathol. Lab. Med. 112:1032-1040. USDA (U.S. Department of Agriculture3. 1982a. FSIS Policy Memorandum 039. Food Safety and Inspection Service, Washington, D.C. USDA (U.S. Department of Agriculture). 1982b. FSIS Policy Memorandum 046. Food Safety and Inspection Service, Washington, D.C. USDA (U.S. Department of Agriculture). 1984a FSIS Policy Memorandum 049C. Food Safety and Inspection Service, Washington, D.C. USDA (U.S. Department of Agriculture). 1984b. FSIS Policy Memorandum 078. Food Safety and Inspection Service, Washington, D.C. USDA (U.S. Department of Agriculture). 1987. FSIS Policy Memorandum 070B. Food Safety and Inspection Service, Washington, D.C. USDA (U.S. Department of Agriculture). 1989. FSIS Standards and Labeling Policy Book. Food Safety and Inspection Service, Washington, D.C. USDA (U.S. Department of Agriculture). 1990. Report of the Dietary Guidelines Ad- visory Committee on the Dietary Guidelines for Americans, 1990. Government Printing Office, Washington, D.C. 48 pp. USDA/DHHS (U.S. Department of Agriculture and U.S. Department of Health and Hu- man Services). 1985. Nutrition and Your Health: Dietary Guidelines for Americans, 2nd ed. Govemment Printing Office, Washington, D.C. 24 pp.

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202 NUTRITION LABELING Woodwind, CJ.H., and K.K. Carroll. 1988. Nutrition and human heals aspects of marine oils and lipids. Pp. 2-28 in Manne Biogenic Fats and Oils, R.G. Ackman, ed. CRC Press, Boca Raton, Fla. Yudkin, J. 1964. Dietary fat and dietary sugar in relation to ischemic heart disease and diabetes. Lancet 2:~5.