点击显示 收起
1 From the Department of Pediatrics, Baylor College of Medicine, Houston; the University of Iowa Hospitals and Clinics, Iowa City; and the University of Turku, Finland.
2 Presented at the symposium Fat Intake During Childhood, held in Houston, June 8–9, 1998. 3 Address correspondence to DM Bier, Children's Nutrition Research Center, Baylor College of Medicine, 1100 Bates Street, Houston, TX 77030-2600. E-mail: dbier{at}bcm.tmc.edu.
Only 2 fatty acids are indispensable components of the diet, and their intake requirements represent a tiny fraction of dietary energy intake. Despite this, fat is an important dietary component in childhood because it serves both as a vehicle for absorption of fat-soluble vitamins and as a dense source of energy for metabolic processes and growth. In addition, diets that are inordinately low in fat are also responsible, indirectly at least, for impaired immune function that accompanies energy deficiency in childhood.
As detailed by Butte (1) at this symposium, the energy cost of growth is a very small fraction of total daily energy expenditure after the first year of life. Nonetheless, growth failure is one of the most sensitive indicators of energy deficiency in children. In fact, impaired growth is often used to index the lower limits of adequate fat and energy intakes, and reports of growth failure in small numbers of children consuming low-fat diets have led to widespread concerns about limiting the fat intakes of children (2, 3). Data presented at this symposium on children from Japan, Chile, and mainland China with fat intakes <22% of total energy confirmed the consequential growth failure. The correlation between impaired growth and percentage of total energy from fat is not perfect. Four- to 14-y-old vegetarian Chinese children from Hong Kong grew within the normal range while consuming diets that contained an average of 23% of energy from fat.
Nevertheless, also presented at this symposium were the results of 2 large, well-controlled clinical trials conducted in a total of >1700 children in developed countries. These investigations, the Special Turku Coronary Risk Factor Intervention Project (STRIP) for babies (4–6) and the Dietary Intervention in Children (DISC) study (7, 8), clearly showed that growth, development, and macronutrient intakes are not compromised in children consuming 27–30% of dietary energy as fat. These conclusions are now well supported by the results of systematic studies reported by other investigators (9–14), including data from China and Japan presented at this symposium by Chunming (15), Leung et al (16), and Murata (17). Importantly, the STRIP study recruited infants <1 y of age and showed that essential fatty acid adequacy and fat-soluble vitamin requirements can be met in the weaning and toddler age groups with reduced-fat diets in the range of 27–30% energy. This conclusion is also supported by the observation that dietary fat intake in healthy weaning infants is often 30% (8).
Further, Prentice and Paul (18) presented data from doubly labeled water studies of energy expenditure in children living in developing countries, which also support the position that diets commonly low in fat and energy in these countries are sufficient to support growth in healthy children. However, these diets are inadequate for supporting catch-up growth after episodes of diarrhea and other infections. Low-energy-density weaning foods appear to be the major contributor of growth failure in this context. Because dietary fat needs appear to increase when children are subjected to environmental stresses, especially the stress of infection, symposium participants recommended that new indexes of dietary fat inadequacy (eg, immunologic responses to appropriate challenges) be developed and tested.
Overall, however, symposium participants were unable to reach a consensus on the lower limit of fat intake in children that is compatible with adequate growth and development. In addition, they were unable to agree on the range of optimal fat intake in childhood. Nevertheless, from the data presented, certain general guidelines were apparent. First, repeated studies show that growth, development, and micronutrient intakes are not compromised in children consuming 27–30% of their dietary energy as fat, even during the weaning period (4–14). However, although adults appear to maintain fat balance when consuming diets that provide as little as 10% of energy as fat, dietary fat intakes of 17–22% energy have been associated with growth faltering in children. For this reason, and consistent with recommendations from the American Academy of Pediatrics Committee on Nutrition (19) and the International Dietary Energy Consultancy Group (20, 21), dietary fat intakes above a minimum of 23–25% of dietary energy should be maintained and it appears prudent to set a safety margin slightly above this range. It is important to emphasize that these considerations apply only when total dietary energy intake is from all macronutrient sources and when the intakes of other essential nutrients are each sufficient for adequate growth and development.
Beyond growth and development, percentage energy from fat has been associated with the prevalence of hypercholesterolemia and obesity. As discussed in the symposium, lipoprotein responses to dietary fat intake in childhood are affected by many well-described single gene defects and molecular polymorphisms in lipoprotein, lipoprotein receptor, and lipid processing enzyme genes. However, to a large extent, the mechanisms underlying the altered responses are not understood and individual clinical responses to perturbations in dietary fat content and composition have not been consistent. Similarly, nearly 200 genes, or marker loci, linked to obesity and body composition have been studied (22) and 12 mutations in 7 single genes that result in obesity have been identified. Depending on the study, genetic contributions to the development of obesity can account for 50% of the risk of becoming overweight. Nonetheless, genetic polymorphisms in obesity candidate genes appear to explain only 3–5% of body weight variance. Furthermore, genetic mechanisms alone cannot be responsible for the approximate doubling in the prevalence of overweight and obesity in American children over the past decade. Clearly, an individual's environment significantly affects the expression of his or her genetic potential in this regard (23). Nonetheless, it is often difficult to quantify gene-environment interactions because environmental variables are not always determinable or clearly defined. Perhaps this problem is most apparent in assessments of the consequences of dietary change in countries whose dietary habits are in transition between traditional intake patterns and new patterns more consistent with those of more developed countries because there is no uniform definition of a Western diet. Similar limitations exist for studies of the Mediterranean diet.
In the work presented at this symposium, the quality of children's local environments determined to a great extent the relative significance of fat in their diets. Thus, in an environment in which a surfeit of food is available, total fat intake is related to the undesirable development of obesity, as highlighted by data from the United States, Germany, Spain, and Japan and as discussed in detail by other investigators (24). On the other hand, in environments in which dietary energy from foods is marginal, increased consumption of dietary fat is associated with the desirable outcome of improved growth and development, as shown convincingly by the data from China, Japan, and Chile. However, what is also clear from the information discussed at the symposium is the virtual lack of data on children's responses to dietary fat intakes in relation to their genotypes in any environment. Additionally, there is a lack of similarly limited information on the tracking of dietary response variables throughout childhood as a function of both genotype and environment (25). Therefore, more clinical trials with large numbers of children are needed to study the precise effects of genetic polymorphisms on growth, body composition, and circulating lipoprotein responses to defined dietary fat intakes. In addition to the issues of funding and compliance, accomplishing this task is made more difficult by acceptability and ethical constraints of widespread genetic studies in populations. Nevertheless, in the absence of genotypic classification of dietary responses, public health recommendations for populations as a whole will remain untargeted and less than optimal.
From the observations cited above, a fundamental question identified at the symposium was "What recommendations do we give countries in transition whose current fat intake levels are low by comparison to the standards of a developed country?" Over the past 2 decades in the United States, the percentage of dietary energy from fat decreased from 36–37% to 33–34% and the percentage of dietary saturated fats declined from 14% to 12%. Nevertheless, the prevalence of obesity increased dramatically. Over a roughly similar period, fat intakes increased markedly in Spain and Japan. In Spain, children's dietary fat intakes increased to between 38% and 51% of energy intake, with 20% of energy accounted for by monounsaturated fat. This was accompanied by an increase in body mass index and an increment in serum cholesterol to an average equivalent to the 75th percentile value in American children, despite the high intake of monounsaturated fat in Spanish children. In Japan, the dietary fat increment was predominantly animal fat and was accompanied by an increased prevalence of obesity and a rise in serum cholesterol. Now, although the fractional contribution of dietary fat and saturated fat to energy intake in Japanese children is nearly the same as that in American children, serum cholesterol concentrations are higher in Japanese children, implying an increased sensitivity to dietary fat. These observations raise the question of whether these results are due to underlying genetic differences or, conversely, to the fact that individuals, eg, Americans who have been exposed to relatively high-fat diets for generations, have adapted in some fashion to this environmental variable. Thus, more information is necessary to establish guidelines for total fat intake and for the optimal composition of dietary fats in transitional countries. Furthermore, in societies in which the physical labor demands are great, is there a need to limit the dietary fat intakes of persons in energy balance? Or, does prior stunting predispose individuals to obesity when food becomes plentiful and, therefore, should dietary energy and fat intake recommendations be altered for previously stunted children? In addition, there are habitual societal issues. Although a recommendation for high monounsaturated fat intake might be practical in Spain, it is less likely to be achievable in Finland. Stated more generally, is it realistic to expect global harmonization of dietary fat intake guidelines, or should dietary fat intake recommendations be tailored for individual societies because of genetic and environmental variables?
Another critically important question raised during the symposium was the issue of when to recommend a reduction in saturated fat intake to reduce the risk of atheromatous lesions in the coronary arteries. It is now clear from the body of pathologic evidence presented at this symposium that lipid-laden macrophages, which serve as a physiologically important scavenger function, are normally present in the coronary artery walls of 50% of infants during the first 6 mo of life when fat intake from human milk or infant formula is 50% of dietary energy intake. As fat intake decreases during weaning, the prevalence of these macrophages also declines but remains at nearly 40% up to 2 y of age, when the fatty streaks reflecting the presence of lipid laden macrophages begin to regress. In the aorta, on the other hand, some fatty streaks can be identified in almost every North American child >3 y of age. In the first half of the second decade of life, the coronary arteries again show an increase in the accumulation of lipid laden macrophage foam cells, with a prevalence approaching 70%. At this time, however, the macrophages have a different cellular composition accumulating cholesterol and cholesterol ester depositions as a function of scavenging oxidized low-density lipoproteins. Thus, 8% of young teenagers have more advanced lipid deposits manifest as raised lesions. During the ages of 16–20 y, the prevalence of raised, preatheromatous lesions increases to 15%, although these lesions occupy <1% of intimal surface area. Approximately a decade later, about one-third of young adults have well-developed raised lesions occupying 2% of intimal surface area. These conclusions reaffirm recent similar data from the Bogulasa Heart Study (26).
Further pathologic evidence presented at this symposium shows clearly that fatty streaks are the precursors of more advanced arterial lesions, a progression that depends on sex, circulating lipoprotein concentrations, obesity, hypertension, and cigarette smoking. It is also clear, however, that not all fatty streaks become atheromata and that the detrimental progression is reversible before 20 y of age. What is not at all certain is whether arteries in which fatty streaks have regressed are entirely normal arteries or whether they may be more susceptible to the development of atheromatous lesions later in life.
The issues of progression and potential regression of fatty streaks are obviously central to the timing of recommendations to restrict dietary saturated fat intake during childhood or adolescence. Nonetheless, despite the now extensive pathologic data, broad discrepancies remain in recommendations concerning either the need for or the timing of dietary saturated fat reduction in childhood. Some argue that little needs to be done until late in the second decade of life because, before that time, the prevalence of raised lesions is small. Others, however, argue that acceptance of healthy lifestyle recommendations is generally not a hallmark of adolescence and, practically, it is difficult to change behavioral patterns that have become established over 2 decades. Thus, given an absence of harm, the position that reduced dietary fat intakes much earlier in life will be more successful than later interventions is at least an equally plausible hypothesis. Furthermore, because the duration of chronic exposure to detrimental concentrations of a noxious agent is often as important as the exposure dose itself, earlier dietary intervention in childhood might be supported on a duration of risk basis. In any case, none of these hypotheses has been tested specifically or successfully in children and adolescents. Given the importance of the hypotheses to limiting the principal cause of adult deaths in the developed world, experiments should be designed and implemented to address the issue of the timing and type of dietary fat intake interventions during childhood and adolescence in relation to the development of coronary artery disease. Admittedly, these experiments will be both difficult and costly. What is clear, however, is that dietary fat intake measures, necessary to limit the influx of excessive lipoprotein deposition in arterial walls, must be in place before the end of the second decade of life. Equally important, difficult, and costly experiments to test hypothetical causal relations between dietary fat intake and the development of selected cancers are also sorely needed.
DIETARY GUIDELINES
On the basis of the significant knowledge gaps and uncertainties delineated during the symposium, dietary guidelines for fat intake during childhood must be developed within individual countries for their own populations, taking into account the changes in availability and quality of the food supply necessary to meet these guidelines. Thus, each recommendation for dietary change must take into account national consequences pertaining to growth, under- and over nutrition, cardiovascular risk, and the like, both for the population as a whole and for individual ethnic subpopulations. Although guidelines for fat and energy intakes sufficient to maintain normal growth, development, and satisfaction of essential nutrient requirements should be readily accomplished, the extent to which dietary guidelines for children can provide instructions to prevent the development of chronic disease in adult life is less clear. As outlined at the symposium, several key questions must be answered when the dietary fat intakes of children's diets are modified. These include the following:
As with most other complex nutritional issues in childhood, generally applicable answers to these questions are not available. By identifying these questions and the others outlined above, the symposium proved to be successful by bringing together the evidence available from around the world and by highlighting the questions that will form the basis of testable hypotheses in future research studies.
REFERENCES