European Journal of Clinical Nutrition (1997) 51, 387±393 ß 1997 Stockton Press. All rights reserved 0954±3007/97 $12.00 The association between dietary patterns and cardio vascular disease risk indicators in healthy youngsters: Results covering ®fteen years of longitudinal development GB Post, HCG Kemper, J Twisk and W van Mechelen EMGO institute, Faculty of Medicine, Amsterdam Growth and Health Research Group, Vrije Universiteit, Amsterdam, The Netherlands Objective: To examine longitudinal relationships between nutrition and risk indicators for cardio vascular diseases (CVD) during adolescence and young adulthood. Design: A longitudinal study over ®fteen years. Subjects: 98 females and 84 males, from 13 to 27 years. Methods: By means of six interviews dietary patterns were determined. Blood samples were analyzed for serum concentration of total cholesterol (TC), and high-density-lipoprotein (HDL), bloodpressure, body fat and maximal aerobic power (VO2max) were determined. The longitudinal relations were analyzed with generalized estimation equations (GEE), a statistical technique in which relations at different time-points are tested simultaneously. Results: Compared to Dutch recommendations six out of seven macro nutrients appear to be unfavorable with respect to CVD. Borderline or high CVD risk values are apparent at 27 y in more than 25% of the subjects with respect to percentage body fat and serum total cholesterol in both sexes. In males 40% or more show borderline hypertension. The `univariate' longitudinal analyses showed signi®cantly positive relations: (1) between the intake of animal protein, saturated fat (SFA), cholesterol (Chol) and TC, and HDL; (2) between total energy intake (EN) and systolic blood pressure, and VO2max. Signi®cantly negative associations were found: (1) between EN, poly-unsaturated fat (PUFA) and TC concentrations; (2) between EN and sum of four skinfolds (SSF). Conclusions: With increasing age, over a period of 15 y in both sexes the SFA and Chol intake relate signi®cantly to the development of a negative CVD risk pro®le. The intake of PUFA relates positive to a CVD risk pro®le. The signi®cantly negative relation between EN intake and body fat (SSF) is partly explained by the relation between EN and VO2max. Descriptors: diet composition; cardio vascular risk indicators; young females and males; longitudinal study Introduction A diet rich in saturated fat, cholesterol and animal protein is a major factor leading to elevations of total serum cholesterol, whereas a high intake of poly-unsaturated fat (PUFA) plays a role in lowering serum cholesterol levels. High energy intake relates to obesity, and this affects blood pressure. Therefore proper diets appear to exert a favorable in¯uence on CVD by modifying established risk factors and reducing adiposity. (Posner et al, 1993; Shea et al, 1993; Clevidence et al 1992; Anderson et al, 1991; Barr et al, 1992; Edelstein et al, 1992; Grundy & Denke, 1990). In epidemiological research the identi®cation of risk indicators for CVD in adults is well established. More recently interest has focused on CVD risk factors in children and young adults, supposing that atherosclerosis starts early in childhood (Bild et al, 1996; Kelder et al, 1994). Longitudinal studies investigating the relation between dietary patterns and CVD risk indicators in young females and males are scarce (Twisk et al, 1996; Liu et al, 1996; Hunter et al, 1995). Correspondence: Dr. GB Post, EMGO Institute/Faculty of Medicine/ AGGO, Vrije Universiteit, v.d. Boechorststraat 7, 1081 BT, Amsterdam, The Netherlands Received 30 June 1996; revised 1 March 1997; accepted 7 March 1997 The study of potentially deleterious patterns of diet affecting blood lipids and body composition within individuals requires long-term serial measurements. In the `Amsterdam Growth and Health Study' longitudinal observations were made over a period of 15 y in approximately 200 male and female subjects, from the teenage period until the adult age, that is between the ages of 13 and 27 y. (Kemper, 1995). In previous analyses a direct relationship could not be demonstrated in these males and females, between, on the one hand, total energy intake and the energy contributed by total fat and, on the other hand, the sum of four skin folds and the serum cholesterol level. (Post, 1989; Post & Welten, 1995). These ®ndings were explained by the fact that the level of risk factors for hyper-cholesterolemia and obesity was relatively low and did not approach adult risk levels yet. The longitudinal development of CVD risk indicators, however, will not solely be in¯uenced by nutritional factors such as the total intake of energy, fat or saturated fat, but also by biological parameters like cardiopulmonary ®tness and body weight together with other lifestyle factors like physical activity behaviour (Twisk et al, 1996). This present study explores the longitudinal association between nutritional factors, namely the intake of energy, animal protein, saturated fat, poly-unsaturated fat and cholesterol, as independent variables and CVD risk indica- Amsterdam Growth and Health Study GB Post et al 388 tors, namely systolic-, diastolic blood pressure, serum lipids and sum of skin folds, as dependent variables, during adolescence and young adulthood over a period of 15 y. Subjects and methods Study population The study population reported here consists of the longitudinal sample of the Amsterdam Growth and Health Study (Kemper, 1985; Kemper, 1995). In 1977 the study started with 307 pupils of a secondary school in Amsterdam (The Netherlands). During the adolescent period (1977± 1980) there was a drop-out rate of 24% resulting in four measurements taken yearly of 131 girls and 102 boys. Five years later, in 1985, a total of 200 subjects was remeasured. In 1991, a sixth measurement took place on 182 subjects, 98 females and 84 males. No signi®cant drop-out effects were demonstrated with respect to the parameters relevant to the present report (Post & Kemper, 1995). The multiple longitudinal design of the study is described in detail by Kemper (1985, 1995). The present analysis considers the longitudinal data of the 98 females and 84 males from 13 until 27 y. The quality controls of the measured variables was done in two ways: ®rstly all measurements were executed by the same trained testers according the same guidelines over all the years; secondly the test-retest reproducibility of each measurement is checked by a statistical procedure calculating the interperiod correlations between the repeated measurements. All reproducibility coef®cients showed suf®cient values (> 0.60) used in the variables used in this paper. The details are published elsewhere (Kemper et al, 1985; Post, 1989). Cardio vascular disease indicators Risk indicators for CVD used as dependent variables in this study were the sum of four skin folds (SSF), systolic and diastolic blood pressure (SBP and DBP), serum total cholesterol (TC) and serum high-density lipoproteins (HDL) concentrations and maximal aerobic power. Between ages 13 and 27 y, six measurements were taken of anthropometric and other biological characteristics. Body fatness was de®ned by the SSF, namely by the sum of the bicipital, tricipital, sub scapular and supra-iliacal skinfolds (Harpenden skinfold caliper) (Durnin & Ramahan, 1967; Weiner & Lourie, 1969). The SBP and DBP were measured with a sphygmomanometer and a standard pressure cuff at the left upper arm with the subject in a sitting position. Non-fasting TC and HDL were analyzed enzymatically (Lipid Laboratory at the Department of Human Nutrition, Agriculture University, Wageningen, The Netherlands). Analyses met the criteria of the WHO reference laboratories: TC was determined according to the methods of Huang et al (1961) and Abell et al (1952), the HDL cholesterol fraction was analyzed according to the method of Burstein & Samaille (1960). Cardio respiratory ®tness was determined by measuring maximal aerobic power (VO2max). It was assessed with a direct method using a standard running test on a treadmill until exhaustion and was expressed in ml min71. kg72/3 (Kemper, 1985). The longitudinal development of several CVD risk indicators are different for females and males, and in¯uenced by sexual maturation (Berenson et al, 1981). Before full maturity is reached biological age can be different from calendar age. Rapidly maturing subjects have higher biological ages than calendar ages, and slowly maturing subjects have lower biological ages than calendar ages. During the adolescent period of the study biological age was determined by measuring skeletal age from X-rays of the left hand, according to the Tanner-Whitehouse II method (Tanner et al, 1975). In the statistical analyses, corrections are made for gender and biological age. Dietary assessment Daily food intake data were collected with a detailed crosscheck dietary history interview (Burke, 1947; Beal, 1967) adapted to the Amsterdam Growth and Health longitudinal study (Post, 1989). This method provided information about the usual food consumption pattern preceding the interview. The measurement of food intake was consistently executed in the same period of the year, namely in the months January until May, to avoid seasonal bias, by the same dietician. Study participants were asked to recall their usual food consumption pattern during the past month. Frequency, amounts and methods of preparations of the foods consumed were assessed in household measures or common portion sizes. A variety of visual aids were used in depicting portion sizes. Only the food items eaten at least twice monthly were recorded. Information on foods consumed during regular meals as well as in between meals (so-called snacks) were collected separately for the ®ve school or work days and for the two weekend days. A Dutch food-composition database was used in calculating energy and mean daily nutrient intakes (NEVO Table, 1991). As far as the concerned nutrients in this study the percentage of missing values are below 1%. A detailed description of the dietary assessment methodology and the reproducibility of the dietary history used in this study was reported previously. (Kemper, 1995; Post, 1989). Dietary characteristics as independent variables relevant for the present analysis included the intake of total energy (En, in MJ), animal protein (AProt), saturated fat (SFA), poly unsaturated fat (PUFA), and cholesterol (Chol). Because a higher energy intake mostly results in a higher intake of nutrients, the nutritional factors AProt, SFA, PUFA, and Chol were adjusted for energy intake. Data analysis A longitudinal correlation coef®cient was calculated between nutritional factors and risk indicators for CVD using the generalized estimating equations (GEE) technique. (Zeger & Liang, 1986). The following statistical model was used: P P Yit b0 b1j Xijt b2t time-dependent covariates P time-independent covariates where: Yit observations of subject i at time t; b0 intercept; blj standardized regression coef®cient of independent variable j; Xijt independent variable j of subject i at time t; b2 regression coef®cient of time. This model tests the relation between separate risk indicators for CVD (Yit) and each of the nutritional factors (Xit) simultaneously at each point in time, resulting in a standardized regression coef®cient (b), which can be interpreted as a longitudinal correlation coef®cient. This method corrects for time-dependent covariates, like year of measurement (time) and biological age, and time-independent covariates like gender. Because the longitudinal character- Amsterdam Growth and Health Study GB Post et al istics of the same subject (Yit) are not independent of each other, the parameters of the model have to be estimated adjusting for these intra-subject correlations. With GEE the relations were calculated between the longitudinal development of the risk indicators for CVD (Yit; TC, HDL, SBP, DBP, SSF and VO2max) and separate of the dietary parameters (Xit; EN, AProt, SFA, PUFA, Chol.) over the entire longitudinal period of 15 y. First of all, the nutritional factors were entered individually into the statistical model and if signi®cant relations (P 0.05) were found with more than one of the nutritional factors, a multivariate GEE was carried out. Differences between the mean intakes of the subjects with Dutch recommended daily allowances (RDAs) are tested with paired t-tests. Results The EN intake in females ( 9.5 MJ) showed no signi®cant age trend between 13 and 27 y (see Figure 1). The males showed during the adolescent period a signi®cant increase until adult age (from 11.6 MJ to 13.8 MJ, P 0.001), and thereafter a signi®cant decrease appeared at adult age (12.7 MJ). Throughout the same age period the contribution of protein to the energy intake increased from 13±14% in females and in males from 12±13% (both P 0.001), in particular due to the AProt intake. The intake of carbohydrates decreased with increasing age, from about 47±44 energy per cent in females, and from 46 to 45 energy per cent in males (P 0.01). The contribution of total daily fat intake decreased (P 0.01) from about 42% of total energy to about 39.5%, in females as well as in males. Finally during this age period the intake of Chol ¯uctuated between the 26±33 mg/MJ, with a peak intake at young adult age (females 33 mg/MJ, males 30 mg/MJ). The CVD risk indicators showed in our population with increasing age increasing value in females and males for SSF (see Figure 2), blood pressure (see Figure 3), and TC and HDL concentration (see Figure 4). The SSF increased in females about 40% (P 0.001), between the age 13 and 21 y, followed by a signi®cant decrease at age 27 y (Figure Figure 1 The longitudinal change in total daily energy intake (MJ) (mean and s.d.) for females and males from 13±27 y of age. Figure 2 The longitudinal change in sum of skinfolds (mm) (mean and s.d.) for females and males from 13±27 y of age. 389 Amsterdam Growth and Health Study GB Post et al 390 Figure 3 The longitudinal change in systolic bloodpressure (SBP) and diastolic bloodpressure (DBP) in mm Hg (mean and s.d.) for females and males from 13±27 y of age. 2). Males showed a gradual increase in the SSF from the age of 15 y until the age of 27 y of about 30% (P 0.001). In females the SBP remained more or less constant through adolescence and young adulthood, and the DBP increased slightly but signi®cantly (P 0.001) (Figure 3). In males a gradual increasing SBP was found (P 0.001) with increasing age. DBP increased by about 10% (P 0.001) from age 21 until age of 27 y. The serum TC and HDL concentration in females showed hardly any change between the ages of 13 and 16 y, but over the young adult and the adult period (®fth and sixth measurement) the TC concentration increased by almost 20% (P 0.001) (Figure 4). The HDL concentration increased only during the adult period (P 0.001). Initially, during adolescence, males TC concentration decreased by 10%, followed by a 10% increase thereafter (both P 0.001). The HDL concentration decreased between ages 13 and 21 y (P 0.001), with no further changes at age 27 y. The signi®cant relations, resulting from the `univariate' GEE analyses between the longitudinal changes of the nutritional factors on the one hand and the longitudinal changes of CVD indicators on the other hand, are shown in Table 1. The GEE analyses showed no interaction with gender, so the relations were not different for males and females. The univariate analysis showed that the changes in EN intake were signi®cantly but negatively related to the changes in the SSF (P 0.015); positively related to blood pressure (especially the SBP, P 0.04); negatively Figure 4 The longitudinal change in serum concentration of total cholesterol (TC) and high density lipoproteins (HDL) (mmol/L) (mean and s.d.) for females and males from 13±27 y of age. Amsterdam Growth and Health Study GB Post et al Table 1 The signi®cant associations estimated by the GEE `univariate' analyses regarding the longitudinal development of CVD risk indicatorsa in relation to nutritional characteristicsb, corrected for time, gender and biological age. The Amsterdam Growth and Health Study EN (MJ) AProt (% En) SFA (% En) c DBP SBP TC HDL SSF VO2max b 95% CId P-valuee b 95% CI P-value b 95% CI P-value b 95% CI P-value b 95% CI P-value b 95% CI P-value 0.075 0.00 to 0.15 0.040 70.096 70.16 to 70.04 0.002 PUFA (% En) Chol (mg/MJ) 70.076 70.12 to 70.03 0.001 0.107 0.05 to 0.16 0.000 0.080 0.02 to 0.14 0.013 70.067 0.00 to 70.13 0.049 0.073 0.02 to 0.13 0.012 0.083 0.04 to 0.13 0.001 0.089 0.03 to 0.14 0.002 70.073 70.12 to 70.02 0.005 0.105 0.05 to 0.16 0.000 a TC, serum total cholesterol concentration; HDL, serum high density lipoproteins cholesterol concentration; DBP, diastolic blood pressure; SBP, systolic blood pressure; TC, serum total cholesterol; SSF, sum of 4 skinfolds; VO2max, maximal aerobic power EN, total energy intake; AProt, animal protein intake; SFA, saturated fat intake; PUFA, poly-unsaturated fat intake; Chol, cholesterol intake; MJ, MegaJoules; % En, percentage of energy c Correlation coef®cient d 95% con®dence interval e Signi®cant 0.05. b related to TC concentration (P 0.012); and positively related to VO2max (P 0.001). The changes in intake of AProt (En%) showed a positive relation to the changes in TC concentration (P 0.012). The longitudinal changes in intake of SFA (En%) and of Chol (mg/MJ) were signi®cantly positively related to TC (respectively P 0.001 and P 0.001) as well as to HDL concentration (respectively P 0.012 and P 0.013). SFA intake was also related to the changes in DBP, but the relationship was negative (P 0.05). The intake of PUFA (En%) showed over time a negative relation with the TC concentration (P 0.001). No other signi®cant relations could be demonstrated. Based on the signi®cant associations found with the univariate GEE (Table 1) a multivariate GEE was analyzed relating the longitudinal changes in the TC and HDL concentration to the relevant nutritional characteristics, namely EN, APROT, SFA, PUFA and CHOL (summarized in Table 2). The longitudinal changes in Chol intake and SFA intake remained positively associated with the TC concentration (P 0.03). The EN and PUFA intake remained inversely related to TC (respectively P 0.012 and P 0.04). The relation of AProt with TC disappeared. The association between the changes in SFA intake and the HDL concentration was positive (P 0.014). For Chol intake the relation with HDL concentration was not signi®cant anymore. Table 3 summarizes the comparison between the average composition of the diet and the RDAs, in both sexes over the entire age period. At all ages the differences were signi®cant (paired t-test, P < 0.000) from the RDAs in an unfavorable direction. The average intake of total protein, fat and saturated fat was higher than recommended for a prudent diet, but lower for the PUFA, total carbohydrate and poly saccharides intakes. The cholesterol intake was the only parameter that showed a signi®cant lower and favorable value with respect to the RDAs. One exception was found for females at age 21: with a signi®cant higher value (0.4 mg/MJ, P < 0.000). Table 4 summarizes the percentages of females and males with borderline and/or high risk values for CVD at age 27 y. The results show that less than 5% of the females have high risk values for SBP and DBP and HDL. In males this is only shown for SBP and HDL. In 11% of the females and 12% of the males a borderline DBP is found, and an additional 12% of the males have a hypertensive DBP. A borderline SBP was measured in 9% of the females and in 42% of the males (Kemper, 1995). Table 2 The multivariate signi®cant correlations estimated by GEE regarding the longitudinal development of HDL and TCa concentration in relation to nutritional factorsb, corrected for time, gender and biological age. The Amsterdam Growth and Health Study EN (MJ) c TC HDL a b 95% CId P-valuee b 95% CI P-valuee 70.096 70.16 to 70.04 0.002 AProt (% En) SFA (% En) PUFA (% En) Chol (mg/MJ) 0.060 0.00 to 0.12 0.030 0.072 0.02 to 0.13 0.014 70.049 70.10 to 0.00 0.042 0.061 0.01 to 0.12 0.033 TC, serum total cholesterol concentration; HDL, serum high density lipoproteins cholesterol concentration EN, total energy intake; AProt, animal protein intake; SFA, saturated fat intake; PUFA, poly-unsaturated fat intake; Chol, cholesterol intake; MJ, MegaJoules; % En, percentage of energy c Correlation coef®cient d 95% con®dence interval e Signi®cant 0.05. b 391 Amsterdam Growth and Health Study GB Post et al 392 Table 3 The range of mean differences in intake of seven macronutrients with the Recommended Daily Allowances (RDA) given by the Netherlands Nutrition Council (1989), during adolescence and young adulthood in females and males. Statistical signi®cant differences at all ages with RDAs are indicated Nutrient RDA Range of difference during study females Total protein Total fat Saturated fat Poly unsaturated fat Cholesterol Total carbohydrate Poly saccharides 11 en% 35 en% 10 en% 10 en% 33 mg/MJ 55 en% 30 en% 1.4 4.6 5.5 73.5 74.0 78.4 77.1 Table 4 Percentage of subjects above (or below for HDL) borderline and high risk values for cardio vascular diseases at age 27 y. (Bell et al, 1986; WHO/ISH, 1989; Erkelens, 1991) Value Risk factor Bodyfat (%) SBP (mm Hg) DBP (mm Hg) TC (mmol/l) HDL (mmol/l) Borderline females males females males females males females males females males 25 15 140 140 90 90 5.2 5.2 1.2 1.2 33% 29% 9% 42% 11% 12% 39% 25% 7% 49% High 30 20 160 160 95 95 6.2 6.2 0.9 0.9 15% 10% Ð 2% 3% 12% 14% 11% 1% 5% Discussion Environmental factors, such as lifestyle, are suggested to be the driving forces behind the etiology of CVD. Among these, diet is considered to be highly important. The western diet, with a relatively high fat intake and low in complex carbohydrates, is seen as one of the relatively well-established factors in elevating the risks of CVD (Posner et al, 1993). In this study, females and males, showed a decreasing total fat intake, as well as a decreasing contribution of fat intake to the total energy consumption with increasing age. Nevertheless, at adult age, this study population, on average, exceeds the recommended daily allowances (Netherlands Nutrition Council, 1989). Even the proportion of subjects, at the age of 27 y, consuming a high daily fat diet ( 40 en%) was 49% in females and 46% in males (Post and Welten, 1995). Investigating the long term effects of a dietary pattern with respect to the development of CVD risk indicators, one has to make an estimate of the qualitative aspects of the daily diet over the 15 y period. This was done by comparison with Dutch RDAs (Netherlands Nutrition Council, 1989). In relation to CVD risk indicators it could be shown that in six out of seven selected macro nutrients (see Table 3) the intakes did not meet the recommendations in both sexes. A prudent diet, as recommended by the Dutch Nutrition Council, includes carbohydrates of > 55 En% as well as 30 EN% polysaccharides, because of the inverse relation with the proportion of energy derived from fat. Overall it can be stated that the longitudinal dietary pattern in this population is potentially unhealthy with respect to the development of CVD, because most of the macronutrients do not meet the recommended daily allowances in the Netherlands (1989). The literature de®nes health indicators and risk factors for CVD. (Bell et al, 1986; WHO/ISH, 1989; Erkelens, 1991). to to to to to to to 3.3 6.7 8.8 74.2 0.4 711.2 78.5 males 0.5 to 2.6 4.1 to 7.9 6.6 to 8.5 73.2 to 74.0 73.2 to 77.0 79.0 to 710.6 77.0 to 77.8 Signi®cance in all years (both sexes) < 0.001 < 0.001 < 0.001 < 0.001 < 0.001 < 0.001 < 0.001 High TC is seen as a major risk factor in relation to CVD. The cut-off point for ideal serum TC concentration in the Netherlands is recommended at 5.0 mmol/l. (Erkelens, 1991). The mean TC concentration of males was equal to this level, whereas females, at the age of 27 y, showed higher concentrations (see Figure 4). If the `moderate' risk cut-off point of 5.2 mmol/l is considered, then 25% of the adult males, and 39% of the females were above this point, and another 11% of the males and 14% of the females were above the high risk cut-off point of 6.2 mmol/l. Very low HDL concentration are seen in 1% of the females and 5% of the males, but if borderline low values are included, 7% and 49% respectively are at risk (Table 4). Although cholesterol intake was the only nutrient that showed favorable lower intakes than RDAs this did not ®nd expression in lower percentages of subjects with hypercholesteremia compared to the other CVD risk factors. Body fat can be estimated from the sum of skin folds. If one accepts a percentage of body fat of 30% in females and 20% in males as high risk values for overweight, (see Table 4), then 15% of the female subjects and 10% of the male subjects in our longitudinal study should be regarded as such at age 27 y. At this age 48% of the females and 39% of the males have body fat percentages greater than 25% and 15% respectively. (Kemper, 1995). Although at age 27 y the mean values of our population did not exceed the high risk values, borderline values for CVD risk indicators can be seen rather frequently. In this study the longitudinal relations between nutritional parameters as independent variables and biological risk indicators for CVD as dependent variables were analyzed with generalized estimating equations. The advantage of using GEE is that all longitudinal data are used and the relation can be analyzed under correction of both time-dependent, that is year of measurement, biological age, and time-independent, namely gender, co-variates. (Twisk et al, 1994). The observed negative association between the TC concentration and the PUFA intake (declining CVD risk indicators with age), as well as the positive relation with the intake of SFA and Chol (increasing CVD risk indicators with age), support the literature on these aspects. (Hegsted et al, 1965; Lewis et al, 1981; Weisweiler et al, 1985; Rosenbergh & Schaefer, 1988; Li-Ching et al, 1994). Miller et al (1990) found no relationship between EN intake and adiposity, but demonstrated a higher fat contribution (En%) in obese adults compared to lean subjects, as well as a lower score on exercise activities. In our study an inverse relation was found of the SSF to EN intake (P 0.005) (see Table 1), and a positive association between EN intake and VO2max (P 0.000). The negative relation of the SSF and the EN intake can possibly be Amsterdam Growth and Health Study GB Post et al explained by the positive relation of VO2max with EN, suggesting that subjects with a high VO2max are more physically active, expend more energy and are as a result leaner. Therefore the VO2max and EN were taken into a multivariate GEE for the dependent variable SSF. Although the negative association between SSF and EN decreased (from 70.073 to 70.054, 95% CI 70.003 to 70.105), it remained signi®cant (P 0.036). So, VO2max can only partly explain this relation. Conclusions (1) In comparison with Netherlands Nutrition Council recommendations, the intake of six out of seven macro nutrients appeared to be unfavorable with respect to the development of CVD risk indicators with increasing age, in both sexes. (2) At age 27 y, in this study, the prevalence of borderline CVD risk values is more than 25% for body fat, and serum total cholesterol in both sexes, but even higher in males for systolic-, diastolic blood pressure and serum high density lipoproteins. (3) In this study a dietary pattern with a relatively high saturated fat and high cholesterol intake, between ages 13 and 27 y in both sexes, showed to be signi®cantly and positively related to serum total cholesterol. (4) The longitudinal analysis revealed that the intake of poly-unsaturated fat was negatively related to serum total cholesterol (5) A dietary pattern with a relative high energy intake in both sexes was related in this study to a more favorable coronary risk pro®le, namely a lower amount of body fat, a higher physical ®tness, a lower diastolic blood pressure and a lower serum total cholesterol. References Abell LL, Levy BB & Kendall FE (1952): Simpli®ed method for the estimation of total cholesterol in serum and demonstration of its speci®city. J. Biol. Chem 195, 357±366. Anderson KM, Wilson PW, Odell PM & Kannel WB (1991): An updated coronary risk pro®le. A statement for health professionals. Circulation 83, 356±362. Barr SL, Ramakrishnan R, Johnson C, Holleran S, Dell RP & Ginsberg HN (1992): Reducing total dietary fat without reducing saturated fatty acids does not signi®cantly lower total plasma cholesterol concentrations in normal males. Am. J. Clin. Nutr. 55, 675±681. Beal VA (1967): The nutritional history in longitudinal research. J. Am. Diet. Ass. 51, 425±432. Bell RD, Macek M, Rutenfranz J & Saris WHM (1986): Health indicators and risk factors of cardio vascular diseases during childhood and adolescence. In: Children and Exercise XII, Vol 17 eds. Rutenfranz J, Mocellin R, Klimt F, Int. Series Sports Science, Human Kinetics, Champaign IL. Berenson GS, Srinivasan SR, Cresanta JL, Foster TA, Webber LS (1981): Dynamic changes of serum lipoproteins in children during adolescence and sexual maturation. Am. J. Epidemiol. 113, 157±170. Bild DE, Jacobs DR jr, Liu K, Williams OD, Hilner JE, Perkins LL, Marcovina SM, Hulley SB. (1996): Seven-year trend in plasma lowdensity-lipoprotein-cholesterol in young adults: the CARDIA Study. Ann. Epidemiol. 6, 235±245. Burke BS (1947): The dietary history as a tool in research. J. Am. Diet. Ass. 23, 1041±1046. Burstein M & Samaille J (1960): Sur un dosage rapide du cholesterol lie aux alpha-et betalipoproteinen du serum. Clin. Chim. Acta. 5, 609±611. Clevidence BA, Judd JT, Schatzkin A, Muesing RA, Campbell WS, Brown CC, Taylor PR. (1992): Plasma lipid and lipoprotein concentrations of men consuming a low-fat, high-®ber diet. Am. J. Clin. Nutr. 55, 689± 694. Durnin JVGA & Rahaman MM (1967): The assessment of the amount of fat in the human body from measurements of skinfold thickness. Brit. J. Nutr. 21, 681±689. Edelstein SL, Barrett-Connor EL, Wingard DL & Cohn BA (1992): Increased meal frequency associated with decreased cholesterol concentrations; Rancho Bernardo CA, 1984±1987. Am. J. Clin. Nutr. 55, 664±669. Erkelens DW (1991): Herziening concensus cholesterol. Ned. T. Geneesk. 135±49, 2337±2340. Dutch. Grundy SM & Denke MA (1990): Dietary in¯uences on serum lipids and lipoproteins. J. Lipid Res. 31, 1149±1172. Hegsted DM, McGandy RB, Myers ML & Stare FJ (1965): Quantitative effects of dietary fat on serum cholesterol in man. Am. J. Clin. Nutr. 17, 281±295. Huang TC, Chen CP, Wegler V & Raftery A (1961): A stable reagent for the Liberman-Buchard reaction. Anal. Chem. 33, 1405±1407. Hunter SM, Bao W & Berenson GS (1995): Understanding the development of behavior risk factors for cardiovascular disease in youth: the Bogalusa Heart Study. Am. J. Med. Sci. 310, Suppl 1, S114± S118. Kelder SH, Perry CL, Klepp KI & Lytle LL (1994): Longitudinal tracking of adolescent smoking, physical activity, and food choice behaviours. Am. J. Pub. Health 84, 1121±1126. Kemper HCG (ed) (1985): Growth Health and Fitness of TeenagersÐ Longitudinal research in International perspective. Medicine and Sport Science, Vol 20, Karger. Kemper HCG (ed) (1995): The Amsterdam Growth StudyÐA longitudinal analysis of health, ®tness and lifestyle. HKP Sport Science Monograph Series, Vol 6. Lewis B, Hammett F, Katan M, Kay RM, Merkx I, Nobels A, Miller NE, Swan AV (1981): Towards an improved lipid-lowering diet: additive effects of changes in nutrient intake. Lancet 2, 1310±1313. Li-Ching L, Shieh MJ, Posner BM, Ordovas JM, Dwyer JT, Lichtenstein AH, Cupples LA, Dallal GE, Wilson PW, Schaefer EJ. (1994): Relationship between dietary intake, lipoproteins and apoliproteins in Taipei and Framingham. Am. J. Clin. Nutr. 60; 765±774. Lie K, Ruth KJ, Flack JM, Jones-Webb R, Bunke G, Savage PJ, Hulley SB. (1996): Blood pressure in young blacks and whites: relevance of obesity and lifestyle factors in determining differences. The CARDIA Study. Coronary artery risk development in young adults. Circulation 93, 60±66. Miller MC, Lindeman, AK, Wallace J & Niederpruem M (1990): Diet composition, energy intake, and exercise in relation to body fat in men and women. Am. J. Clin. Nutr. 52; 426±430. Netherlands Nutrition Council (1989): Nederlandse Voedingsnormen. Voedingsraad, Den Haag. (Dutch). NEVO Table (1991): De Nederlandse voedingsmiddelen tabel. (Dutch). Posner BM, Cupples LA, Franz MM & Gagnon DR (1993): Diet and heart disease risk factors in adult American men and women. Int. J. Epidemiol. 22, 1014±1025. Post GB & Kemper HCG (1995): Procedure and subjects. In: The Amsterdam Growth Study, ed. Kemper HCG. HKP Sport Science Monograph Series, Vol 6, pp 17±27. Post GB & Welten DC (1995): The development of nutritional intake during 15 years of follow-up. In: The Amsterdam Growth Study, ed. Kemper HCG, HKP Sport Science Monograph Series, Vol 6, pp 108±134. Post GB (1989): Nutrition in adolescenceÐa longitudinal study in dietary patterns from teenager to adult. PhD Thesis. SO 16, De Vrieseborch, Haarlem, The Netherlands. Rosenberg IH & Schaefer EJ (1988): Dietary saturated fatty acids and blood cholesterol. N. Engl. J. Med. 318, 1270±1271. Shea S, Melnik TA, Stein AD, Zansky SM, Maylahn C & Basch CE (1993): Age, sex, educational attainment, and race/ethnicity in relation to consumption of speci®c foods contributing to the atherogenic potential of diet. Prev. Med. 22, 203±218. Tanner JM, Whitehouse RH, Marshall WA, Healy MJR & Goldstein H (1975): Assessment of Skeletal Maturity and Prediction of Adult Height (TW2 method). London, Academic Press. Twisk JWR, Kemper HCG & Mellenbergh GJ (1994): Mathematical and analytical aspects of tracking. Epidemiol. Rev. 2, 165±183. Twisk JWR, Kemper HCG, Mellenbergh GJ, van Mechelen W & Post GB (1996): Relation between the longitudinal development of lipoprotein levels and lifestyle parameters during adolescence and young adulthood. Ann. Epidemiol. 6, 246±256. Weiner JS & Lourie JA (1969): Human Biology, a Guide to Field Methods. IBP Handbook, number 9, Oxford, Blackwell. Weisweiler P, Janetscheck P & Schwandt P (1985): In¯uence of poly unsaturated fats and fat restriction on serum lipoproteins in humans. Metabolism 34, 83±87. WHO/ISH (1989): 1989 guidelines for the management of mild hypertension: Memorandum from WHO/ISH meeting bulletin of the World Health Organization, 67±5, 493±498. Zeger SL & Liang KY (1986): Longitudinal data analysis for discrete and continuous outcomes. Biometrics 42, 121±130. 393
© Copyright 2026 Paperzz