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ORIGINAL RESEARCH COMMUNICATION |
1 From the Departments of Foods & Nutrition (CWG, PAL, JMJ, LDM, and DT), Health & Kinesiology (RML), and Statistics (GPM), Purdue University, West Lafayette, IN, and the Department of Medicine, Indiana University, Indianapolis, IN (MP)
2 Abstracts presented at Experimental Biology 2002 (New Orleans, LA) and 2004 (Washington, DC).
3 Supported by the National Dairy Council and General Mills, Inc.
4 Address reprint requests to D Teegarden, Department of Foods & Nutrition, Purdue University, Stone Hall-1264, West Lafayette, IN 47907-1264. E-mail: teegarden{at}cfs.purdue.edu.
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ABSTRACT |
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 TOP ABSTRACT INTRODUCTIONSUBJECTS AND METHODSRESULTSDISCUSSIONREFERENCES |
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Objectives: The objectives of the study were to determine whether acute or chronic increased dairy calcium intakes alter postprandial whole-body fat oxidation and whether the increased intake is related to changes in PTH concentrations.
Design: Normal-weight women aged 18–30 y were randomly assigned to a low (<800 mg/d, control; n = 10) or high (1000–1400 mg/d; n = 9) dietary calcium intake group for 1 y. Whole-body fat oxidation was assessed by measuring respiratory gas exchange after each subject consumed 2 isocaloric liquid meals containing 100 or 500 mg Ca at baseline and 1 y. Fasting serum PTH was measured at baseline and 1 y.
Results: The mean 1-y change in fat oxidation was higher in the high-calcium group than in the low-calcium control group after a low-calcium meal (0.10 ± 0.05 compared with 0.005 ± 0.04 g/min; P < 0.001) and a high-calcium meal (0.06 ± 0.05 compared with 0.03 ± 0.04 g/min; P < 0.05). The 1-y change in serum log PTH was negatively associated with the 1-y change in postprandial fat oxidation after a high-calcium meal (partial r = –0.46, P < 0.04) when controlled for the1-y change in total body fat mass.
Conclusions: The results suggest that a chronic diet high in dairy calcium increases whole-body fat oxidation from a meal, and increases in fasting serum PTH relate to decreases in postprandial whole-body fat oxidation.
Key Words: Calcium intake • dairy intake • intervention • fat oxidation • parathyroid hormone • clinical trial
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INTRODUCTION |
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TOPABSTRACTINTRODUCTIONSUBJECTS AND METHODSRESULTSDISCUSSIONREFERENCES |
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A growing body of evidence supports that higher intakes of calcium are associated with weight loss, often with changes specific to fat mass (5–19). For example, in a 2-y exercise intervention trial in 54 healthy young women, calcium intake—controlled for energy—was negatively associated with changes in body weight and fat mass (11). Other studies have supported an effect of calcium intake on body weight and fat mass in children (8, 18), men (15), and women (6, 9, 11, 15, 19). In addition, dairy products may enhance the effect of calcium on weight loss (14, 16).
It has been proposed that high rates of fat oxidation might protect an individual from obesity, whereas low rates of fat oxidation promote body fat accretion (20). Furthermore, data suggest that dietary calcium affects fat mass through an increase in whole-body fat oxidation (21). In a cross-sectional study of nonobese, healthy adults (n = 35; mean age = 31 y), daily energy expenditure and distribution of macronutrient oxidation were measured by using whole-room indirect calorimetry (21). It was shown that acute calcium intake (mg/kcal) was positively correlated with fat oxidation over 24 h (r = 0.38, P = 0.03), during sleep (r = 0.36, P = 0.04), and during light physical activity (r = 0.32, P = 0.07). After correction for fat mass, fat-free mass, energy balance, acute fat intake, and habitual fat intake, the acute calcium intake explained 10% of the variance in 24-h fat oxidation. This suggests that fat oxidation is increased in response to acute increases in dietary calcium. It is unknown, however, whether chronic intakes of high dietary calcium alter fat oxidation regardless of calcium load.
The regulation of serum calcium by parathyroid hormone (PTH) and 1,25 dihydroxyvitamin D (1,25(OH)2D) induced by changes in dietary calcium has been proposed as a mechanism that mediates the effects of dietary calcium on fat mass. High dietary calcium loads can acutely suppress concentrations of serum PTH (22), and it is hypothesized that serum 1,25(OH)2D concentrations parallel these changes. Both PTH and 1,25(OH)2D increase the concentrations of intracellular calcium in adipocytes, which leads to a decrease in lipolysis and an increase in lipogenesis through increases in fatty acid synthase concentrations in the cell (13, 15). A study by Gunther et al (23) showed that the 1-y change in serum PTH was positively associated with the change in fat mass in healthy, normal-weight, young women (18–31 y).
The current study was designed to determine 1) whether there are differences in fat oxidation in response to an acute low or high dietary calcium load in women consuming a chronically low-calcium diet (before randomization), and 2) whether the chronic intake of high dietary calcium affects fat oxidation after either a low or high dietary calcium load. We hypothesized that increased chronic dietary calcium intake increases whole-body fat oxidation, even with a low-calcium meal, and that fat oxidation would inversely relate to serum PTH.
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SUBJECTS AND METHODS |
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TOPABSTRACTINTRODUCTIONSUBJECTS AND METHODSRESULTSDISCUSSIONREFERENCES |
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Exclusion criteria
Exclusion criteria included the following: 1) chronic intake of medication that interferes with calcium metabolism; 2) malabsorptive, skeletal, muscular, kidney, or hormonal disorders that might affect calcium metabolism; 3) >20% overweight or <15% underweight according to the Metropolitan Life Insurance Tables; 4) self-reported history of an eating disorder; 5) high alcohol consumption (>2 drinks/d); 6) pregnancy or lactation during the previous 6 mo; 7) self-reported symptoms of lactose intolerance; and 8) an unwillingness to consume dairy products.
Assessment of calcium and energy intakes
To select participants with low calcium intakes, a short calcium questionnaire (25) was used for initial screening. A food-frequency questionnaire (26) was used to determine whether the inclusion criteria of <800 mg Ca/d was met. During the study, calcium and energy intakes were assessed by 3-d dietary records at baseline and at 6 and 12 mo. Dietary records were reviewed and analyzed by one trained nutritionist using the Nutrition Data System (NDS) for Research (version 4.04; Food and Nutrient Database 28, Minneapolis, MN). The results of the 3-d dietary records were used in the statistical analyses.
Study design
At baseline, the participants (n = 26) were each given a low- and a high-calcium meal challenge (Figure 1
). After the challenge meal, the thermic effect of a meal, respiratory quotient (RQ), and fat oxidation were determined. These studies allowed the comparison of the effects of a low- and high-calcium meal challenge, with each participant serving as their own control. The participants were then randomly assigned to either the low-calcium control group or the high-calcium group and were followed for 1 y. Differences in participant characteristics were compared by group assignment. At the end of the intervention, the low- and high-calcium meal challenges were repeated for each participant, and the changes in thermic effect of a meal, RQ, and fat oxidation after either the low- or high-calcium meal challenge from baseline to 1 y were determined.
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Weight, body-composition measurements, and physical activity
Weight and body composition were assessed at baseline and at 12 mo after the subjects had fasted and between days 3 and 11 of the menstrual cycle. Weight was measured with a calibrated balance scale while the subjects were wearing light clothing and no shoes. Fat and lean mass were assessed by using dual-energy X-ray absorptiometry (software version 4.3e; Lunar Corp, Madison, WI). Three-day records were collected at baseline and at 6-mo intervals to assess physical activity energy expenditure (kcal/d) with the use of a validated questionnaire (27). The average energy expenditure during the study was calculated as the mean value of the 6- and 12-mo assessments.
Postabsorptive resting metabolic rate
Resting metabolic rate (RMR; kcal/min) was estimated by indirect calorimetry with the use of a metabolic cart (VMax 29n; SensorMedics, Anaheim, CA) at baseline and 12 mo. On the day before the testing was conducted, the subjects were instructed to eat a typical diet, maintain a record of foods ingested, refrain from physical activity and exercise, and avoid caffeine, nicotine, and alcohol. The subjects were also instructed to fast for 12 h before testing. On the morning of the test, the subjects completed a compliance questionnaire regarding these requirements and indicated the days of their menstrual cycle. On entering the semidarkened, thermoneutral laboratory, the subjects voided urine and were placed in a supine position on a bed with a clear ventilated respiratory canopy over the head. The subjects were asked to remain motionless and to breathe normally for 45 min. Readings were taken over the final 10 min and averaged to determine of oxygen uptake (L/min) and the respiratory exchange ratio, from which RMR was estimated. Gas exchange was measured with an infrared carbon dioxide analyzer and a paramagnetic analyzer.
Assessment of postprandial fat oxidation
Within 10 d of the measurement of postabsorptive RMR, the subjects returned to the laboratory on 2 separate mornings for the meal challenges. The procedures for indirect calorimetry were the same as for the postabsorptive RMR assessment described above. On the day before fat oxidation was measured, the subjects were asked to eat meals that were similar to what they ate on the day before the previous test. The subjects consumed a low or a high dairy calcium liquid meal, standardized for energy and macronutrient contents, immediately before the measurement of fat oxidation. At baseline, the low- compared with the high-calcium meal challenges tested the acute effect of calcium intake on fat oxidation after chronically low calcium intakes by the subjects. In contrast, after the intervention, the low-calcium meal challenge tested whether there was an overall body modification in the ability to oxidize fats after chronically high intakes (high-calcium group) compared with chronically low intakes (low-calcium control group). The high-calcium meal challenge tested whether the response to a high calcium load was altered after chronically high (high-calcium) compared with chronically low (low-calcium control group) calcium intakes. Thus, to summarize, both a low- and high-calcium liquid meal were designed and administered at baseline and at 1 y to determine the acute and chronic effects on fat oxidation. Immediately after this meal was consumed, expired air was collected for 10 min with the use of a metabolic cart, which was followed by collections every 10 min for 240 min. At 12 mo, the subjects returned to the laboratory for a repeat of all baseline testing procedures. Postprandial values for fat oxidation (g/min) were estimated for the low- and high-calcium test meals.
Experimental meal design
The liquid meals were adjusted to each subject’s daily energy needs. The percentage of macronutrients was standardized for all subjects (55% carbohydrate, 15% protein, and 30% fat), and the meals (low and high calcium) were administered in random order. The energy content of the experimental meals was 50% of each subject’s postabsorptive RMR. The low-calcium (<100 mg) liquid meals contained the following foods to achieve the percentage of macronutrient and calcium goals: powdered chocolate drink mix (Swiss Miss Sensation; ConAgra Foods, Omaha, NE), soy protein, heavy whipping cream, and orange juice. The high-calcium (>500 mg) meals contained the following foods to meet the percentage of macronutrient and calcium goals: yogurt (Yoplait; General Mills, Minneapolis, MN), powdered chocolate drink mix (Swiss Miss Sensation), heavy whipping cream, and 2%-fat milk. The meals were rapidly consumed in their entirety.
Serum analysis
Blood samples were collected at baseline and at 12 mo during days 3–11 of the menstrual cycle (follicular phase) between 0700 and 1100 after a 12-h fast. After the blood samples were collected and allowed to clot, they were centrifuged and the serum was removed and stored at –80°C. Serum samples were analyzed for concentrations of PTH by a 2-site immunoradiometric assay, which assessed the biologically intact 84 amino acid chain of PTH (Allegro Intact PTH Immunoassay; Nichols Institute, San Clemente, CA).
Statistical analyses
All computations were performed by using SAS software (version 8; SAS Institute, Cary, NC). Means and SDs were computed for all variables of interest. Unless stated otherwise, all data are expressed as means ± SDs. Because the distribution of serum PTH (ng/mL) was positively skewed, a log transformation of this variable was used in the analysis. A paired t test was used to determine the response to a low- or high-calcium meal at baseline before randomization. Baseline and 1-y results were analyzed by using a repeated-measures analysis of variance with group (low-calcium compared with high-calcium intervention) as a between factor and meal (low or high-calcium meal challenge) as a within factor. Student’s t tests were used to examine differences between 1) baseline subject characteristics by group assignment, 2) subjects remaining in the study and dropouts; and 3) calcium and energy intakes during the study by group. Correlations and partial correlations were used to examine relations between PTH and fat-oxidation variables. A partial regression plot was used to illustrate the partial correlation between changes in fat oxidation and log PTH, with control for group and change in fat mass.
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RESULTS |
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The subjects who withdrew from the study after baseline testing (n = 3 in the low-calcium control group; n = 4 in the intervention group) had higher body mass index (BMI; in kg/m2; 24.8 ± 2.1 and 22.0 ± 4, P = 0.05) and fat mass (22.4 ± 5.1 and 16.2 ± 6.4 kg; P = 0.03) values than did the subjects who completed the study (n = 19). However, there were no significant differences in mean baseline age (y), weight (kg), height (cm), lean mass (kg), PTH (ng/mL), dietary calcium (mg/d), or energy intake (kcal/d) between those who withdrew from and those who completed the study.
The baseline characteristics of the subjects who completed the study are shown in Table 1 (n = 19). There were significant differences at baseline between groups in body weight (kg), BMI, and fat mass (kg); the intervention group was heavier and fatter. In contrast, there were no significant differences between groups at baseline in lean mass (kg), fasting concentrations of serum PTH (ng/mL), calcium intake (mg/d), energy intake (kcal/d), or physical activity (kcal/d). The mean total calcium intake was <800 mg/d, and energy intakes were <1900 kcal/d for both groups at the beginning of the study.
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Baseline 2-factor analysis of variance with group (low-calcium group compared with high-calcium group) as a between factor and meal (low or high challenge) as a within factor indicated no statistically significant main effects or interactions for the thermic effect of a meal (Table 2). For fat oxidation and RQ, there were statistically significant group-by-meal interactions (P = 0.02 for both). For the low-calcium meal challenge, fat oxidation was higher and RQ was lower in the control group than in the intervention group (P < 0.0001 for both). In contrast, no group differences were evident after the high-calcium meal challenge (P = 0.16 for both).
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). The intervention group had a greater decrease in RQ after both the low-calcium (–0.20 ± 0.09 and –0.004 ± 0.08; P < 0.0001) and high-calcium (–0.12 ± 0.09 and –0.06 ± 0.08; P < 0.006) meal challenges. The intervention group had a greater increase in fat oxidation after both the low-calcium (0.10 ± 0.05 and 0.005 ± 0.04 g/min; P < 0.0001) and high-calcium (0.06 ± 0.05 and 0.03 ± 0.04 g/min; P < 0.009) meal challenges (Figure 2). There was no significant difference within groups for the change in thermic effect of a meal in response to a low-calcium compared with a high-calcium meal challenge (–31.3 + 67.4 and –28.2 ± 75.1 kcal/4 h) in the low-calcium control group (P = 0.73). However, there were within-group differences in the thermic effect of a meal in the low-calcium group (low-calcium meal challenge: 13.2 ± 25.5 kcal/4 h; high-calcium meal challenge: –15.4 ± 26.3 kcal/4 h; P < 0.02; Figure 2). There were significant differences for the change in fat oxidation in response to a low-calcium compared with a high-calcium meal challenge in the low-calcium control group (0.0047 ± 0.038 and 0.0293 ± 0.038, respectively; P < 0.03) and the high-calcium group (0.100 ± 0.050 and 0.060 ± 0.047, respectively; P < 0.002).
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With the high-calcium meal challenge, baseline log PTH did not correlate with the change in fat oxidation (r = 0.23, P = 0.34), even when the results were adjusted for the change in fat mass and group assignment (partial r = 0.25, P = 0.32). However, the 1-y change in log PTH did correlate with the 1-y change in fat oxidation when the 1-y change in total body fat mass or group assignment were controlled (partial r = –0.45, one-sided P < 0.04; Figure 3). Likewise, these results did not change when baseline physical activity, change in physical activity, or physical activity during the study were included as covariates in the model.
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DISCUSSION |
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TOPABSTRACTINTRODUCTIONSUBJECTS AND METHODSRESULTSDISCUSSIONREFERENCES |
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Although it is proposed that higher rates of fat oxidation might protect an individual from overweight and obesity (21), the increased fat oxidation observed in the intervention group in this study did not translate into a measurable body weight loss or prevention of weight gain (high-calcium group: 0.9 ± 2.5 kg; low-calcium control group: 0.8 ± 2.5 kg). Note, though, that the current study was not powered to detect changes in body weight or fat mass, and 1-y may not be a sufficient amount of time to observe a small negative change in body weight in normal-weight young women. Another possible explanation is that the increased fat oxidation observed in the intervention group had an affect on appetite (28), such that these women compensated through increased energy intake or did not substitute sufficiently so that energy intakes in the dairy group were slightly, but not measurably, higher than those in the low-calcium group. Although data collected from 3-d diet records throughout the intervention showed a difference in energy intake between groups, energy intake is difficult to assess (29) and, therefore, may not be accurately reflected in 3-d diet records. One study, which assessed the relation between calcium and body fat mass (11) in subjects similar to those in the current study (healthy young women), showed that dietary calcium, controlled for energy intake, predicted a significant negative change in body weight (R2 = 0.19) and body fat mass (R2 = 0.27) during a 2-y period. Finally, increased fat oxidation may represent a shift in substrate utilization with no change in overall expenditure. Future research is needed to better understand how alterations in whole-body fat oxidation caused by dietary calcium might affect body weight and fat mass.
Finally, a negative partial correlation was found between the 1-y change in log PTH and the 1-y change in whole-body fat oxidation in response to the high-calcium meal challenge after adjustment for the 1-y change in total body fat mass and group. These results suggest that decreases in serum PTH are associated with an increase in fat oxidation from a meal. This supports the concept of PTH as a potential mediator of the relation between an increased content of calcium in the diet and whole-body fat oxidation. Interestingly, though, the 1-y change in log PTH did not relate to the 1-y change in fat oxidation in response to the low-calcium meal challenge. PTH concentrations are unlikely to change substantially after a low-calcium meal challenge. In contrast, a high-calcium meal challenge acutely reduces PTH concentrations, and the homeostatic concentration of PTH suppression may be modified by the chronic intake of high calcium. Thus, the difference in results between the low- and high-calcium meal challenges, on the basis of fasting PTH concentrations, requires further exploration.
The strengths of this study included the following: 1) length, 2) design (controlled, randomized dietary calcium intervention), 3) use of free-living subjects, and 4) repeated analysis of diet and other lifestyle factors throughout the duration of the study. Although a study conducted in a controlled environment might yield more accurate results, the results of this study better reflect what might occur in response to a public health recommendation aimed at young women to increase dairy calcium. It is important to note that the compliance with the intervention was assessed with the use of self-reported diet records, which are known to be poor indicators of actual intake (29); therefore, compliance is difficult to ensure.
To estimate the biological significance of the changes in fat oxidation noted in this study, the regression equation developed (which included the log of PTH and fat mass changes) was used to predict potential changes in fat oxidation:
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In contrast, fat mass accumulation did not differ significantly by dietary group assignment. Unexpectedly, the low-calcium control group did not gain weight over the year, as often happens in the first year of college and as occurred in the low-calcium consumers in our previous study (11). Thus, we were unable to test whether higher calcium intakes prevent weight gain in this cohort. It is intriguing that higher calcium intakes increase fat oxidation and result in a greater thermic effect of a meal, but this did not translate into changes in body weight. It is possible that in a normal-weight population, an increase in calcium intake results in a shift in substrate utilization, which is measured by fat oxidation, without an increase in energy expenditure. Furthermore, normal-weight persons may have compensatory mechanisms to maintain their body weight and prevent excessive weight loss that might be mediated by increased fat oxidation.
In summary, our findings showed that a 1-y dairy calcium intervention increased fat oxidation in response to a low- or high-calcium liquid meal and thermic effect of a meal after a low-calcium meal challenge. Furthermore, it was shown that the 1-y change in log PTH negatively predicted the 1-y change in fat oxidation in response to a high-calcium liquid meal. Together, these results suggest that women who increase their dairy calcium over a prolonged period, while total energy intake is controlled for, will oxidize higher amounts of fat, potentially through suppression of serum PTH. Future research is warranted to further explore the effects of dietary calcium on whole-body fat oxidation and the mechanism by which this might be occurring.
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ACKNOWLEDGMENTS |
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REFERENCES |
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| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
) and the high-calcium intervention group (•). Linear regression analysis indicated that the 1-y change in log PTH negatively predicted the 1-y change in postprandial fat oxidation after a high-calcium liquid meal after control for the 1-y change in total body fat mass (n = 19; R2 = 0.45, model P = 0.01, partial P = 0.03). Addition of group to the model did not significantly alter the results of the model (P = 0.04). The results did not change when the covariates baseline weight, physical activity, fat oxidation, PTH, BMI, fat mass, and changes in physical activity or mean physical activity during the study were included in the model. The multiple regression equation is as follows: 1-y change in fat oxidation (high-calcium meal) = 0.04 –(0.03 x 1-y change in log PTH) + (0.01 x 1-y change in fat mass).