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Keywords:

  • calcium;
  • women;
  • intervention;
  • body composition;
  • fat mass

Abstract

  1. Top of page
  2. Abstract
  3. Introduction
  4. Research Methods and Procedures
  5. Results
  6. Discussion
  7. Acknowledgments
  8. References

Objective: Previous results from this laboratory suggest that a 1-year dairy intake intervention in young women does not alter fat mass. The objective of this study was to determine the impact of the 1-year dairy intervention 6 months after completion of the intervention.

Research Methods and Procedures: Previously, normal-weight young women (n = 154) were randomized to one of three calcium intake groups: control (<800 mg/d), medium dairy (1000 to 1100 mg/d), or high dairy (1300 to 1400 mg/d) for a 1-year trial (n = 135 completed). In the current study, 51 women were assessed 6 months after completion of the intervention trial. Body compositions (body fat, lean mass) were measured using DXA. Self-report questionnaires were utilized to measure activity and dietary intake (kilocalories, calcium).

Results: The high-dairy group (n = 19) maintained an elevated calcium intake (1027 ± 380 mg/d) at 18 months compared with the control group (n = 18, 818 ± 292; p = 0.02). Mean calcium intake over the 18 months predicted a negative change in fat mass (p = 0.04) when baseline BMI was controlled in regression analysis (model R2 = 0.11). 25-Hydroxyvitamin D levels were correlated with fat mass at each time-point (baseline, r = −0.41, p = 0.003; 12 months, r = −0.42, p = 0.002; 18 months, r = −0.32, p = 0.02) but did not predict changes in fat mass.

Discussion: Dietary calcium intake over 18 months predicted a negative change in body fat mass. Thus, increased dietary calcium intakes through dairy products may prevent fat mass accumulation in young, healthy, normal-weight women.


Introduction

  1. Top of page
  2. Abstract
  3. Introduction
  4. Research Methods and Procedures
  5. Results
  6. Discussion
  7. Acknowledgments
  8. References

Obesity is a rapidly growing epidemic world wide. Recent estimates suggest that 30% of adults age 20 years or older are obese (1). In 2003, more than 25% of the adult population in four states were obese (1). Furthermore, 16% of the children and teens in the U.S. were overweight, and this percentage has tripled since 1980 (1). Although genetics play an important role, the rapid rise in the development of obesity supports that lifestyle factors are likely to contribute substantially to this condition (1).

Results from epidemiological research suggest that calcium from dairy products is negatively associated with body weight (2, 3, 4). However, results of intervention trials have been variable. Increased dairy product intake incorporated into weight loss diets leads to decreased fat mass and waist circumference in several randomized intervention trials (6, 7). The results of weight loss trials that include calcium supplementation are more variable (7, 9). Little information is available on the effects of dairy products or calcium intake on prevention of fat mass or weight gain. A 2-year prospective trial (n = 54) showed that calcium intakes, when corrected for energy intakes, were negatively associated with the 2-year change in weight and fat mass (9). Of the 17 calcium supplementation intervention studies reviewed by Barr (10), only one showed less weight gain in the calcium-supplemented group compared with the controls (11, 12). Therefore, the impact of calcium or dairy products on body fat remains controversial.

There are several proposed mechanisms for the negative impact of dietary calcium on body weight regulation. There are data to suggest that high concentrations of calcium intake can decrease absorption of dietary fatty acids through the formation of indigestible calcium soaps in the gastrointestinal tract (13, 14). Dietary calcium regulation of parathyroid hormone (PTH)1 and 1,25 dihydroxyvitamin D3 [1,25(OH)2D3] has also been proposed to mediate the effects of calcium on fat mass. Higher intakes of calcium suppress PTH and subsequently 1,25(OH)2D. Both PTH and 1,25 dihydroxyvitamin D3 increase levels of intracellular calcium in adipocytes, which can lead to a decrease in lipolysis and an increase in lipogenesis through increases in fatty acid synthase levels in the cell (15). This shift in lipid use may lead to an accumulation of fat. In addition, 25-hydroxyvitamin D (25OHD), the marker for vitamin D status, is negatively associated with serum PTH (16, 17). Thus, vitamin D status may be associated with fat mass through regulation of PTH as well.

Gunther et al. (18) reported results from a 1-year dairy product intervention trial in healthy, normal-weight young women. In this trial, women with low calcium intakes were randomized to one of three calcium intake groups: control (<800 mg/d), medium dairy (1000 to 1100 mg/d), or high dairy (1300 to 1400 mg/d), where dairy products were substituted for other diet components to maintain an isocaloric diet. There was no effect on body fat mass or weight during increased dairy product intake in the 1-year intervention trial. However, it is likely that an effect related to prevention of increases in fat mass may be small, albeit significant, over a period of time (3, 4). For example, the difference between the placebo control and the calcium-supplemented groups in the study of Davies et al. (12) was 0.346 kg/yr. This demonstrates a small but significant effect; thus, the length of this trial (∼4 years) may have enhanced the ability to measure these small changes. Trials of shorter duration, small sample sizes, and/or lack of control for individual energy intake may not yield sufficient power to detect small changes in body fat that dietary calcium may elicit.

Therefore, the current study examined the cohort used in the study by Gunther et al. (18) at 6 months after the completion of the 1-year dairy product intervention trial. The current study tested whether differences in fat mass may be detectable when higher calcium intakes are maintained for a longer period of time. The purpose of the current study was to determine whether participation in a 1-year dairy calcium intervention results in changes in calcium intake and changes in body composition 6 months after the completion of the original study.

Research Methods and Procedures

  1. Top of page
  2. Abstract
  3. Introduction
  4. Research Methods and Procedures
  5. Results
  6. Discussion
  7. Acknowledgments
  8. References

Subjects

The current study employed the participants who were willing to return for assessment 6 months after their completion of a 1-year randomized dairy product intervention whose primary endpoints were body composition and weight [n = 154; mean age, 20.1 years (±2.4)]. The parent study is described in detail elsewhere (18). In brief, inclusion criteria included calcium intakes <800 mg/d and energy intakes <2200 kcal/d. Exclusion criteria included >20% overweight or 15% underweight according to the Metropolitan Life Insurance Tables (19). Letters were sent, 1 month before the 18-month time-point, to all subjects who had completed the 1-year trial inviting them to participate in the 6-month follow-up study. Seventy-one subjects expressed interest in the follow-up assessment, and 51 completed all analysis and questionnaires. There was no other contact between the investigators and the participants between the end of the 1-year trial and the 6-month follow-up. The Purdue University Institutional Review Boards approved both studies, and participants provided written, informed consent.

Anthropometric and Body Composition Measurements

Measurements were taken at baseline, 12, and 18 months between Days 3 and 11 of the menstrual cycle (follicular phase) and between 7 am and 11 am after a 12-hour fast. Height of each subject, to the nearest one-tenth of a centimeter, was measured using a stadiometer (Holtain Limited, Crymych, Dyfed, United Kingdom). Weight, to the nearest 0.5 pound (1.1 kg), was measured using a standard physician's balance beam scale (Healthometer, Inc., Bridgeview, IL). These measures were taken with the subject wearing indoor clothes but without shoes. Total body fat mass and lean mass were measured with DXA (software version 4.3e; Lunar Corp., Madison, WI). Body weight and body composition measures are expressed as change at 18 months from baseline (18 months − baseline).

Assessment of Dietary Intake and Other Lifestyle Factors

A food frequency questionnaire (20) was administered to screen participants for eligibility based on daily calcium and energy (kilocalories) intakes. Dietary intake of calcium from all sources was assessed by 3-day food records at baseline, 12, and 18 months. Dietary records were reviewed and analyzed by one trained nutritionist employing the Nutrition Data System for Research, version 4.04, Food and Nutrient Database 28 (Minneapolis, MN). Dietary calcium intake, which includes dairy calcium intake and supplements, is utilized in the analysis. Lifestyle questionnaires assessed previous and current medical history and medication use at baseline, 12, and 18 months.

Laboratory Methods

Blood samples were collected at baseline, 12, and 18 months between Days 3 and 11 of the menstrual cycle (follicular phase) after a 12-hour fast. After collection, blood samples were immediately centrifuged and serum stored at −80 °C. Serum samples were analyzed for levels of 25OHD with enzyme-linked immunosorbent assay (DiaSorin, Inc., Stillwater, MN).

Dairy Product Intervention Protocol

After completion of baseline testing, participants were randomized into one of three groups: a control group (maintain current dietary consumption), a medium-dairy group (1000 to 1100 mg calcium/d from dairy), and a high-dairy group (1300 to 1400 mg/d calcium/d from dairy). Randomization was stratified by oral contraceptive use and energy intake, such that equal numbers of women in each energy decile (1200 to 1299, 1300 to 1399, 1400 to 1499, etc.) would be in each treatment group.

Participants randomized into the dairy calcium groups received individual dietary counseling by trained nutritionists and were instructed to increase daily calcium intakes by substituting dairy products rich in calcium, with an emphasis on non- and low-fat milk. To maintain isocaloric intakes, participants were instructed to remove other dietary components to approximately equal the added dairy intake calories. A record of daily dairy intake and foods removed from the diet to maintain an isocaloric diet were returned monthly by participants in the intervention groups to assess compliance. The logs were checked for accuracy by a nutritionist; if errors were found in the log, the participant was contacted and retrained to follow the dietary protocol. Dietary counseling was provided throughout the duration of the study. Subjects randomized into the control group were instructed to make no changes to their dietary patterns for 12 months after randomization.

Activity

Three-day physical activity records (21) were collected from all subjects at baseline and 3-month intervals throughout the 1-year intervention study and again at 18 months to assess energy expenditure (kilocalories per day). Briefly, participants were counseled to record activity in 15-minute time periods throughout the day using an activity code defined by nine categories. The categories range from 1, lying down (0.26 kcal/kg per 15 minutes) to 9, intense work/activity (1.95 kcal/kg per 15 minutes). An estimate of 24-hour energy expenditure was calculated based on the results.

Statistical Analysis

All data are reported as means ± SD. Data were analyzed using Statistical Analysis System (version 8.2; SAS Institute, Inc., Cary, NC). Univariate analysis was completed on variables. ANOVA, Pearson correlation, and general linear model (GLM) were used as described in the results. Dependent variables include absolute values and changes in fat mass, lean mass, weight, and BMI. Predictive variables include dietary group assignment, calcium intake, and change in calcium intake. Covariates were absolute values and changes in BMI, energy intake, and 25OHD. p < 0.05 was considered significant.

Results

  1. Top of page
  2. Abstract
  3. Introduction
  4. Research Methods and Procedures
  5. Results
  6. Discussion
  7. Acknowledgments
  8. References

Of the 154 participants who were enrolled in the parent study, 135 completed the 12-month intervention, and 51 participants returned at 6 months after completion of the intervention (18 months). The participants who did not complete the 18-month follow-up (n = 83) were older (20.6 ± 2.6 years) at baseline compared with the participants who completed the follow-up (n = 51, 19.4 ± 1.6 years, p < 0.001). There were no other differences between the completers and non-completers. There were no significant differences in baseline characteristics (0 months) by intervention dietary group assignment of the 51 subjects who completed the 18-month follow-up (Table 1). There were also no significant differences in age, weight, fat mass, lean mass, or energy intake at 18 months by intervention dietary group assignment (Table 1).

Table 1.  Baseline and 18-month characteristics of subjects (mean ± standard deviation)*
 Control n = 18Medium dairy n = 14High dairy n = 19
ParameterBaseline18 MonthsBaseline18 MonthsBaseline18 Months
  • *

    Signficantly different from Control 18 months (p = 0.04), and a trend towards a difference from Medium 18 months (p = 0.06).

Age (y)19.6 ± 1.721.2 ± 1.819.1 ± 0.920.9 ± 0.8319.5 ± 2.020.9 ± 1.9
Weight (kg)60.8 ± 11.661.2 ± 10.966.1 ± 13.766.3 ± 14.861.2 ± 7.661.5 ± 7.4
BMI (kg/m2)21.9 ± 3.422.0 ± 3.023.4 ± 4.723.6 ± 5.121.9 ± 2.622.1 ± 2.5
Fat mass (kg)17.0 ± 8.316.6 ± 7.221.3 ± 10.421.1 ± 11.817.4 ± 5.617.0 ± 5.4
Lean mass (kg)40.1 ± 4.740.9 ± 5.040.1 ± 3.441.0 ± 3.439.8 ± 4.540.6 ± 3.7
Calcium intake (mg/d)765 ± 248818 ± 293721 ± 265799 ± 308686 ± 2391028 ± 380*
Energy intake (kcal/d)1786 ± 5231732 ± 3431670 ± 5071605 ± 5191838 ± 3771699 ± 473
25OHD (ng/mL)24.1 ± 7.223.8 ± 7.223.2 ± 8.021.5 ± 8.925.9 + 11.424.9 ± 9.0

The impact of higher dairy product intervention for 12 months on 18-month dietary calcium intakes was assessed. There was a trend toward group assignment predicting 18-month calcium intake (r = 0.07; p = 0.06) in ANOVA. In these analyses, 18-month calcium intake of the high-dairy product intake intervention group was greater than the control (1028 ± 380 vs. 818 ± 293, respectively; p = 0.04) and trending to being greater than the medium-dairy intake intervention group (799 ± 308; p = 0.06) (Table 1). Furthermore, the high-dairy group, but not the control or medium-dairy groups, increased calcium intake from baseline (Table 2). When corrected for 18-month calorie intake in a GLM, intervention group assignment predicted 18-month calcium intake (p = 0.03), indicating that the high-dairy intake group maintained a higher calcium intake. Thus, high-dairy product intake during 1-year intervention trial increased 18-month calcium intakes.

Table 2.  Change in characteristics of subjects from baseline to 18 months (mean ± standard deviation).
Change parameterControl (n = 18)Medium dairy (n = 14)High dairy (n = 19)
  • *

    p = 0.06 main effect of group assessed by ANOVA.

  • p = 0.002 Paired t test difference from zero.

Weight (kg)0.4 ± 1.70.1 ± 6.70.3 ± 3.0
BMI (kg/m2)0.1 ± 0.60.1 ± 1.30.2 ± 1.3
Fat mass (kg)−0.39 ± 1.99−0.32 ± 4.94−0.43 ± 2.8
Lean mass (kg)0.85 ± 1.30.80 ± 1.30.81 ± 1.3
Calcium intake (mg/d)*53 ± 34978 ± 407341 ± 415
Energy intake (kcal/d)−53 ± 646135 ± 521−139 ± 407

The impact of the higher dairy product intake intervention on 18-month body composition measures was assessed. Similar to the results of the participants who completed the 12-month dairy product intervention trial, group assignment did not predict the 12-month change from baseline in fat mass in the participants who completed the 18-month follow-up study (n = 51). In addition, group assignment did not predict change in 18-month fat mass or weight from baseline in a GLM, even when controlled for baseline BMI. There was a trend for 18-month dietary calcium intake to correlate with change in fat mass when uncontrolled (r = −0.25; p = 0.08), and even when controlled for baseline BMI (r = −0.27, p = 0.06). This trend became significant (r = −0.28; p < 0.05) when analyses were controlled for group in addition to baseline BMI. Inclusion of physical activity or mean caloric intake in the model did not alter the results. Consistent with this, the mean calcium intake for the intervention and follow-up combined (mean of 6-, 12-, and 18-month dietary records) (p = 0.04) predicted the 18-month change in fat mass when controlled for baseline BMI in a regression model (R2 = 0.11):

  • image

None of the dietary variables (group assignment nor calcium intakes) was correlated with changes in lean mass, whether or not analyses were controlled for baseline BMI. Thus, the mean dietary calcium intake over 18 months was associated with reduced fat mass.

To further explore the relationship between calcium intake over 18 months and fat mass accumulation, the cohort was subdivided by mean calcium intake of either greater than or less than 800 mg/d. The mean fat mass of each of these subgroups over the time of the intervention and the 18-month follow up are shown in Figure 1. Fat mass was significantly different between these subgroups at 18 months (p = 0.02).

image

Figure 1. Fat mass (kg) from baseline to 18 months by subgroups of < or >800 mg/d calcium intake. (*) p = 0.02 between groups at 18 months.

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The relationship between serum levels of 25OHD and changes in fat mass, weight, and BMI were explored. When 25OHD was added to models to predict changes in body composition, the results were similar to those reported above. Changes in 25OHD at any time-point did not predict changes in any body composition measure. However, 25OHD levels were correlated with fat mass at each time-point (baseline, r = −0.41, p = 0.003; 12 months, r = −0.42, p = 0.002; 18 months, r = −0.32, p = 0.02).

Discussion

  1. Top of page
  2. Abstract
  3. Introduction
  4. Research Methods and Procedures
  5. Results
  6. Discussion
  7. Acknowledgments
  8. References

The results of the current study indicate that increasing dairy product intake through an intervention study promotes increased calcium intakes 6 months after the end of the study period. Furthermore, increased calcium intake leads to a decreased fat mass compared with a low calcium intake over 18 months. There was no effect of group assignment on body fat mass or weight in this cohort (n = 51) at 12 months, which is similar to the total 135 who completed the 12-month study. Thus, the results of the current study support that the impact of calcium intake may be sufficiently small or that fat mass is influenced by other factors, such that it is difficult to detect an effect at 12 months in a normal-weight, healthy young female sample.

The results of this study demonstrate that higher calcium intakes were maintained once the dietary habit was established in a year-long intervention. This is similar to the concept that higher dairy product intake as a child is associated with higher calcium intakes as an adult (22). It is important to develop strategies to promote increased calcium intakes in the U.S. population because intakes are generally far below current recommendations (23). Therefore, increasing dairy product intake in either children or adults for a period of time may lead to enhanced subsequent calcium intakes. The results of this study suggest that participating in an intervention may affect a change in dietary habits for up to 6 months.

Although the perception exists that dairy products will lead to increased weight, in fact, dairy product intake may prevent fat mass gain. In the original cohort (18), the control and low dairy groups did not gain weight over the year; thus, the prevention of weight gain hypothesis was not tested. Our results demonstrate that consuming higher dairy intakes over the 1-year trial promoted increased calcium intakes up to 6 additional months, although not all participants continued to consume higher levels of calcium. In our models, to predict changes in fat mass required high calcium intakes for the year of intervention (group assignment) and continued high calcium intake for another 6 months (18-month calcium intake). Thus, if one consumes higher calcium intakes for 1 year, and then reduces the intake, it may not have a measurable effect on fat mass. However, if one maintains the higher calcium intake for a longer period of time, in this case 18 months, the differences in fat mass become measurable. The current study suggests that women on low calcium intakes will gain fat mass, and higher calcium intakes will reduce fat mass accumulation progressively over 18 months (Figure 1), leading to a small but significant difference in total fat mass between these two populations.

To determine the biological impact, the regression equation described in the results section, which predicted the 18-month fat mass change by mean dietary calcium intake over 18 months when controlled by baseline BMI, was applied. Substituting various calcium intakes into Equation 1 yields, for 500 mg/d, a fat mass gain of 1.26 kg over 18 months, and for 1200 mg/d, a fat mass loss of 0.631 kg over 18 months. The difference in fat mass accumulation is ∼1.89 kg between these two dietary calcium intake exposures over 18 months in normal-weight young women. Although this is a small change, if this effect is maintained over time, it will have a significant impact on the development of obesity. These changes are slightly higher than those of Davies et al. (12), who showed a 0.346 kg/yr difference in weight change between placebo and calcium supplemented (1200 mg/d supplement) in an ∼4-year randomized control trial with post-menopausal women. Although this is a different age group than the current cohort, the estimated size effect is strikingly similar between the two studies. Using the results from specific cohorts from observational studies, Heaney (24) estimated the potential impact of doubling dietary calcium intake in these cohorts. The results suggest that, over time, doubling the dietary calcium intakes of these cohorts predicts a substantial change in overweight and obese prevalence by as much as 60% to 80% (24).

In this study, the influence of calcium on fat mass cannot be separated from other dairy product components because the increase in dietary calcium was achieved through dairy product intake. A few studies (5, 8, 12, 13), but not all (7, 11), suggest an independent effect of calcium; however, longer studies may be necessary to detect differences (3, 4, 11). There is some evidence to support the role of other dairy product components, including amount and type of protein (25, 26) and conjugated linoleic acid (27). Studies in animal models and in humans support that intake of dairy products may enhance effects of calcium intake (6). It is important to understand the mechanism of dietary calcium and other factors (physical activity, adiposity, vitamin D status, and other dairy product components) on body fat mass to predict which individuals are more likely to benefit by manipulation of these factors.

The current results that demonstrate a negative relationship between serum 25OHD levels and fat mass are consistent with previous literature (28, 29). 25OHD negatively correlated with both BMI and body fat mass in the study by Parikh et al. (29). It is proposed that adipose tissue may serve as a reserve for vitamin D storage; thus, greater adiposity reduces serum 25OHD levels. However, it is intriguing to consider that the lower vitamin D status may promote increased adiposity. It is clear that vitamin D status is a key regulator of fasting serum PTH levels (17, 18). In fact, in this cohort, the baseline 25OHD levels were negatively correlated to baseline PTH levels. Thus, it is intriguing to consider that the suppression of PTH levels by improved vitamin D status may also contribute to regulation of fat mass accumulation (3, 28, 29).

The limitations of the current study include that only 38% of the cohort that completed the original trial returned. It is possible that only those who were compliant during the study or who continued to consume dairy products volunteered to return for the follow-up study. However, the medium-dairy intake group who returned did not maintain intervention study calcium intakes and was similar to the control group at 18 months. In addition, group assignment alone did not predict the change in fat mass. Thus, the results of this study suggest that higher calcium intakes over 18 months are associated with reduced body fat, but further research is needed to confirm this association.

In summary, a 1-year dairy product intervention in young women resulted in increased calcium intakes that were sustained for 6 months after the study was stopped. In addition, maintenance of higher dietary calcium intakes over 18 months resulted in a reduced fat mass accumulation compared with low dietary calcium intakes in healthy, normal-weight, young women. Although the effect is small, 18-month maintenance of higher dairy calcium intakes may lead to prevention of slow age-related fat mass gain. Further long-term intervention studies are necessary to more fully understand the influence of calcium and/or dairy products on prevention of fat mass gain.

Acknowledgments

  1. Top of page
  2. Abstract
  3. Introduction
  4. Research Methods and Procedures
  5. Results
  6. Discussion
  7. Acknowledgments
  8. References

This work was supported by Dairy Management, Inc. (Rosemont, IL).

Footnotes
  • 1

    Nonstandard abbreviations: PTH, parathyroid hormone; 25OHD, 25-hydroxyvitamin D; GLM, general linear model.

  • The costs of publication of this article were defrayed, in part, by the payment of page charges. This article must, therefore, be hereby marked “advertisement” in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

References

  1. Top of page
  2. Abstract
  3. Introduction
  4. Research Methods and Procedures
  5. Results
  6. Discussion
  7. Acknowledgments
  8. References
  • 1
    Centers for Disease Control and Prevention Overweight and Obesity: Home http:www.cdc.govnccdphpdnpaobesity (Accessed June 2006).
  • 2
    Parikh, S. J., Yanovski, JA (2003) Calcium intake and adiposity. Am J Clin Nutr 77: 281287.
  • 3
    Teegarden, D. (2005) The impact of dairy product consumption on body composition. J Nutr 135: 27492752.
  • 4
    Heaney, R. P., Davies, K. M., Barger-Lux, MJ (2002) Calcium and weight: clinical studies. J Am Coll Nutr 21: 152S155S.
  • 5
    Zemel, M. B., Thompson, W., Milstead, A., Morris, K., Campbell, P. (2004) Calcium and dairy acceleration of weight and fat loss during energy restriction in obese adults. Obes Res 12: 582590.
  • 6
    Zemel, M. B., Teegarden, D., Van Loan, M., et al. (2004) Role of dairy products in modulating weight and fat loss: a multicenter trial. FASEB J 18: A845A846.
  • 7
    Shapses, S. A., Heshka, S., Heymsfield, SB (2004) Effect of calcium supplementation on weight and fat loss in women. J Clin Endocrinol Metab 89: 632637.
  • 8
    Zemel, M. B., Richards, J., Mathis, S., Milstead, A., Gebhardt, L., Silva, E. (2005) Dairy augmentation of total and central fat loss in obese subjects. Int J Obes Relat Metab Disord 29: 391397.
  • 9
    Lin, Y. C., Lyle, R. M., McCabe, L. D., McCabe, G. P., Weaver, C. M., Teegarden, D. (2000) Dairy calcium is related to changes in body composition during a two-year exercise intervention in young women. J Am Coll Nutr 19: 754760.
  • 10
    Barr, SI (2003) Increased dairy product or calcium intake: is body weight or composition affected in humans? J Nutr 133: 245S248S.
  • 11
    Recker, R. R., Hinders, S., Davies, K. M., et al. (1996) Correcting calcium nutritional deficiency prevents spine fractures in elderly women. J Bone Miner Res 11: 19611966.
  • 12
    Davies, K. M., Heaney, R. P., Recker, R. R., et al. (2000) Calcium intake and body weight. J Clin Endocrinol Metab 85: 46354638.
  • 13
    Papakonstantinou, E., Flatt, W. P., Huth, P. J., Harris, RB (2003) High dietary calcium reduces body fat content, digestibility of fat, and serum vitamin D in rats. Obes Res 11: 387394.
  • 14
    Jacobsen, R., Lorenzen, J. K., Toubro, S., Krog-Mikkelsen, I., Astrup, A. (2005) Effect of short-term high dietary calcium intake on 24-h energy expenditure, fat oxidation, and fecal fat excretion. Int J Obes Relat Metab Disord 29: 292301.
  • 15
    Zemel, M. B., Shi, H., Greer, B., Dirienzo, D., Zemel, PC (2000) Regulation of adiposity by dietary calcium. FASEB J 14: 11321138.
  • 16
    Dawson-Hughes, B., Dallal, G. E., Krall, E. A., Harris, S., Sokoll, L. J., Falconer, G. (1991) Effect of vitamin D supplementation on wintertime and overall bone loss in healthy postmenopausal women. Ann Intern Med 115: 505512.
  • 17
    Krall, E. A., Sahyoun, N., Tannenbaum, S., Dallal, G. E., Dawson-Hughes, B. (1989) Effect of vitamin D intake on seasonal variations in parathyroid hormone secretion in postmenopausal women. N Engl J Med 321: 17771783.
  • 18
    Gunther, C. W., Legowski, P. A., Lyle, R. M., et al. (2005) Dairy products do not lead to alterations in body weight or fat mass in young women in a 1-y intervention. Am J Clin Nutr 81: 751756.
  • 19
    Metropolitan Life Insurance Company (1999) Height and Weight Table for Women Metropolitan Life Insurance Company New York.
  • 20
    Block, G., Woods, M., Potosky, H., Clifford, C. (1998) Validation of a self-administered diet history questionnaire using multiple diet. J Clin Epidemiol 43: 13271335.
  • 21
    Bouchard, C., Tremblay, A., Leblanc, C., Lortie, G., Savard, R., Theriault, G. (1983) A method to assess energy expenditure in children and adults. Am J Clin Nutr 37: 461467.
  • 22
    Teegarden, D., Lyle, R. M., Proulx, W. R., Johnston, C. C., Weaver, CM (1999) Previous milk consumption is associated with greater bone density in young women. Am J Clin Nutr 69: 10141017.
  • 23
    National Center for Health Statistics (1994) Plan and Operation of the Third National Health and Nutrition Examination Survey, 1998–94 US Government Printing Office Washington, DC.
  • 24
    Heaney, RP (2003) Normalizing calcium intake: projected population effects for body weight. J Nutr 133: 268S270S.
  • 25
    Layman, DK (2003) The role of leucine in weight loss diets and glucose homeostasis. J Nutr 133: 261S267S.
  • 26
    Layman, D. K., Baum, JI (2004) Dietary protein impact on glycemic control during weight loss. J Nutr 134: 968S973S.
  • 27
    Wang, Y., Jones, P. (2004) Conjugated linoleic acid and obesity control: efficacy and mechanisms. Int J Obes Relat Metab Disord 28: 941955.
  • 28
    Bell, N. H., Epstein, S., Greene, A., Shary, J., Oexmann, M. J., Shaw, S. (1985) Evidence for alteration of the vitamin-D-endocrine system in obese subjects. J Clin Invest 76: 370373.
  • 29
    Parikh, S. J., Edelman, M., Uwaifo, G. I., et al. (2004) The relationship between obesity and serum 1,25-dihydroxy vitamin D concentrations in healthy adults. J Clin Endocrinol Metab 89: 11961199.