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The Jean Mayer U.S. Department of Agriculture Human Nutrition Research Center on Aging at Tufts University, Boston, Massachusetts 02111
2To whom correspondence should be addressed at Jean Mayer U.S. Department of Agriculture Human Nutrition Research Center on Aging at Tufts University, 711 Washington St., Boston, MA 02111. E-mail: esaltzman{at}hnrc.tufts.edu
| ABSTRACT |
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KEY WORDS: weight loss oats blood pressure cholesterol humans
| INTRODUCTION |
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Although the benefits observed with complex diets are likely not
attributable to single nutrients, it remains possible that particular
classes of food or individual foods can confer particular benefit. In
addition, the introduction of individual dietary classes or
constituents may be preferable to broader dietary changes in terms of
changing dietary behaviors. Thus, definition of the beneficial
individual constituents of a complex diet is needed. One such possible
constituent is oats, a whole-grain cereal that is rich in soluble
fiber. The effects of oats on lipid metabolism are well documented
(Ripsin 1992
), and there is a growing body of literature
to suggest that oats also lower blood pressure or help prevent
CVD. Population studies suggest that diets rich in oats (He et al. 1994
) or other foods containing soluble fiber
(Pietinen et al. 1996
) are associated with lower levels
of blood pressure or rates of coronary disease. The few intervention
trials examining the effect of oats on blood pressure have been
inconclusive (Kestin et al. 1990
, Swain et al. 1990
), and supplementation trials of soluble fiber have
inconsistently reported beneficial effects on blood pressure
(Krotkiewski 1984
, Rossner et al. 1988
,
Saltzman and Roberts 1997
). However, the amount of oats
may have been inadequate in these trials to achieve the desired effect,
as trials using large doses of foods or soluble fiber have more
consistently demonstrated a blood pressure effect (Krotkiewski 1984
, Singh et al. 1993
). Also, oat or oat fiber
consumption has been shown to reduce postprandial glucose and insulin
concentrations (Braaten et al. 1991 and 1994
), and the
reduction in insulin concentration may provide a mechanism by which
blood pressure could be reduced in response to oat consumption
(Tuck 1992
).
We therefore hypothesized that a diet designed for weight loss that contained oats would produce greater improvements in blood pressure and lipid profiles than a hypocaloric diet without oats. To test this hypothesis, subjects consumed hypocaloric diets with or without oats for 6 wk and demonstrated that a diet containing oats resulted in improvements in a number of CVD risk factors compared with a control diet.
| MATERIALS AND METHODS |
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Subjects were recruited for a trial assessing the effects of
hypocaloric diets with and without oats on body weight, blood pressure
and blood lipids, as well as on measures of energy regulation. Because
one purpose of the trial was to measure energy regulation in healthy
adults, subjects were not specifically recruited on the basis of
preexisting hypertension or dyslipidemia. The weight range of subjects
was limited to a body mass index (BMI) of 2035 kg/m2,
which was chosen to allow a comparison of study variables in
normal-weight individuals with those in overweight or mildly to
moderately obese individuals. In addition, the influence of age was
assessed by comparing responses in younger (age 1830 y) and older
(age 6075 y) age groups. To ensure similar characteristics in the two
diet groups, subjects were randomized on the basis of age and gender
and, in younger subjects, by BMI (< or
25 kg/m2).
The subjects were 43 healthy weight-stable men and women
(Table 1
). None smoked or had a history of recent serious acute or chronic
disease, and all were judged to be healthy on the basis of routine
screening physical examination and blood tests. At screening, subjects
had a systolic blood pressure (SBP) of <150 mm Hg and a diastolic
blood pressure (DBP) of <90 mm Hg. Subjects reported habitually
consuming ethanol of
30 g/d and scored
10 on a dietary restraint
scale (Stunkard and Messick 1985
) administered at
screening. Subjects taking any medication known to influence body
weight or blood pressure, those with a significant history of eating
disorders and those who reported strenuous exercise for
1 h/d were
excluded. The study was approved by the Human Investigation Review
Committee of Tufts University School of Medicine and New England
Medical Center, and written informed consent was obtained from all
subjects.
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The study was conducted at the Metabolic Research Unit (MRU) of the Jean Mayer U.S. Department of Agriculture Human Nutrition Research Center on Aging at Tufts University. The 8-wk protocol was divided into a 2-wk weight-maintenance phase (phase 1) followed by a 6-wk weight-loss phase (phase 2). During both phases, all food and caloric beverages were provided to subjects at the MRU. In phase 1, all subjects consumed the same diet of usual food items (control diet), and the level of energy intake needed to maintain body weight was determined over wk 1 and held constant over wk 2. In phase 2, subjects were provided a diet calculated to contain maintenance energy needs minus 4.2 MJ/d. However, a decrease of 4.2 MJ was thought to be too severe for seven subjects whose initial maintenance requirements were low, and smaller decreases of 3.33.7 MJ were used. In phase 2, subjects consumed one of two study diets: the oats group received a hypocaloric diet containing oats (45 g dry weight/4.2 MJ dietary energy, roughly equivalent to 1.5 servings of oatmeal/4.2 MJ), and the control group continued to consume the same diet as in phase 1. During phase 2, a daily multivitamin containing the Recommended Daily Allowance (RDA) for most vitamins (but not containing minerals) was provided because some subjects had energy intakes that were sufficiently low to preclude intake of the RDA of vitamins from provided food.
During each phase, measures of body weight, body composition, energy expenditure, blood pressure, blood tests for metabolic variables and 24-h urine collections were conducted. Subjects slept in the MRU on nights preceding testing but were otherwise permitted to reside at home. They were encouraged to continue their usual levels of physical activity throughout the 8-wk protocol.
Diets.
All food and energy-containing beverages were provided to the subjects. Three meals and one snack were consumed each day. Subjects were required to eat at least four meals per week in the center and were given other meals for carry-out. After wk 1, subjects were required to consume all food and beverages and to rinse and scrape as well as return food containers.
For phase 1, initial energy needs were predicted using the RDA for
energy (National Research Council 1989
) with appropriate
activity factors applied. Protein was provided as 1.1 g/kg body.
Nonprotein energy was provided as carbohydrate (54% of total energy)
and fat (35% of total energy) (Table 2
). Total energy was adjusted daily over 1 wk to maintain weight within
500 g of d 1. The average daily energy provided over the 1st
7 d was then provided daily to subjects for the 2nd wk. During
this 2nd wk, subjects were required to consume all food. In the rare
event of weight changes of
500 g in phase 2, energy intake was again
adjusted.
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Body weight and composition.
Body weight was measured under standardized conditions with an
electronic digital scale to 0.01 kg, and body height was measured by
fixed-wall stadiometer. Body composition was determined by
hydrodensitometry after an overnight fast: twice during phase 1 and
twice during the last days of phase 2. Measurements were repeated until
at least three measures of body fat were within 2% of each other, and
fat-free mass was calculated according to the equations of
Siri (1961
).
Blood pressure and maximal aerobic capacity.
Blood pressure was determined each residence day and at each outpatient
visit to the MRU and was measured after quiet sitting by nursing staff
using a standard aneroid mercury sphygmomanometer and by noting the
first and fifth Korotkoff sounds. To evaluate the effect of phase 2
diet on blood pressure, initial and final SBP and DBP were defined as
averages of each in wk 2 (phase 1) and wk 8 (phase 2), respectively.
Changes in blood pressure (
SBP and
DBP) were defined as phase
2minusphase 1 values.
Maximal aerobic capacity (
O2max) was
determined during phase 1 with a graded exercise treadmill test using a
standard Bruce protocol (Vogel et al. 1986
) with
collection of expired gases.
Metabolic parameters.
Blood was collected via venipuncture and after the placement of intravenous catheters (for metabolic tests) twice during phase 1 and again for similar measurements at the end of phase 2 (wk 8). Unless otherwise noted, all fasting samples were combined to reflect an average value for each phase.
Plasma glucose (Hexokinase/Glucose-6-Phosphate Dehydrogenase method;
Roche Diagnostic Systems, Branchburg, NJ) and insulin
(radioimmunoassay, DA 125I Insulin Kit; ICN Biomedical,
Costa Mesa, CA) were measured after a 12-h overnight fast twice during
phase 1 and twice during the final week of phase 2 (wk 8), and values
were averaged for each phase. Because changes in fasting insulin and
glucose may be insensitive indicators of changes in insulin
sensitivity, additional models to estimate insulin sensitivity in the
fasting and fed states were used. Insulin resistance was calculated
according to the homeostatic model assessment, where insulin
resistance = (fasting glucose x fasting insulin)/22.5
(Matthews et al. 1985
). In addition, a 2-h 75-g oral
glucose tolerance test was performed once in phase 1 (wk 2) and once at
the end of phase 2 (wk 8), and estimates of whole body insulin
sensitivity were calculated according to the model of Matsuda and DeFronzo (1999
), where insulin sensitivity = 10,000/square root of [(fasting insulin x fasting glucose)
x (mean glucose x mean insulin during oral glucose
tolerance test)].
Plasma lipids and lipoproteins were determined during phase 1 and phase
2 (wk 8) from fasting blood samples collected in tubes containing EDTA.
HDL was prepared after precipitation of apolipoprotein Bcontaining
lipoproteins with dextran sulfate-magnesium chloride from
plasma (Warnick 1982
). Total cholesterol and
triglycerides were determined by automated methods (Abbott Spectrum CCX
Analyzer; Abbott, Dallas, TX) using enzymatic reagents (Abbott A-GENT).
Lipid assays were standardized through the Lipid Standardization
Program of the Centers for Disease Control and Prevention, and CVs for
all lipid assays between and within runs were <2.5%. LDL cholesterol
was estimated by the Friedewald formula (Friedewald et al. 1972
).
Three consecutive 24-h collections of urine were conducted in wk 5 and repeated in wk 7 or 8. Urinary sodium and potassium were analyzed by direct current plasma spectrometry (Spectra-Span VI; Beckman Instruments, Fullerton, CA); concentrations of urinary sodium and potassium were determined for each 24-h collection, and the 3 consecutive days averaged. There were no significant differences between averages for the two time points (wk 5 versus wk 7 or 8), so both were averaged to provide a single value for phase 2.
Statistical analysis.
Data are expressed as means ± SD unless otherwise
noted. Students t test for independent samples was
used to compare the two treatment groups at baseline and to compare
mean change scores between the two groups. ANCOVA was used to adjust
differences for age and gender and to assess interactions of treatment
with diet and gender. When statistically significant interactions were
found, the treatment effect was assessed separately for each treatment
group by using Students t test for paired samples.
Differences were considered statistically significant if the observed
significance level was P
0.05. Statistical
calculations were performed with SYSTAT Version 9 (SPSS, Chicago, IL).
| RESULTS |
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Mean baseline blood pressures were in the normotensive range (Table 1)
.
Within each diet group, paired t tests showed that DBP
decreased significantly from phase 1 to phase 2 (
DBP: control -3
± 5 mm Hg, P = 0.013, oats -4 ± 6 mm Hg,
P = 0.007, difference between oats and control
P = 0.04) (Table 4
). By similar analyses, SBP decreased significantly only in the oats
group (
SBP: control -1 ± 10 mm Hg, P = 0.7,
oats -6 ± 7mm Hg, P < 0.0001). ANCOVA to
determine the effect of diet on blood pressure in phase 2 while
controlling for initial blood pressure, initial BMI and weight lost
(absolute and percent initial) revealed a significant advantage of the
oat diet compared with the control diet on decreases in SBP
(P = 0.026) but not DBP (P = 0.8),
suggesting an effect of diet on SBP independent of weight loss. There
were no significant differences in urinary sodium excretion between
diet groups (oats 2769 ± 814 mg/d, control 2498 ± 732
mg/d).
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| DISCUSSION |
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The magnitude of changes in SBP and DBP in this study are consistent
with the range observed in other nutritional interventions to decrease
blood pressure, including those designed to reduce body weight and
those such as the DASH diet (Appel et al. 1997
). These
interventions have been shown to most effectively reduce blood pressure
in hypertensive patients and to have less consistent effects in
normotensive subjects (Mertens and Van Gall 2000
). Thus,
a hypocaloric diet containing oats consumed by hypertensive subjects
may reduce blood pressure to an even greater extent than observed in
this study: this hypothesis, however, remains untested. Also, the
subjects in this trial had overall favorable lipid profiles, and it is
possible that the inclusion of oats in a hypocaloric diet would be more
effective in those with mild to moderate dyslipidemia.
Because overweight and increasing age are associated with increases in
blood pressure and hyperlipidemia, it would be important to determine
whether a diet such as that used in this study was effective in older
populations. Unfortunately, the number of elderly subjects in this
study, as well as their relatively normal blood pressures and lipid
profiles, did not permit such an analysis, and further work is needed
to address these issues. Systolic hypertension may be associated with
increasing morbidity rates in older persons (Applegate 1992
), so an intervention that reduces SBP, as found in the
present study, may be of particular importance.
Diets rich in oats or similar foods have also been associated with
lower blood pressure in epidemiologic studies (He et al. 1994
, Pietinen et al. 1996
), but the
intervention trials to date that used oats or soluble fiber have
inconsistently improved blood pressure when compared with control diets
(Saltzman and Roberts 1997
). The reasons for this
inconsistency remain unclear, but potential factors include the type of
fiber and its viscosity, the physical form of fiber provided (as part
of whole foods or as an isolate), when fiber is consumed (both the
frequency and whether consumed with other food) and the dose. It should
be noted that the present study incorporated soluble fiber as a whole
food, in conjunction with the consumption of other food, at doses
intermediate to those of existing trials and more frequently than in
most prior trials.
The mechanisms by which an oat-containing diet could confer an advantage in decreasing SBP remain unclear. When the macronutrients and micronutrients considered to potentially influence blood pressure are examined, the only substantial difference between the diets was, again, in soluble fiber. However, the mechanisms underlying the effects of diet are unclear. Insulin resistance has been proposed to influence blood pressure via several means, including direct effects on sympathetic tone and effects on natriuresis. In this study, a nonsignificant trend (P = 0.09) for a greater diminution in fasting insulin was observed with the oat diet, but there was no significant correlation (data not shown) between insulin and blood pressure changes. Also, in this trial there was no significant difference in sodium excretion between diet groups.
In this study, the combination of weight loss along with the inclusion
of oats appeared to have an additive influence on reducing lipid
concentrations. It remains unclear whether the advantages of continued
consumption of the oat diet would be associated with lipid (as well as
blood pressure) benefits after weight stabilization. A review of
existing data on effects of weight loss on these variables suggests
that benefits occur early in weight reduction and are at least in part
due to negative energy balance and that lipid-lowering effects may
partially wane over time despite continued weight loss or maintenance
(Mertens and Van Gall 2000
, Trials of Hypertension Prevention Collaborative Research Group 1992
,
Wadden et al. 1999
). Further investigation is required
to determine whether effects on lipids and blood pressure would persist
after weight stabilization.
It is important to stress that these results do not justify the
recommendation of oats in an unhealthy diet as a supplement to lower
blood pressure and lipids during weight loss. The inclusion
of oats in a diet that is also low in fat and rich in fruit and
vegetables does, however, appear to be promising in promoting improved
risk factors for CVD (Rimm et al. 1996
). The ease with
which oats can be incorporated into such a diet was initially
surprising to us; further, the oat diet was accepted readily and no
gastrointestinal complaints were noted. The optimal dose and frequency
of oat consumption are issues that will require further investigation.
In summary, a weight-loss diet containing oats was associated with favorable decreases in SBP and blood lipids compared with a control diet without oats. Further work is needed to determine whether the benefits observed here can be maintained during weight maintenance after weight loss and whether specific populations, such as those who are overweight, hypertensive or hypercholesterolemic, will respond similarly.
| ACKNOWLEDGMENTS |
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| FOOTNOTES |
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3 Abbreviations used: BMI, body mass index; CVD, cardiovascular disease; DBP, diastolic blood pressure; MRU, Metabolic Research Unit; RDA, Recommended Dietary Allowance; SBP, systolic blood pressure. ![]()
Manuscript received August 10, 2000. Initial review completed September 3, 2000. Revision accepted January 30, 2001.
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