Saturated Fat

Citation:
 
Study Design:
Class:
- Click here for explanation of classification scheme.
Quality Rating:
Research Purpose:

To determine whether a low calorie wt loss diet containing oats would produce greater improvements in blood pressure (b/p) and lipid profile than a low cal wt loss diet without oats.

This study also measured energy regulation and influence of age.
Inclusion Criteria:

Wt range limited to BMI of 20-35 kg/m2

Ages 18-75

Men and women

Healthy

Wt stable

Exclusion Criteria:

Taking meds known to influence body wt or b/p

Significant hx of eating d/o

Strenuous exercise of = 1h/d

Description of Study Protocol:

Subjects were recruited.

Neither method of recruitment nor source of subjects were reported.

An 8-week study that took place at the Metabolic Research Unit (MRU) of the Jean Mayer USDA Human Nutrition Research Center on Aging at Tufts University.

First 2 weeks (Phase I) all subjects consumed the same diet of usual food items and the level of calories needed to maintain body wt.

In the 6 week wt loss phase (Phase II) subjects were provided a diet of maintenance energy minus 4.2 MJ/d.

For Phase II subjects were randomized to the control or oat diet on the basis of age and gender to ensure similar characteristics in the 2 Phase II groups.  The younger subjects were further randomized by BMI<25 or =25.

Method of randomization not reported.

The oat-free control diet in Phase II was simply a continuation of the Phase I diet.

The experimental diet contained 45g dry wt/4.2MJ of oats.  A daily multivit w/no minerals was given during Phase II to all subjects due to the inadequate vit content of the low cal diet.

Subjects slept at the MRU on the night before a test only.

Subjects ate 3 meals and 1 snack/d.  The oat diet contained oats in all meals and snacks.

Diets were matched for insoluble fiber, pro, cho, and fat.  Na+ and K+ were held constant at each subject’s level of intake in Phase I.

Subjects were required to eat at least 4 meals/week at the MRU.

 

 

Data Collection Summary:

No blinding used.

During Phase I and II the following measures were done:

*Body wt, body comp, energy expenditure, b/p, blood tests for metabolic variables, 24-h urine.

Body wt and composition

Wt measured with digital electric scale to 0.01 kg.

Ht measured with fixed-wall stadiometer.

Body comp measured with hydrodensitometry after an overnight fast. Done twice during Phase I and twice in Phase II.

Fat free mass calculated using equations of Siri 1961.

Blood Pressure

Taken at each outpatient visit and each stay at MRU after sitting quietly.

Average systolic and diastolic b/p was determined for wk 2 and subtracted from the avg from wk 8 to determine the effect of the Phase II diet on b/p.

Metabolic parameters

Blood was collected twice in Phase I and once in Phase II.

Plasma glc was measured after overnight fast twice during I and once during II.

Oral glc tolerance once in I and II.

Plasma lipids and lipoproteins once in I and II.

Urinary Na+ and K+ were analyzed.  3 consecutive 24-h urine samples collected in wk 5, and repeated in wk 7 or 8.

 

Description of Actual Data Sample:

43 healthy men and women.

*20 men

*23 women

*ages 19-78

control n=21

oat n=22

100% completion rate

 

Summary of Results:

There were no significant differences in the 2 diet groups in age, wt, BMI, %body fat at baseline.

During Phase II both groups had similar wt changes, indicating diet adherence was good. No sig diff between groups in %wt change compared to initial wt.  No sig diff in change in fat mass (Table 1).

There were no effects of initial BMI, initial %body fat, age or gender on wt loss.  No sig diet x age or diet x gender interactions on wt loss (no data).

At baseline mean b/p was normal in both groups.

Diastolic b/p decreased sig within and between both groups after Phase II (Table 1).

Systolic b/p sig decreased only in the oat group after Phase II (Table 1).

Diet appeared to have an effect on SBP independent of wt loss  When controlling for initial b/p, initial BMI, and wt lost, there was a sig diff found in the effect of the oat diet on decreasing SBP (P=0.026) but not DBP (P=0.8).

 

Table 1.  Between and within group differences after treatment.

 

Control

Oats

Between groups

Within group

Absolute wt change

-4.0 ± 1.1 kg

-3.9 ± 1.6 kg

P=0.8

0

Wt change as % of initial wt

-5.3 ± 1.6%

-5.5 ± 2.8%

P=0.76

0

Fat mass change

-2.7 ± 1.6 kg

-2.5 ± 1.3 kg

P=0.65

0

Change SBP

-1 ± 10 mmHg

-6 ± 7 mmHg

0

P=0.7/P=0.0001

Change DBP

-3 ± 5 mmHg

-4 ± 6 mmHg

P=0.4

P=0.013/P=0.007

Urinary Na+ excretion

2498 ± 732 mg/d

2769 ± 814 mg/d

 X

0

Changes in TG mmol/L

-0.22 ± 0.23

-0.36 ± 0.36

X

0

Change in TC

mmo/L

-3.4 ± 0.5

-0.87 ± 0.47

P=0.003

0

Changes in VLDL mmol/L

-0.1± 0.1

-0.16 ± 0.17

X

0

Changes in

LDL mmol/L

-0.2 ± 0.41

-0.6 ± 0.41

P=0.008

0

Changes in HDL mmol/L

-0.04 ± 0.14

0.09 ± 0.13

X

0

X = no significant difference. P value not reported

Author Conclusion:

Adding oats to a wt loss diet may have the benefit of reducing SBP. Sustaining a reduction of SBP to the degree seen in this study (6 mm HG) would have a considerable effect on preventing CVD.

The subjects in this study were normotensive however a low cal wt loss diet that includes oats may have an even greater effect on hypertensive subjects.

The same may be said for subjects with mild to moderate dyslipidemia.

It is unclear if there would continue to be improvement in lipid profiles or b/p after wt stabilization.

The addition of oats to an unhealthy wt loss diet to improve lipids or b/p  is not recommended.

In this study oats were easy to incorporate, was accepted by the subjects and caused no GI complaints.

 

Funding Source:
Government: NIH,US Dept. of Agriculture,
Industry:
Quaker Oates Company
Food Company:
Reviewer Comments:

Small sample size.

No report of how subjects were recruited or from where.

No report on method of randomization.

Control and experimental groups were equal in all characteristics.

Sample included both sexes and huge age span so it shows promise for generalizability if the sample size was larger.

Quality Criteria Checklist: Primary Research
Relevance Questions
  1. Would implementing the studied intervention or procedure (if found successful) result in improved outcomes for the patients/clients/population group? (Not Applicable for some epidemiological studies) Yes
  2. Did the authors study an outcome (dependent variable) or topic that the patients/clients/population group would care about? Yes
  3. Is the focus of the intervention or procedure (independent variable) or topic of study a common issue of concern to dieteticspractice? Yes
  4. Is the intervention or procedure feasible? (NA for some epidemiological studies) Yes
 
Validity Questions
1. Was the research question clearly stated? Yes
  1.1. Was (were) the specific intervention(s) or procedure(s) [independent variable(s)] identified? Yes
  1.2. Was (were) the outcome(s) [dependent variable(s)] clearly indicated? Yes
  1.3. Were the target population and setting specified? Yes
2. Was the selection of study subjects/patients free from bias? Yes
  2.1. Were inclusion/exclusion criteria specified (e.g., risk, point in disease progression, diagnostic or prognosis criteria), and with sufficient detail and without omitting criteria critical to the study? Yes
  2.2. Were criteria applied equally to all study groups? Yes
  2.3. Were health, demographics, and other characteristics of subjects described? Yes
  2.4. Were the subjects/patients a representative sample of the relevant population? Yes
3. Were study groups comparable? Yes
  3.1. Was the method of assigning subjects/patients to groups described and unbiased? (Method of randomization identified if RCT) N/A
  3.2. Were distribution of disease status, prognostic factors, and other factors (e.g., demographics) similar across study groups at baseline? Yes
  3.3. Were concurrent controls or comparisons used? (Concurrent preferred over historical control or comparison groups.) Yes
  3.4. If cohort study or cross-sectional study, were groups comparable on important confounding factors and/or were preexisting differences accounted for by using appropriate adjustments in statistical analysis? N/A
  3.5. If case control study, were potential confounding factors comparable for cases and controls? (If case series or trial with subjects serving as own control, this criterion is not applicable.) N/A
  3.6. If diagnostic test, was there an independent blind comparison with an appropriate reference standard (e.g., "gold standard")? N/A
4. Was method of handling withdrawals described? Yes
  4.1. Were follow-up methods described and the same for all groups? N/A
  4.2. Was the number, characteristics of withdrawals (i.e., dropouts, lost to follow up, attrition rate) and/or response rate (cross-sectional studies) described for each group? (Follow up goal for a strong study is 80%.) N/A
  4.3. Were all enrolled subjects/patients (in the original sample) accounted for? N/A
  4.4. Were reasons for withdrawals similar across groups? N/A
  4.5. If diagnostic test, was decision to perform reference test not dependent on results of test under study? N/A
5. Was blinding used to prevent introduction of bias? No
  5.1. In intervention study, were subjects, clinicians/practitioners, and investigators blinded to treatment group, as appropriate? N/A
  5.2. Were data collectors blinded for outcomes assessment? (If outcome is measured using an objective test, such as a lab value, this criterion is assumed to be met.) N/A
  5.3. In cohort study or cross-sectional study, were measurements of outcomes and risk factors blinded? N/A
  5.4. In case control study, was case definition explicit and case ascertainment not influenced by exposure status? N/A
  5.5. In diagnostic study, were test results blinded to patient history and other test results? N/A
6. Were intervention/therapeutic regimens/exposure factor or procedure and any comparison(s) described in detail? Were interveningfactors described? No
  6.1. In RCT or other intervention trial, were protocols described for all regimens studied? N/A
  6.2. In observational study, were interventions, study settings, and clinicians/provider described? N/A
  6.3. Was the intensity and duration of the intervention or exposure factor sufficient to produce a meaningful effect? N/A
  6.4. Was the amount of exposure and, if relevant, subject/patient compliance measured? N/A
  6.5. Were co-interventions (e.g., ancillary treatments, other therapies) described? N/A
  6.6. Were extra or unplanned treatments described? N/A
  6.7. Was the information for 6.4, 6.5, and 6.6 assessed the same way for all groups? N/A
  6.8. In diagnostic study, were details of test administration and replication sufficient? N/A
7. Were outcomes clearly defined and the measurements valid and reliable? Yes
  7.1. Were primary and secondary endpoints described and relevant to the question? N/A
  7.2. Were nutrition measures appropriate to question and outcomes of concern? N/A
  7.3. Was the period of follow-up long enough for important outcome(s) to occur? N/A
  7.4. Were the observations and measurements based on standard, valid, and reliable data collection instruments/tests/procedures? N/A
  7.5. Was the measurement of effect at an appropriate level of precision? N/A
  7.6. Were other factors accounted for (measured) that could affect outcomes? N/A
  7.7. Were the measurements conducted consistently across groups? N/A
8. Was the statistical analysis appropriate for the study design and type of outcome indicators? Yes
  8.1. Were statistical analyses adequately described and the results reported appropriately? N/A
  8.2. Were correct statistical tests used and assumptions of test not violated? N/A
  8.3. Were statistics reported with levels of significance and/or confidence intervals? N/A
  8.4. Was "intent to treat" analysis of outcomes done (and as appropriate, was there an analysis of outcomes for those maximally exposed or a dose-response analysis)? N/A
  8.5. Were adequate adjustments made for effects of confounding factors that might have affected the outcomes (e.g., multivariate analyses)? N/A
  8.6. Was clinical significance as well as statistical significance reported? N/A
  8.7. If negative findings, was a power calculation reported to address type 2 error? N/A
9. Are conclusions supported by results with biases and limitations taken into consideration? Yes
  9.1. Is there a discussion of findings? N/A
  9.2. Are biases and study limitations identified and discussed? N/A
10. Is bias due to study's funding or sponsorship unlikely? Yes
  10.1. Were sources of funding and investigators' affiliations described? N/A
  10.2. Was the study free from apparent conflict of interest? N/A