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Erschienen in: Diabetology & Metabolic Syndrome 1/2014

Open Access 01.12.2014 | Research

Effects of diet and exercise interventions on diabetes risk factors in adults without diabetes: meta-analyses of controlled trials

verfasst von: J A D Ranga Niroshan Appuhamy, Ermias Kebreab, Mitchell Simon, Rickey Yada, Larry P Milligan, James France

Erschienen in: Diabetology & Metabolic Syndrome | Ausgabe 1/2014

Abstract

Background and aims

Fasting insulin (FI), fasting glucose (FG), systolic blood pressure (SBP), high density lipoproteins (HDL), triacylglycerides (TAG), and body mass index (BMI) are well-known risk factors for type 2 diabetes. Reliable estimates of lifestyle intervention effects on these factors allow diabetes risk to be predicted accurately. The present meta-analyses were conducted to quantitatively summarize effects of diet and exercise intervention programs on FI, FG, SBP, HDL, TAG and BMI in adults without diabetes.

Materials and methods

MEDLINE and EMBASE were searched to find studies involving diet plus exercise interventions. Studies were required to use adults not diagnosed with type 2 diabetes, involve both dietary and exercise counseling, and include changes in diabetes risk factors as outcome measures. Data from 18, 24, 23, 30, 29 and 29 studies were used for the analyses of FI, FG, SBP, HDL, TAG and BMI, respectively. About 60% of the studies included exclusively overweight or obese adults. Mean age and BMI of participants at baseline were 48 years and 30.1 kg/m2. Heterogeneity of intervention effects was first estimated using random-effect models and explained further with mixed-effects models.

Results

Adults receiving diet and exercise education for approximately one year experienced significant (P <0.001) reductions in FI (-2.56 ± 0.58 mU/L), FG (-0.18 ± 0.04 mmol/L), SBP (-2.77 ± 0.56 mm Hg), TAG (-0.258 ± 0.037 mmol/L) and BMI (-1.61 ± 0.13 kg/m2). These risk factor changes were related to a mean calorie intake reduction of 273 kcal/d, a mean total fat intake reduction of 6.3%, and 40 minutes of moderate intensity aerobic exercise four times a week. Lifestyle intervention did not have an impact on HDL. More than 99% of total variability in the intervention effects was due to heterogeneity. Variability in calorie and fat intake restrictions, exercise type and duration, length of the intervention period, and the presence or absence of glucose, insulin, or lipid abnormalities explained 23-63% of the heterogeneity.

Conclusions

Calorie and total fat intake restrictions coupled with moderate intensity aerobic exercises significantly improved diabetes risk factors in healthy normoglycemic adults although normoglycemic adults with glucose, insulin, and lipid abnormalities appear to benefit more.
Hinweise

Electronic supplementary material

The online version of this article (doi:10.​1186/​1758-5996-6-127) contains supplementary material, which is available to authorized users.

Competing interests

The authors declare that they have no competing interests.

Authors’ contributions

JADRN and JF contributed to conception, design, analysis and interpretation of data and drafted the manuscript. EK and MS contributed to design, analysis and interpretation of data and drafted the manuscript. RY and LPM contributed to conception and drafted the manuscript. All authors read and approved the final manuscript.

Introduction

High prevalence of type 2 diabetes is strongly associated with obesity and lack of physical activity. Type 2 diabetes is a major cause of kidney failure, lower-limb amputation, blindness, heart disease and is a leading cause of death among adults in Western countries [1]. Consequently, diabetes creates a major financial burden on national healthcare systems representing, for example, more than 10% of total healthcare expenditures in the USA, Canada and Europe [2].
Type 2 diabetes is a predictable and preventable disease [3]. In addition to pharmacological interventions, type 2 diabetes can be effectively prevented or delayed by lifestyle changes targeting diet and physical activity improvements [4]. Increases in fasting insulin (FI), fasting glucose (FG), systolic blood pressure (SBP), high density lipoproteins (HDL), triacylglycerides (TAG), and body mass index (BMI) are associated with increased risk of developing diabetes and are often used in mathematical models for predicting the risk of developing diabetes [57]. Reliable estimates of risk factor responses to lifestyle interventions can improve the accuracy of diabetes risk predictions and assist in planning effective diabetes prevention programs.
Several published studies have investigated the effects of diet and exercise interventions on diabetes risk factors but the estimated effect sizes are inconsistent across studies. Meta-analyses are widely used to compare and combine treatment effects across studies and achieve consensus about the overall treatment effect size. However, conclusions drawn from combining data can be misleading, especially if the individual studies and datasets are considerably different. Therefore, estimation and explanation of the between-study variability or heterogeneity of effect sizes should be an important goal in undertaking meta-analyses. Meta-analyses using random-effect models assume that the studies are a random sample of the entire population of studies, allowing inferences to be generalized beyond the studies included. Random-effect meta-analyses also allow for estimation and exploration of heterogeneity [8].
Meta-analyses have previously been published on lifestyle intervention effects in adults diagnosed with type 2 diabetes [9, 10]. However, the present study focused on effects among individuals without diabetes as these are directly related to diabetes prevention rather than management. Yamaoka and Tango [11], Gillies et al. [12] and Norris et al. [13] published meta-analyses summarizing the efficacy of diet and exercise interventions among adults with pre-diabetes or impaired glucose tolerance (IGT). We decided to focus on lifestyle intervention effects irrespective of pre-diabetic risk categories. Evidence suggesting the need for lower cutoff levels for diabetes risk categories in Western populations [14] and including more studies in the analyses provided the impetus for this decision. Besides obtaining estimates of effect sizes for overall lifestyle intervention, we were also interested in examining the effects of important intervention aspects such as calorie and fat intake restrictions and improvements in frequency and duration of exercise.
The objectives of the present meta-analyses were to quantitatively summarize 1) overall effect size of lifestyle education programs targeting both diet and physical exercise modifications and 2) effects of important dietary and exercise attributes on FI, FG, SBP, HDL, TAG and BMI in adults without diabetes in Western populations.

Methods

Studies involving both diet and physical exercise interventions where FI, FG, SBP, TAG, HDL and/or BMI were major outcome measures were searched. Study participants were required to be from Western populations, where the majority is Caucasian. This distinction was made to minimize the potential heterogeneity of intervention effects due to ethnic differences. Study participants in the control group were required to continue with their regular exercise and dietary habits and not receive any diet or exercise counseling prior to or during the study period. MEDLINE and EMBASE computer searches [15] were carried out for articles describing human clinical trials published in English before June 30, 2012 using the keywords: “diet or weight loss”, “exercise or physical activity”, “diabetes risk or cardiovascular risk”, “obese or overweight” and “men and women”. Different combinations of key words were searched in both MEDLINE and EMBASE (Table 1). A total of 894 (278 with MEDLINE and 616 with EMBASE) studies were retrieved from the computer searches. Six hand-searched articles were additionally included (Figure 1). 474 duplicates were removed leaving 420 records to be screened. Two authors separately screened the abstracts of the 420 articles and excluded 137 articles because they were about surveys, feasibility studies, trial designs or mathematical and statistical model analyses (Figure 1). Moreover, some of the excluded studies were not from Western countries. The remaining 283 full text articles were assessed for eligibility to be included. The eligibility criteria were 1) trials included adult (men and/or women) participants who were not diagnosed with diabetes, 2) intervention involved both dietary and exercise counseling, 3) dietary counseling targeted calorie and macronutrient intake modifications, 4) outcome measures included changes in diabetes risk factors compared to a control group, 5) availability of mean and variance measures of risk factor changes from baseline in both control and intervention groups, and 6) availability of information on macronutrient intake changes of intervention and control participants. A total of 249 articles were excluded as they did not meet the eligibility criteria (Figure 1). Two [16, 17] of the 34 remaining articles reported risk factors for men and women separately. The male and female groups in these reports were considered two separate studies leaving 36 studies for quality assessment. Quality of the selected studies was evaluated by assessing the risk of four biases [18]: 1) selection bias representing systematic differences between baseline characteristics of intervention and control groups, 2) performance bias regarding exposure to factors other than the interventions of interest, 3) attrition bias involving systematic differences between groups in withdrawals from a study, and 4) publication bias assessed as described below. Baseline characteristics of study participants were not considerably different between control and intervention arms in any of the 36 studies. Although some studies encouraged increased fiber intake and reduced cholesterol intake besides macronutrient intake modifications, these studies were kept in the dataset because fiber and cholesterol intake effects can be accounted for in the analyses as described below. Most of the studies reported no systematic differences between withdrawal groups. However, two articles were excluded because the studies had considerable dropout rates (>30%) with no note on the similarities or differences of the withdrawal groups (Figure 1). Although, the statistical significance (P-values) of the intervention effects did not change, the magnitude of the effect sizes changed notably when these two studies were excluded. Since obtaining accurate effect size estimates for lifestyle interventions regarding diabetes risk was the main objective of the present study, we proceeded with the meta-analyses without these two studies. Therefore, the final data set used for the meta-analyses contained 34 studies (Figure 1 and Table 2).
Table 1
Number of articles retrieved from MEDLINE and EMBASE databases for different key word combinations
Keywords
MEDLINE
EMBASE
Diet, exercise, obese, diabetes risk, men, women
27
56
Diet, exercise, overweight, diabetes risk, men, women
29
50
Diet, exercise, obese, cardiovascular risk, men, women
32
63
Diet, exercise, overweight, cardiovascular risk, men, women
34
69
Diet, physical activity, obese, diabetes risk, men, women
29
67
Diet, physical activity, overweight, diabetes risk, men, women
28
84
Diet, physical activity, obese, cardiovascular risk, men, women
33
77
Diet, physical activity, overweight, cardiovascular risk, men, women
31
97
Weight loss, exercise, obese, diabetes risk, men, women
18
21
Weight loss , exercise, overweight, diabetes risk, men, women
17
32

Data and variables

Data were extracted and put onto structured Excel datasheets designed to capture relevant information in a concise manner. Two authors conducted the screening and data extraction independently using a common set of instructions prepared for the relevant tasks. Sample size (N), mean risk factor levels at baseline and standard deviation (SD) of FI, FG, SBP, HDL, TAG and BMI changes during intervention of the control and intervention arms were essential to the analyses. Mean FI and BMI values were recorded in mU/L and kg/m2, respectively, while the other risk factors were recorded in mmol/L. In the absence of a reported SD, if 95% confidence intervals for the risk factor changes were provided, the SD was calculated assuming the changes were normally distributed. In a few cases, the SD was calculated using the P-values for risk factor changes from baseline and corresponding test statistics. N was the number of participants completing each treatment and undergoing post-treatment risk factor measurements. Information on energy (kcal/d) and the macronutrients: carbohydrate, protein, total fat, and saturated fat intake [% of energy intake (%E)] at baseline and at the end of the interventions were recorded in separate columns of the datasheet. When the macronutrient intakes were reported in g/d (along with daily energy intake), the %E values were calculated using Atwater energy equivalents [19]. Energy and macronutrient intake changes (from baseline) in the control and intervention groups were calculated separately. Difference (d) between these changes mean values are given in Table 3 was then calculated and used in the statistical models.
Table 2
Summary description of the diet plus exercise intervention studies included in the analyses
Study
Authors and year
Country
Age1
Women2
IGT/IR/MetS3
BMI4
Diet intervention guidelines5
Exercise intervention guidelines5
1
Straznicky et al. 2012 [20]
Australia
55
0.41
MS
32.7
~650 kcal/d restriction, 22% protein, 30% TF, 9% SF
aerobic (biking), 40 min/S, 3–4 S/wk
2
Blumenthal et al. 2010 [21]
USA
52
0.69
NA
33.3
~500 kcal/d restriction, 27% TF
aerobic (biking and walking), 40 min/S, 3–4 S/wk
3
Ibanez et al. 2010 [22]
Spain
50
1.00
NA
35.0
500 kcal/d restriction
resistance training, 45–60 min/S, 2 S/wk
4
Straznicky et al. 2010 [23]
Australia
55
0.41
MS
32.4
~500 kcal/d restriction, 30% TF, 9% SF
aerobic (biking), 40 min/S, 3 S/wk
5
Roumen et al. 2008 [24]
Netherlands
56
0.45
IGT
29.4
reduced caloric and reduced fat diet
aerobic plus resistant training, 30 min/S, 5 S/wk
6
Herder et al. 2009 [25]
Finland
56
0.50
IGT
31.2
<30% TF, <10% SF
endurance training, >30 min/S, ~6 S/wk
7
Mosca et al. 2008 [26]
USA
48
0.66
NA
28.1
low-SF and low-cholesterol diet
moderate physical activity (brisk walking), 30–60 min/S
8
Morgan et al. 2009 [27]
UK
41
0.74
NA
31.6
Rosemary Conley's controlled-calorie low-fat diet
Rosemary Conley's Fitness plan with weekly classes
9
Dale et al. 2009 [28]
New Zealand
46
0.67
IR
34.6
400 kcal/d restriction, 27% TF, 9% SF
high intensity training, 30 min/S, 5 S/wk
10
Meckling and Sherfey, 2007 [29]
Canada
43
1.00
NA
29.9
500 kcal/d restriction, high protein (37%) diet
endurance training, 36 min/S, 3 S/wk
11
Burke et al. 2007 [30]
Australia
56
0.56
NA
30.1
<30% TF, <10% SF
moderate intensity, 30 min/S, most days/wk
12
Bo et al. 2007 [31]
Italy
56
0.58
MS
30.0
reduced TF and SF intake
moderate intensity (i. e. brisk walking), ~150 min/wk
13
Arciero et al. 2006 [32]
USA
43
0.48
NA
27.8
high protein (40%) and low fat (20%) diet
resistance and cardiovascular training, 20 min/S, 4–6 S/wk
14
Brekke et al. 2005 [33]
Sweden
42
0.37
NA
26.1
<30% TF intake, <10% SF intake
walking or more intensive exercise, 30 min/S, 4–5 S/wk
15
Watkins et al. 2003 [34]
USA
50
0.50
NA
33.7
500 kcal/d restriction, <20% TF
cycle ergometry and jogging, or walking, ~60 min/S, 3–4 S/wk
16
Lindstrom et al. 2003 [35]
Finland
55
0.66
IGT
31.3
200 kcal/d restriction, <30% TF, <10% SF
endurance exercise & resistance training, >30 min/S
17
Esposito et al. 2003 [36]
Italy
35
1.00
NA
34.5
1400 kcal/d, 55% carbohydrate, 30% TF, <10% SF
aerobic exercise (walking and swimming)
18
Mensink et al. 2003 [37]
Netherlands
56
0.43
IGT
29.5
>55% carbohydrate, <30% TF, <10% SF
moderate physical activity, >30 min/S, 5 S/wk
19
McAuley et al. 2002 [38]
New Zealand
46
0.71
IR
34.5
400 kcal/d restriction, 27% TF, 9% SF
Moderate exercise plus resistance training, >20 min/S, 5 S/wk
20
Miller et al. 2002 [39]
USA
54
0.62
NA
33.7
500 kcal/d restriction, 27% TF, 6% SF
aerobic (brisk walking and biking), 30–45 min/S, 3 S/wk
21
Reseland et al. 2001 [40]
Norway
45
0.00
MS
27.5
400 kcal/d restriction, <30% TF
endurance exercise, 1 h/S, 3 S/wk
22
Oldroyd et al. 2001 [41]
UK
58
0.40
IGT
30.2
<30% TF intake, ~50% carbohydrate
aerobic exercise, 20–30 min/S, 2–3 S/wk
23
Kuller et al. 2001 [42]
USA
47
1.00
NA
25.0
Calorie restriction upto 1300 kcal, 25% TF, 7% SF
increasing physical activity to 1250 kcal expended weekly
24
Ornish et al. 1998 [43]
USA
60
0.09
NA
26.9
10%-fat vegetarian diet
moderate-intensity aerobic, 1 h/S, 5 S/wk
25
Stefanick et al. 1998 (female) [16]
USA
57
1.00
NA
25.6
<30% TF intake, <7% SF intake
aerobic (jogging and brisk walking), 60 min/S, 3 S/wk
26
Stefanick et al. 1998 (male) [16]
USA
48
1.00
NA
27.8
<30% TF intake, <7% SF intake
aerobic (jogging and brisk walking), 60 min/S, 3 S/wk
27
Wing et al. 1998 [44]
USA
46
0.78
NA
36.0
600-700 kcal/d restriction, 20% TF intake
aerobic (brisk walking), 60 min/S, 5 S/wk
28
Simkin-Silverman et al. 1995 [45]
UK
47
1.00
NA
25.1
<25% TF intake, <7% SF intake
brisk walking spending 1000 kcal/wk, 3–5 S/wk
29
Hellenius et al. 1993 [46]
Sweden
46
0.00
NA
25.6
12% daily calorie and 10% TF restriction
aerobic exercise, 30–45 min/S, 2–3 S/wk
30
Svendsen et al. 1993 [47]
Denmark
54
1.00
NA
29.7
800 kcal/d restriction, low fat (25%) diet
aerobic plus resistant training, 75 min/S, 3 S/wk
31
Page et al. 1993 [48]
UK
40
0.23
IGT
25.9
50-55% carbohydrate, 30% TF, high fiber
aerobic weight and circuit training, swimming, >3 S/wk
32
Schuler et al. 1992 [49]
Germany
54
0.00
NA
26.6
<20% TF, 65% carbohydrate, PUSF: SF ratio >1.0
daily exercise (75% MHR), >30 min/S
33
Wood et al. 1991 (male) [17]
USA
38
0.00
NA
33.5
55% carbohydrate, 30% TF, <10% SF
aerobic (brisk walking and jogging), 35 min/S, 3 S/wk
34
Wood et al. 1991 (female) [17]
USA
38
1.00
NA
26.3
55% carbohydrate, 30% TF, <10% SF
aerobic (brisk walking and jogging), 35 min/S, 3 S/wk
1Average age of participants at baseline (years), 2fraction of women participants, 3whether participants had abnormalities such as impaired glucose tolerance (IGT), insulin resistance (IR) and metabolic syndrome (MetS) or no abnormalities (NA), 4average BMI of participants at baseline (kg/m2), 5TF = Total fat (% of energy), SF = Saturated fat (% of energy), and S = exercise session.
d = Nutrient intake change in intervention group Change in control group
When the nutrient intake changes of control participants were not available, they were assumed to be unchanged from baseline during the interventions. With respect to exercise interventions, two explanatory variables: the number of exercise sessions per week (ES) and minutes of exercise per session (EM) were created. Two binary variables were also created to represent presence or absence of dietary counseling regarding fiber intake increase (FB) and cholesterol intake reduction (CH). As some exercise intervention programs included resistance training sessions, a binary variable (ERT; 1 = presence or 0 = absence) was created to examine the impact of resistance training on the diabetes risk factors. When actual ES and EM measures were not available, they were assumed to be equivalent to the exercise intervention guidelines (Table 2). Some studies exclusively recruited people with abnormalities such as impaired glucose tolerance (IGT), insulin resistance (IR), or metabolic syndrome (MetS). Another binary variable (ABN) was created to identify studies that exclusively used participants with such abnormalities. Average age in years, study duration in months and the fraction of women in the study population (ranging from 0, only men to 1, only women) were also extracted. When the biomarker levels were measured at multiple time points, the measures of the nutrient intake at the latest time point were used. For some studies, the selected time point was after a follow-up period. Therefore, an additional binary variable (IFU) was generated to represent presence or absence of a follow-up period.

Statistical analyses

Separate meta-analyses were conducted for each biomarker using the metafor (version 1.6-0) package in R (version 2.12.2) [50]. Mean difference (MD) was chosen as the effect size measure as it allows effect size interpretation in the original units of risk factor measurement.
M D = Mean risk factor change Intervention - Mean risk factor change Control
This choice was further supported by the fact that the metafor package allows for weighting individual studies for corresponding sample variance as described below [50]. The forest plots of each risk factor were also constructed using MD (Figures 2, 3, and 4). In addition to MD, forest plots give average sample size, intervention duration, and absolute risk factor changes in the control and intervention arms.
Let:
y i = θ i + e i
where y i is the observed effect size or MD in the ith study, θ i is the corresponding (unknown) true effect size, e i is the sampling error [e i  ~ N(0, v i )]. Sampling variances (i.e., v i ) are assumed to be known and remained fixed during estimation in order to weight the individual studies when estimating model parameters [50]. Between-study variability (heterogeneity) of the true effects θ i was assumed to be purely random, leading to random-effect models given by:
θ i = μ + u i
where θ i is the true effect size (e.g., MD) in the ith study, μ is the overall true effect size, and u i is the random deviation from the overall effect size (u i  ~ N(0, τ2)), which was unknown but estimated from the data. The true effects were normally distributed with mean μ and variance τ 2 . If τ2 = 0, homogeneity is implied among true effects across individual studies such that μ=θ. Heterogeneity (τ2) was expressed as a percentage of total variability (τ2 plus sample variance) yielding I 2 statistics.
Table 3
Summary statistics for variables across the 34 studies included in the meta-analyses
Variable
Mean ± SD1
Minimum
Maximum
Energy and macronutrient intake at baseline
  
Calorie intake, kcal/d
2100 ± 260
1583
2900
Carbohydrate, %E
46.6 ± 5.0
36.5
58.5
Protein, %E
17.2 ± 2.6
12.3
25
Fat, %E
34.7 ± 3.3
27.5
43.5
Saturated fat, %E
12.9 ± 1.8
9
16.6
Energy and macronutrient intake changes of intervention participants 2
Calorie intake, kcal/d
-273 ± 169
-828
49.5
Carbohydrate, %E
2.9 ± 5.7
-14
11
Protein, %E
3.3 ± 5.6
-3.8
21.3
Fat, %E
-6.3 ± 3.8
-16.5
0.4
Saturated fat, %E
-2.9 ± 2.0
-8
0.0
Exercise intervention
   
Number of sessions per week
4 ± 1.0
2
7
Session length (minutes)
41 ± 13
20
75
Risk factor level measurements at baseline
   
FI
14.9 ± 5.4
3.0
24.1
FG
5.55 ± 0.4
4.83
6.20
SBP
128 ± 10
110
143
HDL
1.25 ± 0.2
0.89
1.74
TAG
1.76 ± 0.9
0.85
5.84
BMI
30.2 ± 3.3
25.0
36.0
Age at baseline, years
49 ± 7
35
60
Fraction of women participants
0.59 ± 0.3
0
1
Duration of intervention (months)3
14 ± 3.5
2
60
1SD, Standard deviation.
2Change from baseline compared to that of control participants.
3Duration from baseline to the risk factor level measurements used in the analyses.
An I2 value greater than 50% indicates considerable heterogeneity. Thus, for response variables (e.g., intervention effects on diabetes risk factors in the present study) with I2 > 50%, the random-effect models were extended to mixed-effect models including fixed effects of explanatory variables (meta-regression analyses) with the potential to explain the heterogeneity in intervention effects. The mixed-effect models were given by:
θ i = β 0 + β 1 x i 1 + + β p x i p + u i
where β0 is the overall true effect size, x ij is the the value of the jth explanatory variable (j = 1, 2, …, p) for the ith study, β j is the change in the true effect size for a unit increase in the jth explanatory variable and u i  ~ N(0, τ2). Here, τ2 denotes the amount of residual heterogeneity [50]. The parameters in the mixed-effect models (β0, …, β p ) were estimated via weighted least squares with weights equal to 1/(v i  + τ2).
The candidate explanatory variables for the mixed-effect models were energy and macronutrient intake changes, the exercise attributes: ES, EM and ERT, baseline risk factor level, baseline age and BMI, time duration from baseline to the post-intervention risk factor measurements, FB, CH, ABN, IFU and fraction of women in the study population. Each continuous explanatory variable was centered on its mean before being used in the mixed-effect models. This allows for interpreting the meta-regression coefficients in terms of changes in intervention effect size for a unit change in a continuous explanatory variable from its mean. Mixed-effect models including individual explanatory variables were first fitted to the data. Full multivariate mixed-effect models were then formed including all explanatory variables having notable effects (P <0.10) when fitted individually. Reduced models were formed via stepwise elimination of one explanatory variable at a time. The final mixed-effect models were chosen by comparing reduced models vs. full models using log-likelihood ratio tests with the maximum likelihood method.

Publication bias and influence diagnosis

Publication bias and presence of influential cases can affect the validity and robustness of the conclusions from a meta-analysis [51, 52]. Studies for which the effect size estimates and their variability are extremely sensitive were recognized using a leave-one-out approach. The leave1out function in metafor package was used to execute this influence diagnostic analysis, which is equivalent to a sensitivity analysis. Cook’s distance and τ 2 estimates (τ2D) were obtained when each study was excluded from the data set. [50]. If a study was related to a Cook’s distance >2 and τ2D two SD below the mean τ2D of the other studies, that study was removed from the dataset. Initially, 19, 25, 25, 31, 30, and 30 of the 34 studies were chosen for FI, FG, SBP, HDL, TAG and BMI analyses respectively, but after the influence analyses 18, 24, 23, 30, 29, and 29 studies were retained, respectively. Presence of publication bias was assessed using funnel plots. Asymmetric funnel plots indicate the presence of publication bias. Egger’s regression test was used to examine funnel plot asymmetry [50]. None of the funnel plots was found to be significantly asymmetric (P-values for funnel plot asymmetry >0.05) indicating absence of publication bias in all cases.

Results

Study characteristics

Of the 34 studies included in meta-analyses, 16, 13, and 5 studies were from Europe, North America, and Australia and New Zealand, respectively (Table 2). Information about ethnic composition of participants was not available in all the articles. Based on the articles reporting the ethnic composition, >60% of the study participants were Caucasian. Average age at baseline ranged from 35 to 60 years with a mean of 49 years, indicating that the majority of study participants were middle-aged. Twenty of the 34 studies recruited exclusively overweight and obese individuals. Average baseline BMI varied from 25.0 to 36.0 kg/m2 with a mean of 30.2 kg/m2 (Table 3). Twelve of the 34 studies examined diet plus exercise intervention specifically in adults with abnormalities such as IGT, IR, or MetS. Average FG of participants in the individual studies ranged between 4.83 and 6.20 mmol/L, with a mean of 5.55 mmol/L. The respective FI range was 3.0 and 24.1 mU/L with a mean of 14.9 mU/L. Time duration from baseline risk factor measurements to the post-intervention measurements varied from 2 to 60 months with a mean of 14 months (Table 3). In a few studies, this duration included a follow-up period in addition to the intervention counselling period. Nine of the studies included only female participants and four used only males while the rest (21 studies) included both males and females. The majority of lifestyle intervention programs aimed to restrict energy intake by 500 kcal/d, total fat ≤30%E, and saturated fat ≤10%E (Table 2) and to improve physical activity through moderate-intensity aerobic exercises such as brisk walking, jogging, cycling, and swimming. About one-third of the intervention programs included instructions for resistance training. Overall, the intervention programs involved an average of 4 exercise sessions a week each lasting 41 minutes (Table 3).

Heterogeneity

Random-effect model analyses (Table 4) revealed substantial heterogeneity (τ2, P <0.001) of lifestyle intervention effects on all risk factors. The I2 estimates (τ2/τ2 + sample variance) were >99.0% in all cases (Table 4) indicating that between-study variability of intervention effects (τ2) were >110 times greater than within-study variability (sample variance). Therefore the random-effect models were extended to mixed-effect models to explore heterogeneity.
Table 4
Heterogeneity ( τ 2 ) of lifestyle intervention effects and statistical significance of funnel plot asymmetry from random-effect models
Risk factor1
Number of studies included
N2
Heterogeneity2
Funnel plot asymmetry ( P-value)3
I 2 (%)2
τ 2
P-value
FI (mU/L)
18
1756
99.5
3.762 ± 1.511
<0.001
0.519
FG (mmol/L)
24
3897
99.4
0.013 ± 0.005
<0.001
0.774
SBP (mm Hg)
23
3443
99.4
7.474 ± 2.894
<0.001
0.771
HDL (mmol/L)
30
4218
99.8
0.007 ± 0.002
<0.001
0.577
TAG (mmol/L)
29
3908
99.8
0.050 ± 0.015
<0.001
0.855
BMI (kg/m2)
29
4160
99.8
0.881 ± 0.256
<0.001
0.587
1FI: Fasting insulin, FG: Fasting glucose, SBP: Systolic blood pressure, HDL: High density lipoprotein, TAG: Triacylglyceride, BMI: Body mass index.
2total number of participants, who concluded the interventions.
2I 2  = heterogeneity (τ 2 ) expressed as a percentage of total variance (τ 2  + sample error).
3From Egger’s regression test.

Intervention effect size estimates from mixed-effect models

Calorie intake restrictions, abnormalities such as IGT or IR, and resistance training exercises influenced FI responses to lifestyle interventions (P <0.10) and accounted for 60% of the heterogeneity [τ2 = 3.762 (Table 4) vs. 1.523 (Table 5)]. Lifestyle interventions reduced FI by 2.56 ± 0.58 mU/L (Table 5) in normal adults engaging in moderate intensity aerobic exercise. This decrease in FI was related to a mean 273 kcal/d restriction (Table 3). The negative parameter estimate of calorie restriction in Table 5 shows that an additional 100 kcal/d restriction would have reduced FI by an additional 0.68 ± 0.26 mU/L. On the other hand, incorporation of resistance training into the exercise intervention impeded the expected FI decline by 1.72 ± 0.81 mU/L. Hence, the expected FI change among adults engaging in resistance training was -0.84 mU/L (-2.56 + 1.72 mU/L). Regardless of the degree of calorie restriction and exercise intensity, adults with metabolic abnormalities tended (P = 0.082) to experience an extra FI reduction of 1.20 ± 0.69 mm Hg (Table 5).
Table 5
Estimates of intervention effect size and total amount of residual heterogeneity ( τ 2 ) from final mixed-effect models
Risk factor1
Overall effect size
Effect size change for intervention attributes and other factors
Residual heterogeneity
Estimate ± SE
P- value
Explanatory Variables2
Estimate ± SE3
P-value
τ2
P-value
FI (mU/L)
-2.56 ± 0.58
<0.001
Presence of IGT, IR or MetS
-1.20 ± 0.69
0.082
1.523 ± 0.773
<0.001
   
Calorie restriction (100 kcal/d)
-0.68 ± 0.26
0.009
  
   
Incorporation of resistance training
1.72 ± 0.81
0.034
  
FG (mmol/L)
-0.18 ± 0.04
<0.001
Presence of IGT, IR or MetS
-0.08 ± 0.05
0.098
0.010 ± 0.004
<0.001
   
After a follow-up period
0.13 ± 0.06
0.034
  
SBP (mm Hg)
-2.77 ± 0.56
<0.001
Presence of IGT, IR or MetS
-3.23 ± 1.00
0.001
2.796 ± 1.419
<0.001
   
Calorie restriction (100 kcal/d)
-0.64 ± 0.23
0.006
  
   
Length of intervention (months)
0.13 ± 0.03
<0.001
  
HDL (mmol/L)
-0.015 ± 0.015
0.305
Age at baseline (years)
-0.006 ± 0.002
0.021
0.005 ± 0.002
<0.001
   
Fraction of women participants
-0.086 ± 0.046
0.065
  
TAG (mmol/L)
-0.258 ± 0.037
<0.001
Calorie restriction (100 kcal/d)
-0.061 ± 0.017
<0.001
0.029 ± 0.009
<0.001
   
Baseline TAG (mmol/L)
-0.243 ± 0.076
0.001
  
BMI (kg/m2)
-1.61 ± 0.13
<0.001
Calorie restriction (100 kcal/d)
-0.22 ± 0.08
0.003
0.353 ± 0.125
<0.001
   
Fat intake restriction (% Energy)
-0.10 ± 0.03
0.003
  
   
Exercise session duration (10 min)
-0.24 ± 0.12
0.055
  
   
Baseline BMI (kg/m2)
-0.07 ± 0.04
0.095
  
1FI: Fasting insulin, FG: Fasting glucose, SBP: Systolic blood pressure, HDL: High density lipoprotein, TAG: Triacylglyceride, BMI: Body mass index.
2IGT = Impaired glucose tolerance, IR = Insulin resistance and MetS = Metabolic syndrome.
3Standard error of the estimate.
Diet plus exercise interventions reduced FG by 0.18 ± 0.04 mmol/L (P <0.001) in normoglycemic healthy adults. The metabolic abnormality and follow-up period variables considerably explained the heterogeneity of the intervention effects on FG. Heterogeneity was reduced by 23% when these factors were included in the final model (τ2 = 0.013 vs. 0.010). Participants experienced less (by 0.13 ± 0.06 mmol/L) FG decline as they entered a follow-up period, during which rigorous intervention counselling was not provided. Regardless of undergoing a follow-up period or not, adults with metabolic abnormalities tended (P = 0.098) to experience a greater FG decline (by 0.08 ± 0.05 mmol/L) compared to normal adults (Table 5). Diet and exercise interventions reduced SBP by 2.77 ± 0.56 mm Hg (P <0.001, Table 5). However, study participants with abnormalities experienced an extra SBP decline of 3.23 ± 1.00 mm Hg (Table 5). Extending intervention by a month reduced the expected SBP decline by 0.13 ± 0.03 mm Hg. Calorie restriction increased by 100 kcal/d was associated with an additional SBP decline of -0.64 ± 0.23 mm Hg (P = 0.006). Presence or absence of abnormalities, intervention duration, and degree of calorie intake restriction explained collectively 63% [τ2 = 7.474 (Table 4) vs. 2.796 (Table 5)] of heterogeneity of the intervention effect on SBP.
The diet plus exercise interventions did not have a significant impact (P = 0.305) on HDL (Table 5). Nonetheless, age of participants at baseline and percentage of women in the study population explained 29% of heterogeneity in HDL changes in intervention participants compared to control participants. The lifestyle interventions reduced TAG by 0.258 ± 0.037 mmol/L (P <0.001). This drop in TAG was related to a mean net energy intake restriction of 273 kcal/d and a mean baseline TAG of 1.76 mmol/L (Table 3). An additional 100 kcal/d energy restriction would have further improved the decrease in TAG by 0.061 ± 0.017 mmol/L. A unit increase in TAG at baseline was associated with an additional TAG drop of 0.243 ± 0.076 mmol/L.
Adult participants experienced a 1.61 ± 0.13 kg/m2 (P <0.001) BMI decline when engaged in a diet plus exercise lifestyle intervention program. The extent of calorie and total fat intake restrictions, duration of exercise sessions, and baseline BMI considerably affected the degree of BMI change (P <0.060, Table 5). An extra 100 kcal/d energy intake restriction, a unit increase in total fat intake restriction and an additional 10 minutes of exercise would have further reduced BMI by 0.22 ± 0.08, 0.10 ± 0.03 and 0.24 ± 0.12 kg/m2, respectively. Obese adults appeared to respond more to the interventions than normal and overweight adults because a unit increase in BMI at baseline from the mean (30.1 kg/m2) was associated (P = 0.095) with an additional 0.07 ± 0.04 kg/m2 BMI decline. The final mixed-effect model including calorie and fat restrictions, exercise duration, and BMI at baseline explained 60% of the heterogeneity in lifestyle intervention effect on BMI [τ2 = 0.881 (Table 4) vs. 0.353 (Table 5)].

Discussion

Although meta-analytic applications are increasingly used to summarize results from clinical trials, much uncertainty remains about which approach to use, particularly when significant between-study variability of results or heterogeneity is present [53]. Random-effect methods provide an attractive approach for summarizing heterogeneous results [53]. The lifestyle intervention effects of individual studies included in the present meta-analyses were very heterogeneous (Figures 2, 3 and 4). Therefore, the overall effect sizes and total amount of heterogeneity (τ2) was estimated using random-effect approaches. In addition to determining the overall effect size, random-effect approaches allow for exploring factors responsible for heterogeneity. These approaches involve mixed-effect models and are similar to meta-regression approaches. Thus, mixed-effect models were used to explore heterogeneity and estimate the impacts of important attributes of lifestyle interventions on risk factor changes. Such estimates are difficult to find in the literature but would improve diabetes risk prediction models. For example, Appuhamy and colleagues [54] developed a mathematical model for predicting diabetes incidence using BMI. Incorporating the effect size estimates of BMI (Table 5) should enable their model to predict diabetes incidence changes in response to lifestyle modifications. The present meta-analyses summarized effects of lifestyle modifications on other diabetes risk factors such as FI, FG, SBP, HDL and TAG. These factors are also used in mathematical models for predicting diabetes risk [57].
Fasting insulin in normoglycemic adults is an important predictor of diabetes risk independent of whether they have insulin resistance or not [55]. Thus, lowering FI could be an option in primary diabetes prevention [55]. The present meta-analyses showed that non-diabetic adults engaging in a diet plus exercise intervention program experienced a 17% reduction in FI from baseline. Although dietary guidelines in the studies advocate on average a 500 kcal/d energy restriction, the average net energy intake reduction among intervention participants was 273 kcal/d. A greater compliance with calorie restriction would have further decreased FI because FI was found to decrease linearly by 0.68 mU/L for each additional 100 kcal/d reduction. Hence an actual 500 kcal/d energy restriction would have reduced FI by 4.10 mU/L. Participants with impaired glucose tolerance or insulin resistance had their FI improved to a greater extent than normal participants. When resistance training was incorporated into moderate intensity aerobic exercises, the expected FI improvement for lifestyle interventions was significantly reduced by 1.72 mU/L. This agrees with Holten et al. [56] who demonstrated that strength training could increase FI levels in non-diabetic adults.
Fasting glucose is often used in diabetes risk prediction models [57], although plasma glucose based on the oral glucose tolerance test (OGTT) or the IGT test (IGTT) would better predict diabetes risk [58]. The greater cost and inconvenience associated with these tests generally impede their use in diabetes prediction models [59]. Furthermore, we chose FG over OGTT and IGTT-based glucose because FG was measured in many of the searched studies. Diet and exercise interventions were associated with a decline in FG of 0.18 mmol/L, representing a 3% drop from baseline (P <0.001). Elevating FG from normoglycemic levels to impaired fasting glucose (IFG) levels doubles the risk of developing diabetes [60, 61]. The mean baseline FG of 5.55 mmol/L indicates that many of the study participants were at a high risk of developing diabetes especially considering the fact that the current cutoff for IFG (5.60 mmol/L) needs to be reduced for some Western populations [14]. Therefore, this 3% FG reduction should delay diabetes development in Western adults. Our results showed that continuous dietary counselling and physical activity improvement were necessary for a persistent FG decline. Moreover, the FG levels of adults with abnormalities such as IGT or MetS improved more than those of normal adults.
Hypertension is recognized as an independent predictor of diabetes incidence in various populations. Systolic blood pressure above 120 mm Hg is associated with twice the diabetes risk of SBP below 100 mm Hg [62]. The present meta-analyses showed that diet plus exercise intervention counseling reduced (P <0.001) SBP by 2.77 mm Hg. This decline in SBP could be associated with a considerable reduction in diabetes risk as Dotevall et al. [63] reported a 0.10 diabetes hazard ratio increase for every unit increase in SBP above 130 mm Hg. Normoglycemic adults with abnormalities such as IGT or MetS experienced greater declines in SBP, suggesting more lifestyle intervention benefits for them than for ordinary adults. An improved compliance with calorie restriction guidelines, particularly as the intervention program progressed, could have resulted in a greater SBP decline.
Dyslipidaemia, characterized by elevated TAG and reduced HDL, is usually associated with increased risk of developing diabetes mellitus [64]. Diet plus exercise interventions reduced TAG by 0.258 mmol/L (P <0.001). This could be associated with a considerably reduced risk of developing diabetes as Tirosh et al. [65] reported a 13% reduction in diabetes risk for each 0.20 mmol/L decline in TAG in non-diabetic men. The declines in TAG were greater as baseline TAG levels increased, suggesting more lifestyle intervention benefits for dyslipidaemic adults than normolipidaemic adults. Greater calorie restrictions further enhanced the TAG declines, in agreement with the findings of Fontana et al. [66]. When summarized over 30 studies, diet plus exercise interventions did not have a significant impact on HDL. Fourteen studies were associated with reduced HDL (the negative mean differences in Figure 4A) while the rest showed zero or positive responses. Differences in baseline age and percentage of women in the study population explained 29% of the heterogeneity in HDL responses to lifestyle interventions.
Body mass index is a leading diabetes risk predictor as evidenced by the high correlation between obesity and diabetes prevalence. Curioni and Lourenco [67] and Schaar et al. [68] have summarized diet plus exercise intervention effects on weight loss in adults regardless of diabetes status. These analyses together examined 22 studies and found significant weight loss in response to intervention. We found a consistent reduction in BMI (P <0.001) of 1.61 kg/m2 (5.3% from baseline BMI) for diet plus exercise interventions. Such a BMI reduction could be associated with a considerable reduction in diabetes risk as Chiu et al. [69] estimated a 30% diabetes incidence drop in response to a BMI reduction from 30.0 to 28.0 kg/m2. Moreover, the mathematical model developed by Appuhamy et al. [53] predicts that a 1.61 kg/m2 in BMI decline can lead to a 20% diabetes incidence reduction in non-diabetic middle-aged adults. The heterogeneity in lifestyle intervention effect on BMI was significant (Figure 2B and Table 4). However, degrees of calorie and total fat intake restrictions, duration of exercise and BMI at baseline explained 60% of the heterogeneity. An additional 100 kcal/d calorie intake reduction, an extra unit reduction in total fat intake, and extending the exercise session length by 10 minutes could collectively result in an additional 0.56 kg/m2 decline in BMI. BMI decline significantly improved as baseline BMI increased, suggesting greater lifestyle intervention benefit for obese adults than for adults of normal weight.
Considerable unexplained heterogeneity still remained (residual heterogeneity estimates in Table 5), indicating that factors other than those taken into consideration in the present analyses could be responsible for between-study variability of lifestyle intervention effects. In addition to carbohydrate, fat and protein as explanatory variables, the present meta-analyses also accounted for saturated fat and cholesterol intake restrictions, and fiber intake improvements. However, they did not significantly (P >0.10) explain heterogeneity of lifestyle intervention effects. Data on food sources of fatty acids could have explained heterogeneity to some extent [70, 71] but availability of such data was extremely limited in the studies considered. Representations of exercise intensity (e.g., percent maximum heart rate and percent maximum oxygen consumption) may have explained some of the heterogeneity. Furthermore, representation of degree of compliance with diet and exercise guidelines [72] and ethnic composition of participants [73] could have further explained heterogeneity. As the selected articles [2049] did not consistently report sufficient information to create such variables, we were unable to explore their contribution to heterogeneity.
In summary, lifestyle interventions targeting calorie and total fat intake restrictions and increase in moderate intensity aerobic exercises were associated with significant improvements in diabetes risk factors among normoglycemic adults. Differences in some intervention attributes such as energy and fat intake restrictions, exercise type and session duration, length of intervention, and baseline characteristics of study participants accounted for 23-63% of the heterogeneity. Having explained such proportions of heterogeneity, lifestyle interventions were associated with significant declines in FI, FG, SBP, TAG, and BMI of 2.56 mU/L, 0.18 mmol/L, 2.77 mm Hg, 0.258 mmol/L, and 1.61 kg/m2 respectively in healthy normoglycemic adults. However, normoglycemic adults having abnormalities such as IGT, insulin resistance, metabolic syndrome or hyperlipidemia appeared to benefit more from diet plus exercise intervention programs than healthy normoglycemic adults.
This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://​creativecommons.​org/​licenses/​by/​4.​0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver (http://​creativecommons.​org/​publicdomain/​zero/​1.​0/​) applies to the data made available in this article, unless otherwise stated.

Competing interests

The authors declare that they have no competing interests.

Authors’ contributions

JADRN and JF contributed to conception, design, analysis and interpretation of data and drafted the manuscript. EK and MS contributed to design, analysis and interpretation of data and drafted the manuscript. RY and LPM contributed to conception and drafted the manuscript. All authors read and approved the final manuscript.
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Literatur
1.
Zurück zum Zitat Williams R, Van Gaal L, Lucioni C: Assessing the impact of complications on the costs of type II diabetes. Diabetologia. 2002, 45: S13-S17. 10.1007/s00125-002-0859-9.CrossRefPubMed Williams R, Van Gaal L, Lucioni C: Assessing the impact of complications on the costs of type II diabetes. Diabetologia. 2002, 45: S13-S17. 10.1007/s00125-002-0859-9.CrossRefPubMed
2.
Zurück zum Zitat Zhang P, Zhang X, Brown J, Vistisen D, Sicree R, Shaw J, Nichols G: Global healthcare expenditure on diabetes for 2010 and 2030. Diabetes Res Clin Pract. 2010, 87: 293-301. 10.1016/j.diabres.2010.01.026.CrossRefPubMed Zhang P, Zhang X, Brown J, Vistisen D, Sicree R, Shaw J, Nichols G: Global healthcare expenditure on diabetes for 2010 and 2030. Diabetes Res Clin Pract. 2010, 87: 293-301. 10.1016/j.diabres.2010.01.026.CrossRefPubMed
4.
Zurück zum Zitat Karve A, Hayward RA: Prevalence, diagnosis, and treatment of impaired fasting glucose and impaired glucose tolerance in nondiabetic U.S. adults. Diabetes Care. 2010, 33: 2355-2359. 10.2337/dc09-1957.PubMedCentralCrossRefPubMed Karve A, Hayward RA: Prevalence, diagnosis, and treatment of impaired fasting glucose and impaired glucose tolerance in nondiabetic U.S. adults. Diabetes Care. 2010, 33: 2355-2359. 10.2337/dc09-1957.PubMedCentralCrossRefPubMed
5.
Zurück zum Zitat Hjellvik V, Sakshaug S, Strom H: Body mass index, triglycerides, glucose, and blood pressure as predictors of type 2 diabetes in a middle-aged Norwegian cohort of men and women. Clin Epidemiol. 2012, 4: 213-224.PubMedCentralCrossRefPubMed Hjellvik V, Sakshaug S, Strom H: Body mass index, triglycerides, glucose, and blood pressure as predictors of type 2 diabetes in a middle-aged Norwegian cohort of men and women. Clin Epidemiol. 2012, 4: 213-224.PubMedCentralCrossRefPubMed
6.
Zurück zum Zitat McNeely MJ, Boyko EJ, Leonetti DL, Kahn SE, Fujimoto WY: Comparison of a clinical model, the oral glucose tolerance test, and fasting glucose for prediction of type 2 diabetes risk in Japanese Americans. Diabetes Care. 2003, 26: 758-763. 10.2337/diacare.26.3.758.CrossRefPubMed McNeely MJ, Boyko EJ, Leonetti DL, Kahn SE, Fujimoto WY: Comparison of a clinical model, the oral glucose tolerance test, and fasting glucose for prediction of type 2 diabetes risk in Japanese Americans. Diabetes Care. 2003, 26: 758-763. 10.2337/diacare.26.3.758.CrossRefPubMed
7.
Zurück zum Zitat Boutayeb A, Chetouani A: A critical review of mathematical models and data used in diabetology. Biomed Eng Online. 2006, 5: 43-10.1186/1475-925X-5-43.PubMedCentralCrossRefPubMed Boutayeb A, Chetouani A: A critical review of mathematical models and data used in diabetology. Biomed Eng Online. 2006, 5: 43-10.1186/1475-925X-5-43.PubMedCentralCrossRefPubMed
8.
Zurück zum Zitat DerSimonian R, Kacker R: Random-effects models for meta-analysis of clinical trials: an update. Contemp Clin Trials. 2007, 28: 105-114. 10.1016/j.cct.2006.04.004.CrossRefPubMed DerSimonian R, Kacker R: Random-effects models for meta-analysis of clinical trials: an update. Contemp Clin Trials. 2007, 28: 105-114. 10.1016/j.cct.2006.04.004.CrossRefPubMed
9.
Zurück zum Zitat Norris SL, Lau J, Smith SJ, Schmid CH, Engelgau MM: Self-management education for adults with type 2 diabetes: a meta-analysis of the effect on glycemic control. Diabetes Care. 2002, 25: 1159-1171. 10.2337/diacare.25.7.1159.CrossRefPubMed Norris SL, Lau J, Smith SJ, Schmid CH, Engelgau MM: Self-management education for adults with type 2 diabetes: a meta-analysis of the effect on glycemic control. Diabetes Care. 2002, 25: 1159-1171. 10.2337/diacare.25.7.1159.CrossRefPubMed
10.
Zurück zum Zitat Brand-Miller J, Hayne S, Petocz P, Colagiuri S: Low-glycemic index diets in the management of diabetes: a meta-analysis of randomized controlled trials. Diabetes Care. 2003, 26: 2261-2267. 10.2337/diacare.26.8.2261.CrossRefPubMed Brand-Miller J, Hayne S, Petocz P, Colagiuri S: Low-glycemic index diets in the management of diabetes: a meta-analysis of randomized controlled trials. Diabetes Care. 2003, 26: 2261-2267. 10.2337/diacare.26.8.2261.CrossRefPubMed
11.
Zurück zum Zitat Yamaoka K, Tango T: Efficacy of lifestyle education to prevent type 2 diabetes: a meta-analysis of randomized controlled trials. Diabetes Care. 2005, 28: 2780-2786. 10.2337/diacare.28.11.2780.CrossRefPubMed Yamaoka K, Tango T: Efficacy of lifestyle education to prevent type 2 diabetes: a meta-analysis of randomized controlled trials. Diabetes Care. 2005, 28: 2780-2786. 10.2337/diacare.28.11.2780.CrossRefPubMed
12.
Zurück zum Zitat Gillies CL, Abrams KR, Lambert PC, Cooper NJ, Sutton AJ, Hsu RT, Khunti K: Pharmacological and lifestyle interventions to prevent or delay type 2 diabetes in people with impaired glucose tolerance: systematic review and meta-analysis. BMJ. 2007, 334: 299-10.1136/bmj.39063.689375.55.PubMedCentralCrossRefPubMed Gillies CL, Abrams KR, Lambert PC, Cooper NJ, Sutton AJ, Hsu RT, Khunti K: Pharmacological and lifestyle interventions to prevent or delay type 2 diabetes in people with impaired glucose tolerance: systematic review and meta-analysis. BMJ. 2007, 334: 299-10.1136/bmj.39063.689375.55.PubMedCentralCrossRefPubMed
13.
Zurück zum Zitat Norris SL, Zhang X, Avenell A, Gregg E, Schmid CH, Lau J: Long-term non-pharmacological weight loss interventions for adults with prediabetes. Cochrane Database Syst Rev. 2005, CD005270- Norris SL, Zhang X, Avenell A, Gregg E, Schmid CH, Lau J: Long-term non-pharmacological weight loss interventions for adults with prediabetes. Cochrane Database Syst Rev. 2005, CD005270-
14.
Zurück zum Zitat Valdes S, Botas P, Delgado E, Alvarez F, Cadorniga FD: Does the new American Diabetes Association definition for impaired fasting glucose improve its ability to predict type 2 diabetes mellitus in Spanish persons? The Asturias Study. Metabolism. 2008, 57: 399-403. 10.1016/j.metabol.2007.10.017.CrossRefPubMed Valdes S, Botas P, Delgado E, Alvarez F, Cadorniga FD: Does the new American Diabetes Association definition for impaired fasting glucose improve its ability to predict type 2 diabetes mellitus in Spanish persons? The Asturias Study. Metabolism. 2008, 57: 399-403. 10.1016/j.metabol.2007.10.017.CrossRefPubMed
15.
Zurück zum Zitat Wilkins T, Gillies RA, Davies K: EMBASE versus MEDLINE for family medicine searches: can MEDLINE searches find the forest or a tree?. Can Fam Physician. 2005, 51: 848-849.PubMed Wilkins T, Gillies RA, Davies K: EMBASE versus MEDLINE for family medicine searches: can MEDLINE searches find the forest or a tree?. Can Fam Physician. 2005, 51: 848-849.PubMed
16.
Zurück zum Zitat Stefanick ML, Mackey S, Sheehan M, Ellsworth N, Haskell WL, Wood PD: Effects of diet and exercise in men and postmenopausal women with low levels of HDL cholesterol and high levels of LDL cholesterol. N Engl J Med. 1998, 339: 12-20. 10.1056/NEJM199807023390103.CrossRefPubMed Stefanick ML, Mackey S, Sheehan M, Ellsworth N, Haskell WL, Wood PD: Effects of diet and exercise in men and postmenopausal women with low levels of HDL cholesterol and high levels of LDL cholesterol. N Engl J Med. 1998, 339: 12-20. 10.1056/NEJM199807023390103.CrossRefPubMed
17.
Zurück zum Zitat Wood PD, Stefanick ML, Williams PT, Haskell WL: The effects on plasma lipoproteins of a prudent weight-reducing diet, with or without exercise, in overweight men and women. N Engl J Med. 1991, 325: 461-466. 10.1056/NEJM199108153250703.CrossRefPubMed Wood PD, Stefanick ML, Williams PT, Haskell WL: The effects on plasma lipoproteins of a prudent weight-reducing diet, with or without exercise, in overweight men and women. N Engl J Med. 1991, 325: 461-466. 10.1056/NEJM199108153250703.CrossRefPubMed
18.
Zurück zum Zitat Higgins JPT, Altman DG: Chapter 8: assessing risk of bias in included studies. Cochrane Handbook for Systematic Reviews of Interventions. Edited by: Higgins JPT, Green S. 2008, Chichester: John Wiley & Sons Ltd, 187-241.CrossRef Higgins JPT, Altman DG: Chapter 8: assessing risk of bias in included studies. Cochrane Handbook for Systematic Reviews of Interventions. Edited by: Higgins JPT, Green S. 2008, Chichester: John Wiley & Sons Ltd, 187-241.CrossRef
19.
Zurück zum Zitat Merrill AL, Watt BK: Energy value of foods: basis and derivation. Agriculture Handbook. 1973, Washington, DC: US Department of Agriculture, Agricultural Research Service, 74 Merrill AL, Watt BK: Energy value of foods: basis and derivation. Agriculture Handbook. 1973, Washington, DC: US Department of Agriculture, Agricultural Research Service, 74
20.
Zurück zum Zitat Straznicky NE, Lambert EA, Grima MT, Eikelis N, Nestel PJ, Dawood T, Schlaich MP, Masuo K, Chopra R, Chopora R, Sari CI, Dixon JB, Tilbrook AJ, Lambert GW: The effects of dietary weight loss with or without exercise training on liver enzymes in obese metabolic syndrome subjects. Diabetes Obes Metab. 2012, 14: 139-148. 10.1111/j.1463-1326.2011.01497.x.CrossRefPubMed Straznicky NE, Lambert EA, Grima MT, Eikelis N, Nestel PJ, Dawood T, Schlaich MP, Masuo K, Chopra R, Chopora R, Sari CI, Dixon JB, Tilbrook AJ, Lambert GW: The effects of dietary weight loss with or without exercise training on liver enzymes in obese metabolic syndrome subjects. Diabetes Obes Metab. 2012, 14: 139-148. 10.1111/j.1463-1326.2011.01497.x.CrossRefPubMed
21.
Zurück zum Zitat Blumenthal JA, Babyak MA, Sherwood A, Craighead L, Lin PH, Johnson J, Watkins LL, Wang JT, Kuhn C, Feinglos M, Hinderliter A: Effects of the dietary approaches to stop hypertension diet alone and in combination with exercise and caloric restriction on insulin sensitivity and lipids. Hypertension. 2010, 55: 1199-1205. 10.1161/HYPERTENSIONAHA.109.149153.PubMedCentralCrossRefPubMed Blumenthal JA, Babyak MA, Sherwood A, Craighead L, Lin PH, Johnson J, Watkins LL, Wang JT, Kuhn C, Feinglos M, Hinderliter A: Effects of the dietary approaches to stop hypertension diet alone and in combination with exercise and caloric restriction on insulin sensitivity and lipids. Hypertension. 2010, 55: 1199-1205. 10.1161/HYPERTENSIONAHA.109.149153.PubMedCentralCrossRefPubMed
22.
Zurück zum Zitat Ibanez J, Izquierdo M, Martinez-Labari C, Ortega F, Grijalba A, Forga L, Idoate F, Garcia-Unciti M, Fernandez-Real JM, Gorostiaga EM: Resistance training improves cardiovascular risk factors in obese women despite a significative decrease in serum adiponectin levels. Obesity (Silver Spring). 2010, 18: 535-541. 10.1038/oby.2009.277.CrossRef Ibanez J, Izquierdo M, Martinez-Labari C, Ortega F, Grijalba A, Forga L, Idoate F, Garcia-Unciti M, Fernandez-Real JM, Gorostiaga EM: Resistance training improves cardiovascular risk factors in obese women despite a significative decrease in serum adiponectin levels. Obesity (Silver Spring). 2010, 18: 535-541. 10.1038/oby.2009.277.CrossRef
23.
Zurück zum Zitat Straznicky NE, Lambert EA, Nestel PJ, McGrane MT, Dawood T, Schlaich MP, Masuo K, Eikelis N, De Courten B, Mariani JA, Esler MD, Socratous F, Chopra R, Sari CI, Paul E, Lambert GW: Sympathetic neural adaptation to hypocaloric diet with or without exercise training in obese metabolic syndrome subjects. Diabetes. 2010, 59: 71-79. 10.2337/db09-0934.PubMedCentralCrossRefPubMed Straznicky NE, Lambert EA, Nestel PJ, McGrane MT, Dawood T, Schlaich MP, Masuo K, Eikelis N, De Courten B, Mariani JA, Esler MD, Socratous F, Chopra R, Sari CI, Paul E, Lambert GW: Sympathetic neural adaptation to hypocaloric diet with or without exercise training in obese metabolic syndrome subjects. Diabetes. 2010, 59: 71-79. 10.2337/db09-0934.PubMedCentralCrossRefPubMed
24.
Zurück zum Zitat Roumen C, Corpeleijn E, Feskens EJ, Mensink M, Saris WH, Blaak EE: Impact of 3-year lifestyle intervention on postprandial glucose metabolism: the SLIM study. Diabet Med. 2008, 25: 597-605. 10.1111/j.1464-5491.2008.02417.x.CrossRefPubMed Roumen C, Corpeleijn E, Feskens EJ, Mensink M, Saris WH, Blaak EE: Impact of 3-year lifestyle intervention on postprandial glucose metabolism: the SLIM study. Diabet Med. 2008, 25: 597-605. 10.1111/j.1464-5491.2008.02417.x.CrossRefPubMed
25.
Zurück zum Zitat Herder C, Peltonen M, Koenig W, Sutfels K, Lindstrom J, Martin S, Ilanne-Parikka P, Eriksson JG, Aunola S, Keinanen-Kiukaanniemi S, Valle TT, Uusitupa M, Kolb H, Tuomilehto J: Anti-inflammatory effect of lifestyle changes in the Finnish Diabetes Prevention Study. Diabetologia. 2009, 52: 433-442. 10.1007/s00125-008-1243-1.CrossRefPubMed Herder C, Peltonen M, Koenig W, Sutfels K, Lindstrom J, Martin S, Ilanne-Parikka P, Eriksson JG, Aunola S, Keinanen-Kiukaanniemi S, Valle TT, Uusitupa M, Kolb H, Tuomilehto J: Anti-inflammatory effect of lifestyle changes in the Finnish Diabetes Prevention Study. Diabetologia. 2009, 52: 433-442. 10.1007/s00125-008-1243-1.CrossRefPubMed
26.
Zurück zum Zitat Mosca L, Mochari H, Liao M, Christian AH, Edelman DJ, Aggarwal B, Oz MC: A novel family-based intervention trial to improve heart health: FIT Heart: results of a randomized controlled trial. Circ Cardiovasc Qual Outcomes. 2008, 1: 98-106. 10.1161/CIRCOUTCOMES.108.825786.PubMedCentralCrossRefPubMed Mosca L, Mochari H, Liao M, Christian AH, Edelman DJ, Aggarwal B, Oz MC: A novel family-based intervention trial to improve heart health: FIT Heart: results of a randomized controlled trial. Circ Cardiovasc Qual Outcomes. 2008, 1: 98-106. 10.1161/CIRCOUTCOMES.108.825786.PubMedCentralCrossRefPubMed
27.
Zurück zum Zitat Morgan LM, Griffin BA, Millward DJ, DeLooy A, Fox KR, Baic S, Bonham MP, Wallace JM, MacDonald I, Taylor MA, Truby H: Comparison of the effects of four commercially available weight-loss programmes on lipid-based cardiovascular risk factors. Public Health Nutr. 2009, 12: 799-807. 10.1017/S1368980008003236.CrossRefPubMed Morgan LM, Griffin BA, Millward DJ, DeLooy A, Fox KR, Baic S, Bonham MP, Wallace JM, MacDonald I, Taylor MA, Truby H: Comparison of the effects of four commercially available weight-loss programmes on lipid-based cardiovascular risk factors. Public Health Nutr. 2009, 12: 799-807. 10.1017/S1368980008003236.CrossRefPubMed
28.
Zurück zum Zitat Dale KS, Mann JI, McAuley KA, Williams SM, Farmer VL: Sustainability of lifestyle changes following an intensive lifestyle intervention in insulin resistant adults: follow-up at 2-years. Asia Pac J Clin Nutr. 2009, 18: 114-120.PubMed Dale KS, Mann JI, McAuley KA, Williams SM, Farmer VL: Sustainability of lifestyle changes following an intensive lifestyle intervention in insulin resistant adults: follow-up at 2-years. Asia Pac J Clin Nutr. 2009, 18: 114-120.PubMed
29.
Zurück zum Zitat Meckling KA, Sherfey R: A randomized trial of a hypocaloric high-protein diet, with and without exercise, on weight loss, fitness, and markers of the Metabolic Syndrome in overweight and obese women. Appl Physiol Nutr Metab. 2007, 32: 743-752. 10.1139/H07-059.CrossRefPubMed Meckling KA, Sherfey R: A randomized trial of a hypocaloric high-protein diet, with and without exercise, on weight loss, fitness, and markers of the Metabolic Syndrome in overweight and obese women. Appl Physiol Nutr Metab. 2007, 32: 743-752. 10.1139/H07-059.CrossRefPubMed
30.
Zurück zum Zitat Burke V, Beilin LJ, Cutt HE, Mansour J, Williams A, Mori TA: A lifestyle program for treated hypertensives improved health-related behaviors and cardiovascular risk factors, a randomized controlled trial. J Clin Epidemiol. 2007, 60: 133-141. 10.1016/j.jclinepi.2006.05.012.CrossRefPubMed Burke V, Beilin LJ, Cutt HE, Mansour J, Williams A, Mori TA: A lifestyle program for treated hypertensives improved health-related behaviors and cardiovascular risk factors, a randomized controlled trial. J Clin Epidemiol. 2007, 60: 133-141. 10.1016/j.jclinepi.2006.05.012.CrossRefPubMed
31.
Zurück zum Zitat Bo S, Ciccone G, Baldi C, Benini L, Dusio F, Forastiere G, Lucia C, Nuti C, Durazzo M, Cassader M, Gentile L, Pagano G: Effectiveness of a lifestyle intervention on metabolic syndrome. a randomized controlled trial. J Gen Intern Med. 2007, 22: 1695-1703. 10.1007/s11606-007-0399-6.PubMedCentralCrossRefPubMed Bo S, Ciccone G, Baldi C, Benini L, Dusio F, Forastiere G, Lucia C, Nuti C, Durazzo M, Cassader M, Gentile L, Pagano G: Effectiveness of a lifestyle intervention on metabolic syndrome. a randomized controlled trial. J Gen Intern Med. 2007, 22: 1695-1703. 10.1007/s11606-007-0399-6.PubMedCentralCrossRefPubMed
32.
Zurück zum Zitat Arciero PJ, Gentile CL, Martin-Pressman R, Ormsbee MJ, Everett M, Zwicky L, Steele CA: Increased dietary protein and combined high intensity aerobic and resistance exercise improves body fat distribution and cardiovascular risk factors. Int J Sport Nutr Exerc Metab. 2006, 16: 373-392.PubMed Arciero PJ, Gentile CL, Martin-Pressman R, Ormsbee MJ, Everett M, Zwicky L, Steele CA: Increased dietary protein and combined high intensity aerobic and resistance exercise improves body fat distribution and cardiovascular risk factors. Int J Sport Nutr Exerc Metab. 2006, 16: 373-392.PubMed
33.
Zurück zum Zitat Brekke HK, Jansson PA, Lenner RA: Long-term (1- and 2-year) effects of lifestyle intervention in type 2 diabetes relatives. Diabetes Res Clin Pract. 2005, 70: 225-234. 10.1016/j.diabres.2005.03.027.CrossRefPubMed Brekke HK, Jansson PA, Lenner RA: Long-term (1- and 2-year) effects of lifestyle intervention in type 2 diabetes relatives. Diabetes Res Clin Pract. 2005, 70: 225-234. 10.1016/j.diabres.2005.03.027.CrossRefPubMed
34.
Zurück zum Zitat Watkins LL, Sherwood A, Feinglos M, Hinderliter A, Babyak M, Gullette E, Waugh R, Blumenthal JA: Effects of exercise and weight loss on cardiac risk factors associated with syndrome X. Arch Intern Med. 2003, 163: 1889-1895. 10.1001/archinte.163.16.1889.CrossRefPubMed Watkins LL, Sherwood A, Feinglos M, Hinderliter A, Babyak M, Gullette E, Waugh R, Blumenthal JA: Effects of exercise and weight loss on cardiac risk factors associated with syndrome X. Arch Intern Med. 2003, 163: 1889-1895. 10.1001/archinte.163.16.1889.CrossRefPubMed
35.
Zurück zum Zitat Lindstrom J, Louheranta A, Mannelin M, Rastas M, Salminen V, Eriksson J, Uusitupa M, Tuomilehto J: The Finnish Diabetes Prevention Study (DPS): lifestyle intervention and 3-year results on diet and physical activity. Diabetes Care. 2003, 26: 3230-3236. 10.2337/diacare.26.12.3230.CrossRefPubMed Lindstrom J, Louheranta A, Mannelin M, Rastas M, Salminen V, Eriksson J, Uusitupa M, Tuomilehto J: The Finnish Diabetes Prevention Study (DPS): lifestyle intervention and 3-year results on diet and physical activity. Diabetes Care. 2003, 26: 3230-3236. 10.2337/diacare.26.12.3230.CrossRefPubMed
36.
Zurück zum Zitat Esposito K, Pontillo A, Di Palo C, Giugliano G, Masella M, Marfella R, Giugliano D: Effect of weight loss and lifestyle changes on vascular inflammatory markers in obese women: a randomized trial. JAMA. 2003, 289: 1799-1804. 10.1001/jama.289.14.1799.CrossRefPubMed Esposito K, Pontillo A, Di Palo C, Giugliano G, Masella M, Marfella R, Giugliano D: Effect of weight loss and lifestyle changes on vascular inflammatory markers in obese women: a randomized trial. JAMA. 2003, 289: 1799-1804. 10.1001/jama.289.14.1799.CrossRefPubMed
37.
Zurück zum Zitat Mensink M, Feskens EJ, Saris WH, De Bruin TW, Blaak EE: Study on Lifestyle Intervention and Impaired Glucose Tolerance Maastricht (SLIM): preliminary results after one year. Int J Obes Relat Metab Disord. 2003, 27: 377-384. 10.1038/sj.ijo.0802249.CrossRefPubMed Mensink M, Feskens EJ, Saris WH, De Bruin TW, Blaak EE: Study on Lifestyle Intervention and Impaired Glucose Tolerance Maastricht (SLIM): preliminary results after one year. Int J Obes Relat Metab Disord. 2003, 27: 377-384. 10.1038/sj.ijo.0802249.CrossRefPubMed
38.
Zurück zum Zitat McAuley KA, Williams SM, Mann JI, Goulding A, Chisholm A, Wilson N, Story G, McLay RT, Harper MJ, Jones IE: Intensive lifestyle changes are necessary to improve insulin sensitivity: a randomized controlled trial. Diabetes Care. 2002, 25: 445-452. 10.2337/diacare.25.3.445.CrossRefPubMed McAuley KA, Williams SM, Mann JI, Goulding A, Chisholm A, Wilson N, Story G, McLay RT, Harper MJ, Jones IE: Intensive lifestyle changes are necessary to improve insulin sensitivity: a randomized controlled trial. Diabetes Care. 2002, 25: 445-452. 10.2337/diacare.25.3.445.CrossRefPubMed
39.
Zurück zum Zitat Miller ER, Erlinger TP, Young DR, Jehn M, Charleston J, Rhodes D, Wasan SK, Appel LJ: Results of the diet, exercise, and weight loss intervention trial (DEW-IT). Hypertension. 2002, 40: 612-618. 10.1161/01.HYP.0000037217.96002.8E.CrossRefPubMed Miller ER, Erlinger TP, Young DR, Jehn M, Charleston J, Rhodes D, Wasan SK, Appel LJ: Results of the diet, exercise, and weight loss intervention trial (DEW-IT). Hypertension. 2002, 40: 612-618. 10.1161/01.HYP.0000037217.96002.8E.CrossRefPubMed
40.
Zurück zum Zitat Reseland JE, Anderssen SA, Solvoll K, Hjermann I, Urdal P, Holme I, Drevon CA: Effect of long-term changes in diet and exercise on plasma leptin concentrations. Am J Clin Nutr. 2001, 73: 240-245.PubMed Reseland JE, Anderssen SA, Solvoll K, Hjermann I, Urdal P, Holme I, Drevon CA: Effect of long-term changes in diet and exercise on plasma leptin concentrations. Am J Clin Nutr. 2001, 73: 240-245.PubMed
41.
Zurück zum Zitat Oldroyd JC, Unwin NC, White M, Imrie K, Mathers JC, Alberti KG: Randomised controlled trial evaluating the effectiveness of behavioural interventions to modify cardiovascular risk factors in men and women with impaired glucose tolerance: outcomes at 6 months. Diabetes Res Clin Pract. 2001, 52: 29-43. 10.1016/S0168-8227(00)00244-8.CrossRefPubMed Oldroyd JC, Unwin NC, White M, Imrie K, Mathers JC, Alberti KG: Randomised controlled trial evaluating the effectiveness of behavioural interventions to modify cardiovascular risk factors in men and women with impaired glucose tolerance: outcomes at 6 months. Diabetes Res Clin Pract. 2001, 52: 29-43. 10.1016/S0168-8227(00)00244-8.CrossRefPubMed
42.
Zurück zum Zitat Kuller LH, Simkin-Silverman LR, Wing RR, Meilahn EN, Ives DG: Women's healthy lifestyle project: a randomized clinical trial: results at 54 months. Circulation. 2001, 103: 32-37. 10.1161/01.CIR.103.1.32.CrossRefPubMed Kuller LH, Simkin-Silverman LR, Wing RR, Meilahn EN, Ives DG: Women's healthy lifestyle project: a randomized clinical trial: results at 54 months. Circulation. 2001, 103: 32-37. 10.1161/01.CIR.103.1.32.CrossRefPubMed
43.
Zurück zum Zitat Ornish D, Scherwitz LW, Billings JH, Brown SE, Gould KL, Merritt TA, Sparler S, Armstrong WT, Ports TA, Kirkeeide RL, Hogeboom C, Brand RJ: Intensive lifestyle changes for reversal of coronary heart disease. JAMA. 1998, 280: 2001-2007. 10.1001/jama.280.23.2001.CrossRefPubMed Ornish D, Scherwitz LW, Billings JH, Brown SE, Gould KL, Merritt TA, Sparler S, Armstrong WT, Ports TA, Kirkeeide RL, Hogeboom C, Brand RJ: Intensive lifestyle changes for reversal of coronary heart disease. JAMA. 1998, 280: 2001-2007. 10.1001/jama.280.23.2001.CrossRefPubMed
44.
Zurück zum Zitat Wing RR, Venditti E, Jakicic JM, Polley BA, Lang W: Lifestyle intervention in overweight individuals with a family history of diabetes. Diabetes Care. 1998, 21: 350-359. 10.2337/diacare.21.3.350.CrossRefPubMed Wing RR, Venditti E, Jakicic JM, Polley BA, Lang W: Lifestyle intervention in overweight individuals with a family history of diabetes. Diabetes Care. 1998, 21: 350-359. 10.2337/diacare.21.3.350.CrossRefPubMed
45.
Zurück zum Zitat Simkin-Silverman L, Wing RR, Hansen DH, Klem ML, Pasagian-Macaulay AP, Meilahn EN, Kuller LH: Prevention of cardiovascular risk factor elevations in healthy premenopausal women. Prev Med. 1995, 24: 509-517. 10.1006/pmed.1995.1081.CrossRefPubMed Simkin-Silverman L, Wing RR, Hansen DH, Klem ML, Pasagian-Macaulay AP, Meilahn EN, Kuller LH: Prevention of cardiovascular risk factor elevations in healthy premenopausal women. Prev Med. 1995, 24: 509-517. 10.1006/pmed.1995.1081.CrossRefPubMed
46.
Zurück zum Zitat Hellenius ML, de Faire U, Berglund B, Hamsten A, Krakau I: Diet and exercise are equally effective in reducing risk for cardiovascular disease. results of a randomized controlled study in men with slightly to moderately raised cardiovascular risk factors. Atherosclerosis. 1993, 103: 81-91. 10.1016/0021-9150(93)90042-S.CrossRefPubMed Hellenius ML, de Faire U, Berglund B, Hamsten A, Krakau I: Diet and exercise are equally effective in reducing risk for cardiovascular disease. results of a randomized controlled study in men with slightly to moderately raised cardiovascular risk factors. Atherosclerosis. 1993, 103: 81-91. 10.1016/0021-9150(93)90042-S.CrossRefPubMed
47.
Zurück zum Zitat Svendsen OL, Hassager C, Christiansen C: Effect of an energy-restrictive diet, with or without exercise, on lean tissue mass, resting metabolic rate, cardiovascular risk factors, and bone in overweight postmenopausal women. Am J Med. 1993, 95: 131-140. 10.1016/0002-9343(93)90253-L.CrossRefPubMed Svendsen OL, Hassager C, Christiansen C: Effect of an energy-restrictive diet, with or without exercise, on lean tissue mass, resting metabolic rate, cardiovascular risk factors, and bone in overweight postmenopausal women. Am J Med. 1993, 95: 131-140. 10.1016/0002-9343(93)90253-L.CrossRefPubMed
48.
Zurück zum Zitat Page RC, Harnden KE, Walravens NK, Onslow C, Sutton P, Levy JC, Hockaday DT, Turner RC: ‘Healthy living’ and sulphonylurea therapy have different effects on glucose tolerance and risk factors for vascular disease in subjects with impaired glucose tolerance. Q J Med. 1993, 86: 145-154.PubMed Page RC, Harnden KE, Walravens NK, Onslow C, Sutton P, Levy JC, Hockaday DT, Turner RC: ‘Healthy living’ and sulphonylurea therapy have different effects on glucose tolerance and risk factors for vascular disease in subjects with impaired glucose tolerance. Q J Med. 1993, 86: 145-154.PubMed
49.
Zurück zum Zitat Schuler G, Hambrecht R, Schlierf G, Niebauer J, Hauer K, Neumann J, Hoberg E, Drinkmann A, Bacher F, Grunze M, Kubler W: Regular physical exercise and low-fat diet. effects on progression of coronary artery disease. Circulation. 1992, 86: 1-11. 10.1161/01.CIR.86.1.1.CrossRefPubMed Schuler G, Hambrecht R, Schlierf G, Niebauer J, Hauer K, Neumann J, Hoberg E, Drinkmann A, Bacher F, Grunze M, Kubler W: Regular physical exercise and low-fat diet. effects on progression of coronary artery disease. Circulation. 1992, 86: 1-11. 10.1161/01.CIR.86.1.1.CrossRefPubMed
50.
Zurück zum Zitat Viechtbauer W: Conducting meta-analyses in R with the metafor package. J Stat Softw. 2010, 36: 1-48.CrossRef Viechtbauer W: Conducting meta-analyses in R with the metafor package. J Stat Softw. 2010, 36: 1-48.CrossRef
51.
Zurück zum Zitat Sutton AJ, Duval SJ, Tweedie RL, Abrams KR, Jones DR: Empirical assessment of effect of publication bias on meta-analyses. BMJ. 2000, 320: 1574-1577. 10.1136/bmj.320.7249.1574.PubMedCentralCrossRefPubMed Sutton AJ, Duval SJ, Tweedie RL, Abrams KR, Jones DR: Empirical assessment of effect of publication bias on meta-analyses. BMJ. 2000, 320: 1574-1577. 10.1136/bmj.320.7249.1574.PubMedCentralCrossRefPubMed
52.
Zurück zum Zitat Viechtbauer W, Cheung MWL: Outlier and influence diagnostics for meta-analysis. Res Synthesis Methods. 2010, 1: 112-125. 10.1002/jrsm.11.CrossRef Viechtbauer W, Cheung MWL: Outlier and influence diagnostics for meta-analysis. Res Synthesis Methods. 2010, 1: 112-125. 10.1002/jrsm.11.CrossRef
53.
Zurück zum Zitat Engels EA, Schmid CH, Terrin N, Olkin I, Lau J: Heterogeneity and statistical significance in meta-analysis: an empirical study of 125 meta-analyses. Stat Med. 2000, 19: 1707-1728. 10.1002/1097-0258(20000715)19:13<1707::AID-SIM491>3.0.CO;2-P.CrossRefPubMed Engels EA, Schmid CH, Terrin N, Olkin I, Lau J: Heterogeneity and statistical significance in meta-analysis: an empirical study of 125 meta-analyses. Stat Med. 2000, 19: 1707-1728. 10.1002/1097-0258(20000715)19:13<1707::AID-SIM491>3.0.CO;2-P.CrossRefPubMed
54.
Zurück zum Zitat Appuhamy JA, Kebreab E, France J: A mathematical model for determining age-specific diabetes incidence and prevalence using body mass index. Ann Epidemiol. 2013, 23: 248-254. 10.1016/j.annepidem.2013.03.011.CrossRefPubMed Appuhamy JA, Kebreab E, France J: A mathematical model for determining age-specific diabetes incidence and prevalence using body mass index. Ann Epidemiol. 2013, 23: 248-254. 10.1016/j.annepidem.2013.03.011.CrossRefPubMed
55.
Zurück zum Zitat Lillioja S, Mott DM, Spraul M, Ferraro R, Foley JE, Ravussin E, Knowler WC, Bennett PH, Bogardus C: Insulin resistance and insulin secretory dysfunction as precursors of non-insulin-dependent diabetes mellitus. prospective studies of Pima Indians. N Engl J Med. 1993, 329: 1988-1992. 10.1056/NEJM199312303292703.CrossRefPubMed Lillioja S, Mott DM, Spraul M, Ferraro R, Foley JE, Ravussin E, Knowler WC, Bennett PH, Bogardus C: Insulin resistance and insulin secretory dysfunction as precursors of non-insulin-dependent diabetes mellitus. prospective studies of Pima Indians. N Engl J Med. 1993, 329: 1988-1992. 10.1056/NEJM199312303292703.CrossRefPubMed
56.
Zurück zum Zitat Holten MK, Zacho M, Gaster M, Juel C, Wojtaszewski JF, Dela F: Strength training increases insulin-mediated glucose uptake, glut4 content, and insulin signaling in skeletal muscle in patients with type 2 diabetes. Diabetes. 2004, 53: 294-305. 10.2337/diabetes.53.2.294.CrossRefPubMed Holten MK, Zacho M, Gaster M, Juel C, Wojtaszewski JF, Dela F: Strength training increases insulin-mediated glucose uptake, glut4 content, and insulin signaling in skeletal muscle in patients with type 2 diabetes. Diabetes. 2004, 53: 294-305. 10.2337/diabetes.53.2.294.CrossRefPubMed
57.
Zurück zum Zitat Abdul-Ghani MA, Williams K, DeFronzo RA, Stern M: What is the best predictor of future type 2 diabetes?. Diabetes Care. 2007, 30: 1544-1548. 10.2337/dc06-1331.CrossRefPubMed Abdul-Ghani MA, Williams K, DeFronzo RA, Stern M: What is the best predictor of future type 2 diabetes?. Diabetes Care. 2007, 30: 1544-1548. 10.2337/dc06-1331.CrossRefPubMed
58.
Zurück zum Zitat Stern MP, Williams K, Haffner SM: Identification of persons at high risk for type 2 diabetes mellitus: do we need the oral glucose tolerance test?. Ann Intern Med. 2002, 136: 575-581. 10.7326/0003-4819-136-8-200204160-00006.CrossRefPubMed Stern MP, Williams K, Haffner SM: Identification of persons at high risk for type 2 diabetes mellitus: do we need the oral glucose tolerance test?. Ann Intern Med. 2002, 136: 575-581. 10.7326/0003-4819-136-8-200204160-00006.CrossRefPubMed
59.
Zurück zum Zitat Wang JJ, Yuan SY, Zhu LX, Fu HJ, Li HB, Hu G, Tuomilehto J: Effects of impaired fasting glucose and impaired glucose tolerance on predicting incident type 2 diabetes in a Chinese population with high post-prandial glucose. Diabetes Res Clin Pract. 2004, 66: 183-191. 10.1016/j.diabres.2004.03.002.CrossRefPubMed Wang JJ, Yuan SY, Zhu LX, Fu HJ, Li HB, Hu G, Tuomilehto J: Effects of impaired fasting glucose and impaired glucose tolerance on predicting incident type 2 diabetes in a Chinese population with high post-prandial glucose. Diabetes Res Clin Pract. 2004, 66: 183-191. 10.1016/j.diabres.2004.03.002.CrossRefPubMed
60.
Zurück zum Zitat Rathmann W, Strassburger K, Heier M, Holle R, Thorand B, Giani G, Meisinger C: Incidence of type 2 diabetes in the elderly German population and the effect of clinical and lifestyle risk factors: KORA S4/F4 cohort study. Diabet Med. 2009, 26: 1212-1219. 10.1111/j.1464-5491.2009.02863.x.CrossRefPubMed Rathmann W, Strassburger K, Heier M, Holle R, Thorand B, Giani G, Meisinger C: Incidence of type 2 diabetes in the elderly German population and the effect of clinical and lifestyle risk factors: KORA S4/F4 cohort study. Diabet Med. 2009, 26: 1212-1219. 10.1111/j.1464-5491.2009.02863.x.CrossRefPubMed
61.
Zurück zum Zitat Janghorbani M, Amini M: Comparison of systolic and diastolic blood pressure with pulse pressure and mean arterial pressure for prediction of type 2 diabetes: the Isfahan Diabetes Prevention Study. Endokrynol Pol. 2011, 62: 324-330.PubMed Janghorbani M, Amini M: Comparison of systolic and diastolic blood pressure with pulse pressure and mean arterial pressure for prediction of type 2 diabetes: the Isfahan Diabetes Prevention Study. Endokrynol Pol. 2011, 62: 324-330.PubMed
62.
Zurück zum Zitat Geiss LS, Pan L, Cadwell B, Gregg EW, Benjamin SM, Engelgau MM: Changes in incidence of diabetes in U.S. adults, 1997–2003. Am J Prev Med. 2006, 30: 371-377. 10.1016/j.amepre.2005.12.009.CrossRefPubMed Geiss LS, Pan L, Cadwell B, Gregg EW, Benjamin SM, Engelgau MM: Changes in incidence of diabetes in U.S. adults, 1997–2003. Am J Prev Med. 2006, 30: 371-377. 10.1016/j.amepre.2005.12.009.CrossRefPubMed
63.
Zurück zum Zitat Dotevall A, Johansson S, Wilhelmsen L, Rosengren A: Increased levels of triglycerides, BMI and blood pressure and low physical activity increase the risk of diabetes in Swedish women. a prospective 18-year follow-up of the BEDA study. Diabet Med. 2004, 21: 615-622. 10.1111/j.1464-5491.2004.01189.x.CrossRefPubMed Dotevall A, Johansson S, Wilhelmsen L, Rosengren A: Increased levels of triglycerides, BMI and blood pressure and low physical activity increase the risk of diabetes in Swedish women. a prospective 18-year follow-up of the BEDA study. Diabet Med. 2004, 21: 615-622. 10.1111/j.1464-5491.2004.01189.x.CrossRefPubMed
64.
Zurück zum Zitat Fukui M, Tanaka M, Toda H, Senmaru T, Sakabe K, Ushigome E, Asano M, Yamazaki M, Hasegawa G, Imai S, Nakamura N: Risk factors for development of diabetes mellitus, hypertension and dyslipidemia. Diabetes Res Clin Pract. 2011, 94: e15-e18. 10.1016/j.diabres.2011.07.006.CrossRefPubMed Fukui M, Tanaka M, Toda H, Senmaru T, Sakabe K, Ushigome E, Asano M, Yamazaki M, Hasegawa G, Imai S, Nakamura N: Risk factors for development of diabetes mellitus, hypertension and dyslipidemia. Diabetes Res Clin Pract. 2011, 94: e15-e18. 10.1016/j.diabres.2011.07.006.CrossRefPubMed
65.
Zurück zum Zitat Tirosh A, Shai I, Bitzur R, Kochba I, Tekes-Manova D, Israeli E, Shochat T, Rudich A: Changes in triglyceride levels over time and risk of type 2 diabetes in young men. Diabetes Care. 2008, 31: 2032-2037. 10.2337/dc08-0825.PubMedCentralCrossRefPubMed Tirosh A, Shai I, Bitzur R, Kochba I, Tekes-Manova D, Israeli E, Shochat T, Rudich A: Changes in triglyceride levels over time and risk of type 2 diabetes in young men. Diabetes Care. 2008, 31: 2032-2037. 10.2337/dc08-0825.PubMedCentralCrossRefPubMed
66.
Zurück zum Zitat Fontana L, Meyer TE, Klein S, Holloszy JO: Long-term calorie restriction is highly effective in reducing the risk for atherosclerosis in humans. Proc Natl Acad Sci U S A. 2004, 101: 6659-6663. 10.1073/pnas.0308291101.PubMedCentralCrossRefPubMed Fontana L, Meyer TE, Klein S, Holloszy JO: Long-term calorie restriction is highly effective in reducing the risk for atherosclerosis in humans. Proc Natl Acad Sci U S A. 2004, 101: 6659-6663. 10.1073/pnas.0308291101.PubMedCentralCrossRefPubMed
67.
Zurück zum Zitat Curioni CC, Lourenco PM: Long-term weight loss after diet and exercise: a systematic review. Int J Obes (Lond). 2005, 29: 1168-1174. 10.1038/sj.ijo.0803015.CrossRef Curioni CC, Lourenco PM: Long-term weight loss after diet and exercise: a systematic review. Int J Obes (Lond). 2005, 29: 1168-1174. 10.1038/sj.ijo.0803015.CrossRef
68.
Zurück zum Zitat Schaar B, Moose-Thiele C, Platen P: Effects of exercise, diet, and a combination of exercise and diet in overweight and obese adults – a meta-analysis of the data. Open Sport Med J. 2010, 4: 17-28. 10.2174/1874387001004010017.CrossRef Schaar B, Moose-Thiele C, Platen P: Effects of exercise, diet, and a combination of exercise and diet in overweight and obese adults – a meta-analysis of the data. Open Sport Med J. 2010, 4: 17-28. 10.2174/1874387001004010017.CrossRef
69.
Zurück zum Zitat Chiu M, Austin PC, Manuel DG, Shah BR, Tu JV: Deriving ethnic-specific BMI cutoff points for assessing diabetes risk. Diabetes Care. 2011, 34: 1741-1748. 10.2337/dc10-2300.PubMedCentralCrossRefPubMed Chiu M, Austin PC, Manuel DG, Shah BR, Tu JV: Deriving ethnic-specific BMI cutoff points for assessing diabetes risk. Diabetes Care. 2011, 34: 1741-1748. 10.2337/dc10-2300.PubMedCentralCrossRefPubMed
70.
Zurück zum Zitat Mozaffarian D, Cao H, King IB, Lemaitre RN, Song X, Siscovick DS, Hotamisligil GS: Trans-palmitoleic acid, metabolic risk factors, and new-onset diabetes in U.S. adults: a cohort study. Ann Intern Med. 2010, 153: 790-799. 10.7326/0003-4819-153-12-201012210-00005.PubMedCentralCrossRefPubMed Mozaffarian D, Cao H, King IB, Lemaitre RN, Song X, Siscovick DS, Hotamisligil GS: Trans-palmitoleic acid, metabolic risk factors, and new-onset diabetes in U.S. adults: a cohort study. Ann Intern Med. 2010, 153: 790-799. 10.7326/0003-4819-153-12-201012210-00005.PubMedCentralCrossRefPubMed
71.
Zurück zum Zitat Micha R, Mozaffarian D: Saturated fat and cardiometabolic risk factors, coronary heart disease, stroke, and diabetes: a fresh look at the evidence. Lipids. 2010, 45: 893-905. 10.1007/s11745-010-3393-4.PubMedCentralCrossRefPubMed Micha R, Mozaffarian D: Saturated fat and cardiometabolic risk factors, coronary heart disease, stroke, and diabetes: a fresh look at the evidence. Lipids. 2010, 45: 893-905. 10.1007/s11745-010-3393-4.PubMedCentralCrossRefPubMed
72.
Zurück zum Zitat Rickel KA, Milsom VA, Ross KM, Hoover VJ, Peterson ND, Perri MG: Differential response of African American and Caucasian women to extended-care programs for obesity management. Ethn Dis. 2011, 21: 170-175.PubMedCentralPubMed Rickel KA, Milsom VA, Ross KM, Hoover VJ, Peterson ND, Perri MG: Differential response of African American and Caucasian women to extended-care programs for obesity management. Ethn Dis. 2011, 21: 170-175.PubMedCentralPubMed
73.
Zurück zum Zitat Hertogh EM, Schuit AJ, Peeters PH, Monninkhof EM: Noncompliance in lifestyle intervention studies: the instrumental variable method provides insight into the bias. J Clin Epidemiol. 2010, 63: 900-906. 10.1016/j.jclinepi.2009.10.007.CrossRefPubMed Hertogh EM, Schuit AJ, Peeters PH, Monninkhof EM: Noncompliance in lifestyle intervention studies: the instrumental variable method provides insight into the bias. J Clin Epidemiol. 2010, 63: 900-906. 10.1016/j.jclinepi.2009.10.007.CrossRefPubMed
Metadaten
Titel
Effects of diet and exercise interventions on diabetes risk factors in adults without diabetes: meta-analyses of controlled trials
verfasst von
J A D Ranga Niroshan Appuhamy
Ermias Kebreab
Mitchell Simon
Rickey Yada
Larry P Milligan
James France
Publikationsdatum
01.12.2014
Verlag
BioMed Central
Erschienen in
Diabetology & Metabolic Syndrome / Ausgabe 1/2014
Elektronische ISSN: 1758-5996
DOI
https://doi.org/10.1186/1758-5996-6-127

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