Background
Child and adolescent overweight and obesity has increased globally, and can be associated with significant short‐ and long‐term health consequences. This is an update of a Cochrane review ...published first in 2003, and updated previously in 2009. However, the update has now been split into six reviews addressing different childhood obesity treatments at different ages.
Objectives
To assess the effects of diet, physical activity and behavioural interventions (behaviour‐changing interventions) for the treatment of overweight or obese children aged 6 to 11 years.
Search methods
We searched CENTRAL, MEDLINE, Embase, PsycINFO, CINAHL, LILACS as well as trial registers ClinicalTrials.gov and ICTRP Search Portal. We checked references of studies and systematic reviews. We did not apply any language restrictions. The date of the last search was July 2016 for all databases.
Selection criteria
We selected randomised controlled trials (RCTs) of diet, physical activity, and behavioural interventions (behaviour‐changing interventions) for treating overweight or obese children aged 6 to 11 years, with a minimum of six months' follow‐up. We excluded interventions that specifically dealt with the treatment of eating disorders or type 2 diabetes, or included participants with a secondary or syndromic cause of obesity.
Data collection and analysis
Two review authors independently screened references, extracted data, assessed risk of bias, and evaluated the quality of the evidence using the GRADE instrument. We contacted study authors for additional information. We carried out meta‐analyses according to the statistical guidelines in the Cochrane Handbook for Systematic Reviews of Interventions.
Main results
We included 70 RCTs with a total of 8461 participants randomised to either the intervention or control groups. The number of participants per trial ranged from 16 to 686. Fifty‐five trials compared a behaviour‐changing intervention with no treatment/usual care control and 15 evaluated the effectiveness of adding an additional component to a behaviour‐changing intervention. Sixty‐four trials were parallel RCTs, and four were cluster RCTs. Sixty‐four trials were multicomponent, two were diet only and four were physical activity only interventions. Ten trials had more than two arms. The overall quality of the evidence was low or very low and 62 trials had a high risk of bias for at least one criterion. Total duration of trials ranged from six months to three years. The median age of participants was 10 years old and the median BMI z score was 2.2.
Primary analyses demonstrated that behaviour‐changing interventions compared to no treatment/usual care control at longest follow‐up reduced BMI, BMI z score and weight. Mean difference (MD) in BMI was ‐0.53 kg/m2 (95% confidence interval (CI) ‐0.82 to ‐0.24); P < 0.00001; 24 trials; 2785 participants; low‐quality evidence. MD in BMI z score was ‐0.06 units (95% CI ‐0.10 to ‐0.02); P = 0.001; 37 trials; 4019 participants; low‐quality evidence and MD in weight was ‐1.45 kg (95% CI ‐1.88 to ‐1.02); P < 0.00001; 17 trials; 1774 participants; low‐quality evidence.
Thirty‐one trials reported on serious adverse events, with 29 trials reporting zero occurrences RR 0.57 (95% CI 0.17 to 1.93); P = 0.37; 4/2105 participants in the behaviour‐changing intervention groups compared with 7/1991 participants in the comparator groups). Few trials reported health‐related quality of life or behaviour change outcomes, and none of the analyses demonstrated a substantial difference in these outcomes between intervention and control. In two trials reporting on minutes per day of TV viewing, a small reduction of 6.6 minutes per day (95% CI ‐12.88 to ‐0.31), P = 0.04; 2 trials; 55 participants) was found in favour of the intervention. No trials reported on all‐cause mortality, morbidity or socioeconomic effects, and few trials reported on participant views; none of which could be meta‐analysed.
As the meta‐analyses revealed substantial heterogeneity, we conducted subgroup analyses to examine the impact of type of comparator, type of intervention, risk of attrition bias, setting, duration of post‐intervention follow‐up period, parental involvement and baseline BMI z score. No subgroup effects were shown for any of the subgroups on any of the outcomes. Some data indicated that a reduction in BMI immediately post‐intervention was no longer evident at follow‐up at less than six months, which has to be investigated in further trials.
Authors' conclusions
Multi‐component behaviour‐changing interventions that incorporate diet, physical activity and behaviour change may be beneficial in achieving small, short‐term reductions in BMI, BMI z score and weight in children aged 6 to 11 years. The evidence suggests a very low occurrence of adverse events. The quality of the evidence was low or very low. The heterogeneity observed across all outcomes was not explained by subgrouping. Further research is required of behaviour‐changing interventions in lower income countries and in children from different ethnic groups; also on the impact of behaviour‐changing interventions on health‐related quality of life and comorbidities. The sustainability of reduction in BMI/BMI z score and weight is a key consideration and there is a need for longer‐term follow‐up and further research on the most appropriate forms of post‐intervention maintenance in order to ensure intervention benefits are sustained over the longer term.
This is a protocol for a Cochrane Review (Intervention). The objectives are as follows:
To determine the effectiveness of following a vegan dietary pattern for the primary and secondary prevention of ...CVD.
Background
Vitamin C is an essential micronutrient and powerful antioxidant. Observational studies have shown an inverse relationship between vitamin C intake and major cardiovascular events and ...cardiovascular disease (CVD) risk factors. Results from clinical trials are less consistent.
Objectives
To determine the effectiveness of vitamin C supplementation as a single supplement for the primary prevention of CVD.
Search methods
We searched the following electronic databases on 11 May 2016: the Cochrane Central Register of Controlled Trials (CENTRAL) in the Cochrane Library; MEDLINE (Ovid); Embase Classic and Embase (Ovid); Web of Science Core Collection (Thomson Reuters); Database of s of Reviews of Effects (DARE); Health Technology Assessment Database and Health Economics Evaluations Database in the Cochrane Library. We searched trial registers on 13 April 2016 and reference lists of reviews for further studies. We applied no language restrictions.
Selection criteria
Randomised controlled trials of vitamin C supplementation as a single nutrient supplement lasting at least three months and involving healthy adults or adults at moderate and high risk of CVD were included. The comparison group was no intervention or placebo. The outcomes of interest were CVD clinical events and CVD risk factors.
Data collection and analysis
Two review authors independently selected trials for inclusion, ed the data and assessed the risk of bias.
Main results
We included eight trials with 15,445 participants randomised. The largest trial with 14,641 participants provided data on our primary outcomes. Seven trials reported on CVD risk factors. Three of the eight trials were regarded at high risk of bias for either reporting or attrition bias, most of the 'Risk of bias' domains for the remaining trials were judged as unclear, with the exception of the largest trial where most domains were judged to be at low risk of bias.
The composite endpoint, major CVD events was not different between the vitamin C and placebo group (hazard ratio (HR) 0.99, 95% confidence interval (CI) 0.89 to 1.10; 1 study; 14,641 participants; low‐quality evidence) in the Physicians Health Study II over eight years of follow‐up. Similar results were obtained for all‐cause mortality HR 1.07, 95% CI 0.97 to 1.18; 1 study; 14,641 participants; very low‐quality evidence, total myocardial infarction (MI) (fatal and non‐fatal) HR 1.04 (95% CI 0.87 to 1.24); 1 study; 14,641 participants; low‐quality evidence, total stroke (fatal and non‐fatal) HR 0.89 (95% CI 0.74 to 1.07); 1 study; 14,641 participants; low‐quality evidence, CVD mortality HR 1.02 (95% 0.85 to 1.22); 1 study; 14,641 participants; very low‐quality evidence, self‐reported coronary artery bypass grafting (CABG)/percutaneous transluminal coronary angioplasty (PTCA) HR 0.96 (95% CI 0.86 to 1.07); 1 study; 14,641 participants; low‐quality evidence, self‐reported angina HR 0.93 (95% CI 0.84 to 1.03); 1 study; 14,641 participants; low‐quality evidence.
The evidence for the majority of primary outcomes was downgraded (low quality) because of indirectness and imprecision. For all‐cause mortality and CVD mortality, the evidence was very low because more factors affected the directness of the evidence and because of inconsistency.
Four studies did not state sources of funding, two studies declared non‐commercial funding and two studies declared both commercial and non‐commercial funding.
Authors' conclusions
Currently, there is no evidence to suggest that vitamin C supplementation reduces the risk of CVD in healthy participants and those at increased risk of CVD, but current evidence is limited to one trial of middle‐aged and older male physicians from the USA. There is limited low‐ and very low‐quality evidence currently on the effect of vitamin C supplementation and risk of CVD risk factors.
Background
Child overweight and obesity has increased globally, and can be associated with short‐ and long‐term health consequences.
Objectives
To assess the effects of diet, physical activity, and ...behavioural interventions for the treatment of overweight or obesity in preschool children up to the age of 6 years.
Search methods
We performed a systematic literature search in the databases Cochrane Library, MEDLINE, EMBASE, PsycINFO, CINAHL, and LILACS, as well as in the trial registers ClinicalTrials.gov and ICTRP Search Portal. We also checked references of identified trials and systematic reviews. We applied no language restrictions. The date of the last search was March 2015 for all databases.
Selection criteria
We selected randomised controlled trials (RCTs) of diet, physical activity, and behavioural interventions for treating overweight or obesity in preschool children aged 0 to 6 years.
Data collection and analysis
Two review authors independently assessed risk of bias, evaluated the overall quality of the evidence using the GRADE instrument, and extracted data following the Cochrane Handbook for Systematic Reviews of Interventions. We contacted trial authors for additional information.
Main results
We included 7 RCTs with a total of 923 participants: 529 randomised to an intervention and 394 to a comparator. The number of participants per trial ranged from 18 to 475. Six trials were parallel RCTs, and one was a cluster RCT. Two trials were three‐arm trials, each comparing two interventions with a control group. The interventions and comparators in the trials varied. We categorised the comparisons into two groups: multicomponent interventions and dietary interventions. The overall quality of the evidence was low or very low, and six trials had a high risk of bias on individual 'Risk of bias' criteria. The children in the included trials were followed up for between six months and three years.
In trials comparing a multicomponent intervention with usual care, enhanced usual care, or information control, we found a greater reduction in body mass index (BMI) z score in the intervention groups at the end of the intervention (6 to 12 months): mean difference (MD) ‐0.3 units (95% confidence interval (CI) ‐0.4 to ‐0.2); P < 0.00001; 210 participants; 4 trials; low‐quality evidence, at 12 to 18 months' follow‐up: MD ‐0.4 units (95% CI ‐0.6 to ‐0.2); P = 0.0001; 202 participants; 4 trials; low‐quality evidence, and at 2 years' follow‐up: MD ‐0.3 units (95% CI ‐0.4 to ‐0.1); 96 participants; 1 trial; low‐quality evidence.
One trial stated that no adverse events were reported; the other trials did not report on adverse events. Three trials reported health‐related quality of life and found improvements in some, but not all, aspects. Other outcomes, such as behaviour change and parent‐child relationship, were inconsistently measured.
One three‐arm trial of very low‐quality evidence comparing two types of diet with control found that both the dairy‐rich diet (BMI z score change MD ‐0.1 units (95% CI ‐0.11 to ‐0.09); P < 0.0001; 59 participants) and energy‐restricted diet (BMI z score change MD ‐0.1 units (95% CI ‐0.11 to ‐0.09); P < 0.0001; 57 participants) resulted in greater reduction in BMI than the comparator at the end of the intervention period, but only the dairy‐rich diet maintained this at 36 months' follow‐up (BMI z score change in MD ‐0.7 units (95% CI ‐0.71 to ‐0.69); P < 0.0001; 52 participants). The energy‐restricted diet had a worse BMI outcome than control at this follow‐up (BMI z score change MD 0.1 units (95% CI 0.09 to 0.11); P < 0.0001; 47 participants). There was no substantial difference in mean daily energy expenditure between groups. Health‐related quality of life, adverse effects, participant views, and parenting were not measured.
No trial reported on all‐cause mortality, morbidity, or socioeconomic effects.
All results should be interpreted cautiously due to their low quality and heterogeneous interventions and comparators.
Authors' conclusions
Muticomponent interventions appear to be an effective treatment option for overweight or obese preschool children up to the age of 6 years. However, the current evidence is limited, and most trials had a high risk of bias. Most trials did not measure adverse events. We have identified four ongoing trials that we will include in future updates of this review.
The role of dietary interventions is more equivocal, with one trial suggesting that dairy interventions may be effective in the longer term, but not energy‐restricted diets. This trial also had a high risk of bias.
Omega-6 fats are polyunsaturated fats vital for many physiological functions, but their effect on cardiovascular disease (CVD) risk is debated.
To assess effects of increasing omega-6 fats (linoleic ...acid (LA), gamma-linolenic acid (GLA), dihomo-gamma-linolenic acid (DGLA) and arachidonic acid (AA)) on CVD and all-cause mortality.
We searched CENTRAL, MEDLINE and Embase to May 2017 and clinicaltrials.gov and the World Health Organization International Clinical Trials Registry Platform to September 2016, without language restrictions. We checked trials included in relevant systematic reviews.
We included randomised controlled trials (RCTs) comparing higher versus lower omega-6 fat intake in adults with or without CVD, assessing effects over at least 12 months. We included full texts, abstracts, trials registry entries and unpublished studies. Outcomes were all-cause mortality, CVD mortality, CVD events, risk factors (blood lipids, adiposity, blood pressure), and potential adverse events. We excluded trials where we could not separate omega-6 fat effects from those of other dietary, lifestyle or medication interventions.
Two authors independently screened titles/abstracts, assessed trials for inclusion, extracted data, and assessed risk of bias of included trials. We wrote to authors of included studies. Meta-analyses used random-effects analysis, while sensitivity analyses used fixed-effects and limited analyses to trials at low summary risk of bias. We assessed GRADE quality of evidence for 'Summary of findings' tables.
We included 19 RCTs in 6461 participants who were followed for one to eight years. Seven trials assessed the effects of supplemental GLA and 12 of LA, none DGLA or AA; the omega-6 fats usually displaced dietary saturated or monounsaturated fats. We assessed three RCTs as being at low summary risk of bias.Primary outcomes: we found low-quality evidence that increased intake of omega-6 fats may make little or no difference to all-cause mortality (risk ratio (RR) 1.00, 95% confidence interval (CI) 0.88 to 1.12, 740 deaths, 4506 randomised, 10 trials) or CVD events (RR 0.97, 95% CI 0.81 to 1.15, 1404 people experienced events of 4962 randomised, 7 trials). We are uncertain whether increasing omega-6 fats affects CVD mortality (RR 1.09, 95% CI 0.76 to 1.55, 472 deaths, 4019 randomised, 7 trials), coronary heart disease events (RR 0.88, 95% CI 0.66 to 1.17, 1059 people with events of 3997 randomised, 7 trials), major adverse cardiac and cerebrovascular events (RR 0.84, 95% CI 0.59 to 1.20, 817 events, 2879 participants, 2 trials) or stroke (RR 1.36, 95% CI 0.45 to 4.11, 54 events, 3730 participants, 4 trials), as we assessed the evidence as being of very low quality. We found no evidence of dose-response or duration effects for any primary outcome, but there was a suggestion of greater protection in participants with lower baseline omega-6 intake across outcomes.Additional key outcomes: we found increased intake of omega-6 fats may reduce myocardial infarction (MI) risk (RR 0.88, 95% CI 0.76 to 1.02, 609 events, 4606 participants, 7 trials, low-quality evidence). High-quality evidence suggests increasing omega-6 fats reduces total serum cholesterol a little in the long term (mean difference (MD) -0.33 mmol/L, 95% CI -0.50 to -0.16, I
= 81%; heterogeneity partially explained by dose, 4280 participants, 10 trials). Increasing omega-6 fats probably has little or no effect on adiposity (body mass index (BMI) MD -0.20 kg/m
, 95% CI -0.56 to 0.16, 371 participants, 1 trial, moderate-quality evidence). It may make little or no difference to serum triglycerides (MD -0.01 mmol/L, 95% CI -0.23 to 0.21, 834 participants, 5 trials), HDL (MD -0.01 mmol/L, 95% CI -0.03 to 0.02, 1995 participants, 4 trials) or low-density lipoprotein (MD -0.04 mmol/L, 95% CI -0.21 to 0.14, 244 participants, 2 trials, low-quality evidence).
This is the most extensive systematic assessment of effects of omega-6 fats on cardiovascular health, mortality, lipids and adiposity to date, using previously unpublished data. We found no evidence that increasing omega-6 fats reduces cardiovascular outcomes other than MI, where 53 people may need to increase omega-6 fat intake to prevent 1 person from experiencing MI. Although benefits of omega-6 fats remain to be proven, increasing omega-6 fats may be of benefit in people at high risk of MI. Increased omega-6 fats reduce serum total cholesterol but not other blood fat fractions or adiposity.
Background
Child and adolescent overweight and obesity have increased globally, and are associated with short‐ and long‐term health consequences.
Objectives
To assess the efficacy of diet, physical ...activity and behavioural interventions delivered to parents only for the treatment of overweight and obesity in children aged 5 to 11 years.
Search methods
We performed a systematic literature search of databases including the Cochrane Library, MEDLINE, EMBASE, PsycINFO, CINAHL and LILACS as well trial registers. We checked references of identified trials and systematic reviews. We applied no language restrictions. The date of the last search was March 2015 for all databases.
Selection criteria
We selected randomised controlled trials (RCTs) of diet, physical activity and behavioural interventions delivered to parents only for treating overweight or obesity in children aged 5 to 11 years.
Data collection and analysis
Two review authors independently assessed trials for risk of bias and evaluated overall study quality using the GRADE instrument. Where necessary, we contacted authors for additional information.
Main results
We included 20 RCTs, including 3057 participants. The number of participants ranged per trial between 15 and 645. Follow‐up ranged between 24 weeks and two years. Eighteen trials were parallel RCTs and two were cluster RCTs. Twelve RCTs had two comparisons and eight RCTs had three comparisons. The interventions varied widely; the duration, content, delivery and follow‐up of the interventions were heterogeneous. The comparators also differed. This review categorised the comparisons into four groups: parent‐only versus parent‐child, parent‐only versus waiting list controls, parent‐only versus minimal contact interventions and parent‐only versus other parent‐only interventions.
Trial quality was generally low with a large proportion of trials rated as high risk of bias on individual risk of bias criteria.
In trials comparing a parent‐only intervention with a parent‐child intervention, the body mass index (BMI) z score change showed a mean difference (MD) at the longest follow‐up period (10 to 24 months) of ‐0.04 (95% confidence interval (CI) ‐0.15 to 0.08); P = 0.56; 267 participants; 3 trials; low quality evidence. In trials comparing a parent‐only intervention with a waiting list control, the BMI z score change in favour of the parent‐only intervention at the longest follow‐up period (10‐12 months) had an MD of ‐0.10 (95% CI ‐0.19 to ‐0.01); P = 0.04; 136 participants; 2 trials; low quality evidence. BMI z score change of parent‐only interventions when compared with minimal contact control interventions at the longest follow‐up period (9 to 12 months) showed an MD of 0.01 (95% CI ‐0.07 to 0.09); P = 0.81; 165 participants; 1 trial; low quality evidence. There were few similarities between interventions and comparators across the included trials in the parent‐only intervention versus other parent‐only interventions and we did not pool these data. Generally, these trials did not show substantial differences between their respective parent‐only groups on BMI outcomes.
Other outcomes such as behavioural measures, parent‐child relationships and health‐related quality of life were reported inconsistently. Adverse effects of the interventions were generally not reported, two trials stated that there were no serious adverse effects. No trials reported on all‐cause mortality, morbidity or socioeconomic effects.
All results need to be interpreted cautiously because of their low quality, the heterogeneous interventions and comparators, and the high rates of non‐completion.
Authors' conclusions
Parent‐only interventions may be an effective treatment option for overweight or obese children aged 5 to 11 years when compared with waiting list controls. Parent‐only interventions had similar effects compared with parent‐child interventions and compared with those with minimal contact controls. However, the evidence is at present limited; some of the trials had a high risk of bias with loss to follow‐up being a particular issue and there was a lack of evidence for several important outcomes. The systematic review has identified 10 ongoing trials that have a parent‐only arm, which will contribute to future updates. These trials will improve the robustness of the analyses by type of comparator, and may permit subgroup analysis by intervention component and the setting. Trial reports should provide adequate details about the interventions to be replicated by others. There is a need to conduct and report cost‐effectiveness analyses in future trials in order to establish whether parent‐only interventions are more cost‐effective than parent‐child interventions.
Background
Omega‐6 fats are polyunsaturated fats vital for many physiological functions, but their effect on cardiovascular disease (CVD) risk is debated.
Objectives
To assess effects of increasing ...omega‐6 fats (linoleic acid (LA), gamma‐linolenic acid (GLA), dihomo‐gamma‐linolenic acid (DGLA) and arachidonic acid (AA)) on CVD and all‐cause mortality.
Search methods
We searched CENTRAL, MEDLINE and Embase to May 2017 and clinicaltrials.gov and the World Health Organization International Clinical Trials Registry Platform to September 2016, without language restrictions. We checked trials included in relevant systematic reviews.
Selection criteria
We included randomised controlled trials (RCTs) comparing higher versus lower omega‐6 fat intake in adults with or without CVD, assessing effects over at least 12 months. We included full texts, s, trials registry entries and unpublished studies. Outcomes were all‐cause mortality, CVD mortality, CVD events, risk factors (blood lipids, adiposity, blood pressure), and potential adverse events. We excluded trials where we could not separate omega‐6 fat effects from those of other dietary, lifestyle or medication interventions.
Data collection and analysis
Two authors independently screened titles/s, assessed trials for inclusion, extracted data, and assessed risk of bias of included trials. We wrote to authors of included studies. Meta‐analyses used random‐effects analysis, while sensitivity analyses used fixed‐effects and limited analyses to trials at low summary risk of bias. We assessed GRADE quality of evidence for 'Summary of findings' tables.
Main results
We included 19 RCTs in 6461 participants who were followed for one to eight years. Seven trials assessed the effects of supplemental GLA and 12 of LA, none DGLA or AA; the omega‐6 fats usually displaced dietary saturated or monounsaturated fats. We assessed three RCTs as being at low summary risk of bias.
Primary outcomes: we found low‐quality evidence that increased intake of omega‐6 fats may make little or no difference to all‐cause mortality (risk ratio (RR) 1.00, 95% confidence interval (CI) 0.88 to 1.12, 740 deaths, 4506 randomised, 10 trials) or CVD events (RR 0.97, 95% CI 0.81 to 1.15, 1404 people experienced events of 4962 randomised, 7 trials). We are uncertain whether increasing omega‐6 fats affects CVD mortality (RR 1.09, 95% CI 0.76 to 1.55, 472 deaths, 4019 randomised, 7 trials), coronary heart disease events (RR 0.88, 95% CI 0.66 to 1.17, 1059 people with events of 3997 randomised, 7 trials), major adverse cardiac and cerebrovascular events (RR 0.84, 95% CI 0.59 to 1.20, 817 events, 2879 participants, 2 trials) or stroke (RR 1.36, 95% CI 0.45 to 4.11, 54 events, 3730 participants, 4 trials), as we assessed the evidence as being of very low quality. We found no evidence of dose‐response or duration effects for any primary outcome, but there was a suggestion of greater protection in participants with lower baseline omega‐6 intake across outcomes.
Additional key outcomes: we found increased intake of omega‐6 fats may reduce myocardial infarction (MI) risk (RR 0.88, 95% CI 0.76 to 1.02, 609 events, 4606 participants, 7 trials, low‐quality evidence). High‐quality evidence suggests increasing omega‐6 fats reduces total serum cholesterol a little in the long term (mean difference (MD) −0.33 mmol/L, 95% CI −0.50 to −0.16, I2 = 81%; heterogeneity partially explained by dose, 4280 participants, 10 trials). Increasing omega‐6 fats probably has little or no effect on adiposity (body mass index (BMI) MD −0.20 kg/m2, 95% CI −0.56 to 0.16, 371 participants, 1 trial, moderate‐quality evidence). It may make little or no difference to serum triglycerides (MD −0.01 mmol/L, 95% CI −0.23 to 0.21, 834 participants, 5 trials), HDL (MD −0.01 mmol/L, 95% CI −0.03 to 0.02, 1995 participants, 4 trials) or low‐density lipoprotein (MD −0.04 mmol/L, 95% CI −0.21 to 0.14, 244 participants, 2 trials, low‐quality evidence).
Authors' conclusions
This is the most extensive systematic assessment of effects of omega‐6 fats on cardiovascular health, mortality, lipids and adiposity to date, using previously unpublished data. We found no evidence that increasing omega‐6 fats reduces cardiovascular outcomes other than MI, where 53 people may need to increase omega‐6 fat intake to prevent 1 person from experiencing MI. Although benefits of omega‐6 fats remain to be proven, increasing omega‐6 fats may be of benefit in people at high risk of MI. Increased omega‐6 fats reduce serum total cholesterol but not other blood fat fractions or adiposity.
Omega 6 plays a vital role in many physiological functions but there is controversy concerning its effect on cardiovascular disease (CVD) risk. There is conflicting evidence whether increasing or ...decreasing omega 6 intake results in beneficial effects.
The two primary objectives of this Cochrane review were to determine the effectiveness of:1. Increasing omega 6 (Linoleic acid (LA), Gamma-linolenic acid (GLA), Dihomo-gamma-linolenic acid (DGLA), Arachidonic acid (AA), or any combination) intake in place of saturated or monounsaturated fats or carbohydrates for the primary prevention of CVD.2. Decreasing omega 6 (LA, GLA, DGLA, AA, or any combination) intake in place of carbohydrates or protein (or both) for the primary prevention of CVD.
We searched the following electronic databases up to 23 September 2014: the Cochrane Central Register of Controlled Trials (CENTRAL) on the Cochrane Library (Issue 8 of 12, 2014); MEDLINE (Ovid) (1946 to September week 2, 2014); EMBASE Classic and EMBASE (Ovid) (1947 to September 2014); Web of Science Core Collection (Thomson Reuters) (1990 to September 2014); Database of Abstracts of Reviews of Effects (DARE) and Health Technology Assessment Database, and Health Economics Evaluations Database on the Cochrane Library (Issue 3 of 4, 2014). We searched trial registers and reference lists of reviews for further studies. We applied no language restrictions.
Randomised controlled trials (RCTs) of interventions stating an intention to increase or decrease omega 6 fatty acids, lasting at least six months, and including healthy adults or adults at high risk of CVD. The comparison group was given no advice, no supplementation, a placebo, a control diet, or continued with their usual diet. The outcomes of interest were CVD clinical events (all-cause mortality, cardiovascular mortality, non-fatal end points) and CVD risk factors (changes in blood pressure, changes in blood lipids, occurrence of type 2 diabetes). We excluded trials involving exercise or multifactorial interventions to avoid confounding.
Two review authors independently selected trials for inclusion, extracted the data, and assessed the risk of bias in the included trials.
We included four RCTs (five papers) that randomised 660 participants. No ongoing trials were identified. All included trials had at least one domain with an unclear risk of bias. There were no RCTs of omega 6 intake reporting CVD clinical events. Three trials investigated the effect of increased omega 6 intake on lipid levels (total cholesterol, low density lipoprotein (LDL-cholesterol), and high density lipoprotein (HDL-cholesterol)), two trials reported triglycerides, and two trials reported blood pressure (diastolic and systolic blood pressure). Two trials, one with two relevant intervention arms, investigated the effect of decreased omega 6 intake on blood pressure parameters and lipid levels (total cholesterol, LDL-cholesterol, and HDL-cholesterol) and one trial reported triglycerides. Our analyses found no statistically significant effects of either increased or decreased omega 6 intake on CVD risk factors.Two studies were supported by funding from the UK Food Standards Agency and Medical Research Council. One study was supported by Lipid Nutrition, a commercial company in the Netherlands and the Dutch Ministry of Economic Affairs. The final study was supported by grants from the Finnish Food Research Foundation, Finnish Heart Research Foundation, Aarne and Aili Turnen Foundation, and the Research Council for Health, Academy of Finland.
We found no studies examining the effects of either increased or decreased omega 6 on our primary outcome CVD clinical endpoints and insufficient evidence to show an effect of increased or decreased omega 6 intake on CVD risk factors such as blood lipids and blood pressure. Very few trials were identified with a relatively small number of participants randomised. There is a need for larger well conducted RCTs assessing cardiovascular events as well as cardiovascular risk factors.
Background
There is evidence from observational studies that whole grains can have a beneficial effect on risk for cardiovascular disease (CVD). Earlier versions of this review found mainly ...short‐term intervention studies. There are now longer‐term randomised controlled trials (RCTs) available. This is an update and expansion of the original review conducted in 2007.
Objectives
The aim of this systematic review was to assess the effect of whole grain foods or diets on total mortality, cardiovascular events, and cardiovascular risk factors (blood lipids, blood pressure) in healthy people or people who have established cardiovascular disease or related risk factors, using all eligible RCTs.
Search methods
We searched CENTRAL (Issue 8, 2016) in the Cochrane Library, MEDLINE (1946 to 31 August 2016), Embase (1980 to week 35 2016), and CINAHL Plus (1937 to 31 August 2016) on 31 August 2016. We also searched ClinicalTrials.gov on 5 July 2017 and the World Health Organization International Clinical Trials Registry Platform (WHO ICTRP) on 6 July 2017. We checked reference lists of relevant articles and applied no language restrictions.
Selection criteria
We selected RCTs assessing the effects of whole grain foods or diets containing whole grains compared to foods or diets with a similar composition, over a minimum of 12 weeks, on cardiovascular disease and related risk factors. Eligible for inclusion were healthy adults, those at increased risk of CVD, or those previously diagnosed with CVD.
Data collection and analysis
Two review authors independently selected studies. Data were extracted and quality‐checked by one review author and checked by a second review author. A second review author checked the analyses. We assessed treatment effect using mean difference in a fixed‐effect model and heterogeneity using the I2 statistic and the Chi2 test of heterogeneity. We assessed the overall quality of evidence using GRADE with GRADEpro software.
Main results
We included nine RCTs randomising a total of 1414 participants (age range 24 to 70; mean age 45 to 59, where reported) to whole grain versus lower whole grain or refined grain control groups. We found no studies that reported the effect of whole grain diets on total cardiovascular mortality or cardiovascular events (total myocardial infarction, unstable angina, coronary artery bypass graft surgery, percutaneous transluminal coronary angioplasty, total stroke). All included studies reported the effect of whole grain diets on risk factors for cardiovascular disease including blood lipids and blood pressure. All studies were in primary prevention populations and had an unclear or high risk of bias, and no studies had an intervention duration greater than 16 weeks.
Overall, we found no difference between whole grain and control groups for total cholesterol (mean difference 0.07, 95% confidence interval ‐0.07 to 0.21; 6 studies (7 comparisons); 722 participants; low‐quality evidence).
Using GRADE, we assessed the overall quality of the available evidence on cholesterol as low. Four studies were funded by independent national and government funding bodies, while the remaining studies reported funding or partial funding by organisations with commercial interests in cereals.
Authors' conclusions
There is insufficient evidence from RCTs of an effect of whole grain diets on cardiovascular outcomes or on major CVD risk factors such as blood lipids and blood pressure. Trials were at unclear or high risk of bias with small sample sizes and relatively short‐term interventions, and the overall quality of the evidence was low. There is a need for well‐designed, adequately powered RCTs with longer durations assessing cardiovascular events as well as cardiovascular risk factors.
Previous research is inconclusive on the effects of mode of delivery on maternal health-related quality-of-life (HRQoL). We conducted a systematic review and meta-analysis to assess the current ...evidence for associations between mode of delivery and postpartum health-related quality-of-life.
Electronic databases MEDLINE ALL (OVID), Web of Science, The Cochrane Library, CINAHL and EMBASE (OVID) were searched for English written articles investigating the relationship between mode of delivery and quality-of-life published form inception to 15th October 2020. Two reviewers independently screened titles and abstracts, assessed full texts, and extracted data. Meta-analysis was conducted where possible.
Twenty-one studies, including 19,879 women, met the inclusion criteria. A meta-analysis of 18 studies found HRQoL scores were significantly higher for women after vaginal delivery in comparison to caesarean (emergency and elective combined) (Effect Size (ES) 0.17, 95% CI 0.01-0.25, n = 7665) with highest scores after assisted vaginal delivery (ES 0.21, 95% CI 0.13-0.30, n = 2547). Physical functioning (ES 11.18, 95% CI = 2.29-20.06, n = 1746), physical role (ES 13.10, 95% CI = 1.16-25.05, n = 1471), vitality (ES 6.31, 95% CI = 1.14-10.29, n = 1746) and social functioning (ES 5.69, 95% CI = 1.26-10.11, n = 1746) were significantly higher after vaginal delivery compared to caesarean.
Health-related quality-of-life scores were higher for women after vaginal delivery in comparison to caesarean section. Consequently, women should be encouraged to deliver vaginally where possible. The findings of this research should be available to the relevant population to help support informed choice.
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