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تاثیر افزایش مصرف میوه و سبزیجات در پیشگیری اولیه از بروز بیماری‌های قلبی‌عروقی

Editorial note

This Cochrane Review has been superseded by a review entitled Vegan dietary pattern for the primary and secondary prevention of cardiovascular diseases (https://www.cochranelibrary.com/cdsr/doi/10.1002/14651858.CD013501.pub2/full).

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پیشینه

شواهد روز‌افزونی وجود دارد که مصرف زیاد میوه و سبزیجات برای پیشگیری از بروز بیماری‌ قلبی‌عروقی (cardiovascular disease; CVD) مفید است.

اهداف

هدف اولیه، تعیین اثربخشی i) توصیه به افزایش مصرف میوه و سبزیجات ii) تدارک میوه و سبزیجات برای افزایش مصرف، در پیشگیری اولیه از بروز CVD است.

روش‌های جست‌وجو

بانک‌های اطلاعاتی الکترونیکی زیر را جست‌وجو کردیم: کتابخانه کاکرین (2012؛ شماره 9؛CENTRAL؛ HTA؛ DARE؛ NEED)، MEDLINE (1946 تا هفته 3 سپتامبر 2012)؛ EMBASE (1980 تا هفته 39 سال 2012) و Conference Proceedings Citation Index ‐ Science on ISI Web of Science (5 اکتبر 2012). پایگاه‌های ثبت کارآزمایی را جست‌وجو و فهرست منابع را غربالگری کردیم و برای کسب اطلاعات بیشتر، هر زمان که لازم بود، با نویسندگان تماس گرفتیم. هیچ محدودیتی از نظر زبان مقاله اعمال نشد.

معیارهای انتخاب

کارآزمایی‌های تصادفی‌سازی و کنترل شده (randomised controlled trials; RCTs) با حداقل سه ماه دوره پیگیری (زمان سپری شده از شروع مداخله) با حضور بزرگسالان سالم یا افراد در معرض خطر بالای ابتلا به CVD. کارآزمایی‌ها، توصیه‌ به افزایش مصرف میوه و سبزیجات (از طریق هر منبع یا روش) را بررسی کردند یا فراهم کردن میوه و سبزیجات را برای افزایش مصرف آنها. گروه مقایسه عبارت بود از عدم انجام مداخله یا انجام‌ مداخله حداقلی. پیامدهای موردنظر عبارت بودند از حوادث بالینی CVD (مورتالیتی ناشی از CVD و همه علل، انفارکتوس میوکارد (myocardial infarction; MI)، پیوند بای‌پس عروق کرونر (coronary artery bypass grafting; CABG) یا آنژیوپلاستی عروق کرونری ترانس‌لومینال از خلال پوست (percutaneous transluminal coronary angioplasty; PTCA)، آنژین پکتورالیس شناسایی شده با آنژیوگرافی، سکته مغزی، اندآرترکتومی کاروتید، بیماری شریانی محیطی (peripheral arterial disease; PAD)) و عوامل خطر اصلی CVD (فشار خون، چربی‌های خون، دیابت نوع 2). کارآزمایی‌های مربوط به مداخلات چند‐‌عاملی در سبک زندگی (از جمله الگوهای مختلف رژیم غذایی، ورزش) یا مواردی که تمرکز بر کاهش وزن داشتند، برای اجتناب از مخدوش‌شدگی کنار گذاشته شدند.

گردآوری و تجزیه‌وتحلیل داده‌ها

دو نویسنده مرور به‌طور مستقل از هم کارآزمایی‌ها را برای ورود انتخاب کردند، داده‌ها را استخراج کرده و خطر سوگیری (bias) را ارزیابی کردند. کارآزمایی‌های مربوط به فراهم کردن میوه و سبزیجات، جداگانه از کارآزمایی‌های توصیه رژیم غذایی، آنالیز شدند.

نتایج اصلی

تعداد 10 کارآزمایی‌ را با مجموع 1730 شرکت‌کننده بزرگسال که تصادفی‌سازی شدند، و یک کارآزمایی در حال انجام را شناسایی کردیم. شش کارآزمایی، تدارک میوه و سبزیجات و چهار کارآزمایی، توصیه به افزایش مصرف میوه و سبزیجات را بررسی کردند. کارآزمایی در حال انجام، تدارک یک رژیم غذایی غنی از آووکادو را بررسی می‌کند. تعداد و نوع اجزای مداخله برای تدارک، و توصیه رژیم غذایی، میان کارآزمایی‌ها متفاوت بودند.

هیچ یک از کارآزمایی‌ها، عوارض بالینی را گزارش نکردند، زیرا همه آنها نسبتا کوتاه‌‐مدت بودند. هیچ شواهد محکمی برای اثبات تاثیر کارآزمایی‌های تکی از تدارک میوه و سبزیجات بر عوامل خطرساز قلبی‌عروقی وجود نداشت، اما کارآزمایی‌ها ناهمگون و کوتاه‐‌مدت بودند. علاوه بر این، در پنج کارآزمایی از شش کارآزمایی، فقط یک نوع میوه یا سبزیجات تدارک دیده شده بود. توصیه‌های رژیم غذایی، تاثیرات مطلوبی را بر فشار‌خون (فشار‌ خون سیستولیک (SBP): تفاوت میانگین (MD): 3.0‐ میلی‌متر جیوه (95% فاصله اطمینان (CI): 4.92‐ تا 1.09‐)، فشار‌خون دیاستولیک (DBP): MD؛ 0.90‐ میلی‌متر جیوه (95% CI؛ 2.03‐ تا 0.24)) و کلسترول لیپوپروتئین با چگالی پائین (LDL) نشان داد، اما آنالیزها فقط بر پایه دو کارآزمایی بودند. سه مورد از 10 کارآزمایی‌ وارد شده، عوارض جانبی را شامل افزایش حرکات روده، بوی بد دهان و بوی بدن را بررسی کردند.

نتیجه‌گیری‌های نویسندگان

در حال حاضر، مطالعات بسیار اندکی به بررسی تدارک، یا توصیه به افزایش مصرف، میوه و سبزیجات در غیاب مداخلات تغذیه‌ای بیشتر یا دیگر مداخلات مربوط به سبک زندگی برای پیشگیری اولیه از بروز بیماری قلبی‌عروقی پرداخته‌اند. شواهد محدود کنونی توصیه به افزایش مصرف میوه و سبزیجات دارند، زیرا یک مداخله تاثیرات مطلوبی بر عوامل خطرساز CVD دارد، اما برای تائید این موضوع، انجام کارآزمایی‌های بیشتری لازم است.

PICOs

Population
Intervention
Comparison
Outcome

The PICO model is widely used and taught in evidence-based health care as a strategy for formulating questions and search strategies and for characterizing clinical studies or meta-analyses. PICO stands for four different potential components of a clinical question: Patient, Population or Problem; Intervention; Comparison; Outcome.

See more on using PICO in the Cochrane Handbook.

تاثیر افزایش مصرف میوه و سبزیجات در پیشگیری از بروز بیماری قلبی‌عروقی

بیماری قلبی‌عروقی (CVD)، یک بار (burden) جهانی بوده و در مناطق مختلف متفاوت است. این تنوع منطقه‌ای تا حدی به عوامل تغذیه‌ای مرتبط بوده و مصرف اندک میوه و سبزیجات، با نرخ بالاتر CVD در ارتباط است. این مرور، اثربخشی افزایش مصرف میوه و سبزیجات را به عنوان یک مداخله تکی بدون تاثیر دیگر الگوهای تغذیه‌ای یا دیگر اصلاحات سبک زندگی در بزرگسالان سالم و افراد در معرض خطر بالای ابتلا به CVD برای پیشگیری از بروز CVD ارزیابی کرد. ما 10کارآزمایی را با حضور 1730 شرکت‌کننده یافتیم که از میان آنها شش مورد فراهم کردن میوه و سبزیجات را برای افزایش مصرف و چهار کارآزمایی توصیه تغذیه‌ای را برای افزایش مصرف میوه و سبزیجات بررسی کردند. در نوع میوه و سبزیجات تدارک دیده شده، تنوع‌هایی وجود داشت، اما همه مداخلات مربوط به تدارک، فقط شامل یک نوع میوه یا سبزیجات بودند. همچنین، در تعداد میوه و سبزیجاتی که به شرکت‏‌کنندگان توصیه می‌شد از آنها استفاده کنند، تنوع‌هایی وجود داشت. برخی مطالعات به شرکت‌کنندگان توصیه کردند که حداقل پنج وعده میوه و سبزیجات در هر روز بخورند، در حالی که دیگر مطالعات، مصرف حداقل هشت یا نه وعده را در روز توصیه کرده‌اند. طول دوره انجام مداخلات، از سه ماه تا یک سال بود. عوارض جانبی در سه مورد از کارآزمایی‌های وارد شده گزارش شدند و شامل افزایش حرکات روده، بوی بد دهان و بوی بدن بودند. هیچ یک از کارآزمایی‌های وارد شده، آنقدر طولانی نبودند که بتواند تاثیر افزایش مصرف میوه و سبزیجات را بر حوادث بیماری قلبی‌عروقی مانند حملات قلبی بررسی کنند. شواهد محکمی وجود نداشت مبنی بر اینکه فراهم آوردن یک نوع میوه یا سبزی تاثیرات مفیدی بر فشار خون و سطح چربی داشته باشد، اما اکثر کارآزمایی‌ها کوتاه‐مدت بودند. شواهدی به دست آمد که توصیه‌های تغذیه‌ای تاثیرات مفیدی بر افزایش مصرف میوه و سبزیجات دارند، اما این شواهد براساس یافته‌های دو کارآزمایی هستند. برای تائید یافته‌های ما، انجام کارآزمایی‌های بیشتر ضروری است.

Authors' conclusions

Implications for practice

Very few trials met the inclusion criteria for our review and none reported our primary outcome. Our strict inclusion criteria was designed to look specifically at the effects of increased fruit and vegetable consumption in the absence of other dietary interventions, but this limited the number of trials included and excluded notably one large trial reporting clinical endpoints (WHI). In our review, favourable effects were seen for outcomes of cardiovascular risk factors in the four trials of dietary advice to increase the consumption of fruit and vegetables, which is promising, but more trials are needed to confirm this and to examine effects over the longer term. Results from trials of the provision of single fruits or vegetables were more limited. Given the limited evidence to date, our review does not make any recommendations about changing practice. Current guidance recommends consumption of at least five portions of fruit and vegetables per day.

Implications for research

There is a lack of randomised controlled trials examining solely the effects of advice to consume more fruit and vegetables and the provision of fruit and vegetables to increase consumption for the primary prevention of CVD. This is surprising given that national and international guidelines recommend the consumption of at least five portions of fruit and vegetables per day. In particular, and most importantly, there is a shortage of randomised controlled trials that look at the effects of interventions to solely increase fruit and vegetable consumption over the longer term to determine the sustainability of such behavioural change, and to examine effects on our primary outcome CVD events. Other large trials of multifactorial dietary interventions including increased fruit and vegetable consumption have shown no benefits of the intervention on CVD clinical events (WHI), and this finding may hold true also for interventions aimed solely at increasing fruit and vegetable consumption, assuming the other components of the dietary intervention did no harm. This evidence is however limited to middle‐aged women and more research is needed in other groups. Furthermore, we found no trials reporting economic evaluations of interventions to increase fruit and vegetable consumption.

Background

Description of the condition

Cardiovascular disease (CVD) is one of the leading causes of death worldwide (WHO 2011). In 2008 it accounted for 30% of total global deaths, with 6.2 million deaths the consequence of stroke and 7.2 million due to coronary heart disease (CHD) (WHO 2011). The burden of CVD also varies substantially between regions (Müller‐Nordhorn 2008), for example, death from Ischaemic heart disease in France is a quarter of that of the United Kingdom (UK) (Law 1999).

Dietary factors may play a vital role in the development of CVD and its risk factors and may contribute to the geographic variability in CVD morbidity and mortality (Scarborough 2011; Yusuf 2001). Such factors are important, not only because they have been linked to CVD development, but also because they can be modified. This makes them one of the main targets for interventions aimed at primary prevention and management of CVD.

One dietary factor that should be considered in the primary prevention of CVD is fruit and vegetable intake. Indeed, a low consumption of fruit and vegetables (less than 400 grammes [g] per day) is thought to be one of the top 10 risk factors for global mortality and is estimated to result in 1.7 million global deaths a year (WHO 2004). Of these global deaths, 14% are from gastrointestinal cancer, 11% are due to ischaemic heart disease and 9% are from stroke. In the European Union, New Zealand and Australia 3.5%, 2.1% and 2.8% respectively of disease burden is considered to be a consequence of low fruit and vegetable intake (Begg 2007; Pomerleau 2004; Tobias 2001), with, in particular, 9.6% of the CVD disease burden in Australia due to a low intake of fruit and vegetables (Begg 2007).

Conversely, it has been shown that a high consumption of fruit and vegetables can have a protective role for some chronic diseases including CVD (Hooper 2007). A number of cohort studies have shown that the risk of CHD is associated with lower consumption of fruit and vegetables (Bazzano 2002; Liu 2000; Liu 2001). Joshipura and colleagues, for example, showed in a large observational study (84,251 women and 42,148 men) that a high intake of fruit of vegetables was associated with reduced risk of developing CHD. This was particularly the case for those fruit and vegetables rich in vitamin C and leafy green vegetables (Joshipura 2001). It has been estimated that an increase in fruit and vegetable intake could reduce the burden of ischaemic stroke and ischaemic heart disease by as much as 19% and 31% respectively (Lock 2005). Furthermore, it is estimated that approximately 2.7 million lives a year could be saved by increasing fruit and vegetable consumption to 400 g per day or over (WHO 2004).

Observational studies have shown that high levels of fruit and vegetable intake are associated with increased psychological well being (Blanchflower 2012), a reduction in the risk of CVD (Joshipura 2001; Liu 2000; Liu 2001) and a reduction in type 2 diabetes (Carter 2010). As a result, many national and international guidelines recommend at least five portions of fruit and/or vegetables a day (a portion equates to 80 g) (Agudo 2004; NHS 2009; U.S. Department of Agriculture 2005). However, such guidelines are not always followed. This appears to be the case in the UK where it is estimated that only 27.7% of the general population reach this target (Maheswaran 2013).

Description of the intervention

There are many complex determinants involved in fruit and vegetable intake. As a consequence of this, a variety of conceptual frameworks are used to help develop interventions aimed at increasing fruit and vegetable consumption (Wolfenden 2012). For instance, a conceptual framework may suggest that interventions aimed at personal and cultural factors are more effective in increasing fruit and vegetable consumption than an intervention targeting only personal factors. It is suggested that for addressing changes to dietary intake, such as fruit and vegetable consumption, a social ecological framework that uses behaviour change theories at different levels of influence is best (Peterson 2002).

The interventions investigated in this review will include those that provide advice to increase fruit and vegetable consumption or those that provide fruit and vegetables themselves to increase consumption. Advice can take many forms in that it may be written or verbal, involve a single or multiple contact and may be delivered by commercial organisations, health professionals or government organisations. Provision may include only one, or more fruit(s) and/or vegetable(s) and be provided in the workplace, at community centres or in the home to name but a few.

How the intervention might work

Evidence from observational and experimental studies suggests that a high consumption of fruit and vegetables, that is more than 400 g or more than five portions a day, may be beneficial for the prevention and treatment of CVD (Ness 1997). However, the exact mechanisms by which increased fruit and vegetable consumption reduce CVD risk are not known. It may be due to fruit and vegetables containing protective elements including vitamins, minerals, antioxidants, micronutrients and phytochemicals (Department of Health 2010; Miller 2000; Van Duyn 2000). There are many potential mechanisms through which these protective elements can act to reduce blood pressure, reduce antioxidant stress, lower the serum level of low‐density lipoprotein cholesterol and improve the regulation of haemostasis (Asgard 2007; Dauchet 2006; Suido 2002).

Theories have been developed to explain the mechanisms by which lifestyle changes such as fruit and vegetable provision and advice interventions influence fruit and vegetable intake. These tend to be based on the Health Belief Model (Rosenstock 1966), The Theory of Planned Behaviour (Ajzen 1991), Social cognitive theory (Bandura 1986) or the Stages of Change Model (Prochaska 1984). All four theories emphasise the dynamic nature of beliefs and suggest that in order for behaviours to change, changes need to be made to a person's perceived norms, attitudes, knowledge, skills, and expectancies (Ogden 2001; Wolfenden 2012). Social‐ecological theories have also been used to explain the mechanisms by which interventions aimed at increasing fruit and vegetable intake may work. These theories suggest that a person's health behaviour is influenced by a multitude of factors including not only intra‐ and interpersonal factors but also organisational and community factors and those relating to public policy (Robinson 2008).

Why it is important to do this review

Many factors determine the intake of fruit and vegetables in adults (Pollard 2002). These include not only demographic and lifestyle factors but also sensory appeal and availability (Anderson 1994; Brug 1995; Clark 1998; Lennernas 1997; Thompson 1999). Although observational studies investigating the factors that determine fruit and vegetable intake provide considerable information to aid in the development of interventions, they do not examine the effectiveness of interventions to increase fruit and vegetable consumption. Some systematic reviews have attempted to do this (Ammerman 2002; Brunner 2007; Contento 1995; Miller 2000a; Pomerleau 2005). Pomerleau et al. (Pomerleau 2005), for example, conducted a systematic review that investigated the effectiveness of interventions designed to promote the intake of fruit and vegetables. They found that the largest increase in fruit and vegetable consumption was for interventions that targeted high‐risk populations or those with a pre‐existing disease, while a small increase of between 0.1 and 1.4 servings of fruit and vegetables a day was found for interventions promoting fruit and vegetable intake in healthy adults. This was similar to the findings of Brunner et al. (Brunner 2007) who found that dietary advice, when compared to no advice, increased the consumption of fruit and vegetables by 1.25 servings per day in healthy adults.

However, these systematic reviews do not always focus solely on the intake of fruit and vegetables (Brunner 2007; Contento 1995). The systematic review by Pomerleau (2005) does not solely focus on CVD (Pomerleau 2005), and other reviews include children (Burchett 2003; Miller 2000a).

We are focusing our attention on adults since a Cochrane review is already being undertaken in assessing the evidence for interventions for increasing fruit and vegetable consumption in children aged up to five years (Wolfenden 2012), and another on community‐based interventions to increase fruit and vegetable consumption for five to 18 year olds (Ganann 2010). A comprehensive systematic review is needed that thoroughly examines interventions providing advice to increase fruit and vegetable consumption and the provision of fruit and vegetables to increase consumption, in healthy adults or those with cardiovascular risk factors to determine their effectiveness in CVD prevention. This will provide guidance not only for national and international governments but also for local authorities, practitioners and members of the public.

Objectives

The primary objective is to determine the effectiveness of i) advice to increase fruit and vegetable consumption ii) the provision of fruit and vegetables to increase consumption, on mortality (cardiovascular and all‐cause), non‐fatal CVD endpoints (myocardial infarction (MI), coronary artery bypass grafting (CABG), percutaneous transluminal coronary angioplasty (PTCA), angina, or angiographically‐defined coronary heart disease (CHD), stroke, carotid endarterectomy, peripheral arterial disease (PAD)), changes in blood pressure (systolic and diastolic blood pressure) and blood lipids (total cholesterol, high‐density lipoprotein (HDL) cholesterol, low‐density lipoprotein (LDL) cholesterol, triglycerides), the occurrence of type 2 diabetes, health‐related quality of life, adverse effects and costs.

Methods

Criteria for considering studies for this review

Types of studies

Randomised controlled trials (RCTs) including cluster‐randomised trials and cross‐over trials.

Types of participants

Adults (people from the age of 18 onwards) of all ages from the general population and those who are at high risk of CVD due to the presence of major CVD risk factors such as smoking, dyslipidaemia or hypertension. The review focused on the effects of fruit and vegetable consumption for the primary prevention of CVD. We therefore excluded studies where more than 25% of participants had CVD at baseline including those who have experienced a previous MI, stroke, revascularisation procedure (CABG or PTCA), those with angina, or angiographically‐defined CHD, cerebrovascular disease (stroke) and PAD. We also excluded studies where more than 25% of the participants had type 2 diabetes as while patients with type 2 diabetes are at increased risk of CVD, interventions for diabetes are covered specifically by the Cochrane Metabolic and Endocrine Disorders review group.

Types of interventions

The interventions included i) specific dietary advice to increase fruit and vegetable consumption or ii) the provision of fruit and vegetables (participants are provided with fruits and vegetables as part of the intervention) as a means to increase consumption. All interventions were to include whole fruit and vegetables only, interventions involving fruit and vegetable extracts were excluded. Both provision and advice interventions could be delivered in any setting, by any individual or modality.

Studies examining advice to increase fruit and vegetable intake were examined separately from those investigating the provision of fruit and vegetables. Multi‐factorial lifestyle interventions (including additional dietary interventions e.g. reduced fat and other lifestyle interventions e.g. exercise) and trials focusing on weight loss were not included in this review to avoid confounding.

We focused on follow‐up periods of three months or more. Follow‐up was considered to be the time elapsed since the start of the intervention and therefore any trials with an intervention duration of less than 12 weeks were excluded. Trials were only considered where the comparison group was no intervention (usual diet) or minimal intervention (e.g. leaflets (dietary or otherwise) with no person‐to‐person interaction or reinforcement).

Types of outcome measures

Endpoints were measured using validated measures.

Primary outcomes

  1. Cardiovascular mortality.

  2. All‐cause mortality.

  3. Non‐fatal endpoints such as MI, CABG, PTCA, angina, or angiographically‐defined CHD, stroke, carotid endarterectomy, PAD.

Secondary outcomes

  1. Changes in blood pressure (systolic and diastolic blood pressure) and blood lipids (total cholesterol, HDL cholesterol, LDL cholesterol, triglycerides).

  2. Occurrence of type 2 diabetes as a major CVD risk factor.

  3. Health‐related quality of life.

  4. Adverse effects (as defined by the authors of the included trials).

  5. Costs.

Search methods for identification of studies

Electronic searches

The following electronic databases were searched: The Cochrane Library (2012, issue 9), (including the Cochrane Central Register of controlled Trials (CENTRAL) and NHS Centre for Reviews and Dissemination (CRD) databases Health Technology Assessment (HTA), Database of Abstracts of Reviews of Effectiveness (DARE) and NHS Economic Evaluation Database (NEED)); MEDLINE (1946 to week 3 September 2012); EMBASE (1980 to 2012 week 39) and the Conference Proceedings Citation Index ‐ Science on ISI Web of Science (5 October 2012). We searched trial registers, screened reference lists and contacted authors for additional information where necessary. No language restrictions were applied.

Medical Subject Headings (MeSH) or equivalent and text word terms were use with searches designed in accordance with Cochrane Heart Group methods and guidance. There were no language restrictions.

Searches were tailored to individual databases. The search strategies for each database are shown in Appendix 1.

Searching other resources

Reference lists of reviews and retrieved articles were checked for additional studies.

We searched the metaRegister of controlled trials (mRCT) (www.controlled-trials.com/mrct), Clinicaltrials.gov (www.clinicaltrials.gov) and the WHO International Clinical Trials Registry Platform (ICTRP) (http://apps.who.int/trialsearch/) for ongoing trials and unpublished or part‐published trials.

Citation searches were performed on key articles. Google Scholar was also used to search for further studies.

We contacted experts in the field for unpublished and ongoing trials and authors were contacted where necessary for additional information.

Data collection and analysis

Selection of studies

Review authors (LH, EI, NF) independently reviewed the titles and abstracts identified from the searching. Following this initial screening, the full text reports of the potentially relevant studies were obtained and the same two review authors (LH, EI) independently selected relevant studies using predetermined inclusion criteria. In all cases, disagreements concerning study inclusion were resolved by consensus, a third review author (Karen Rees (KR)) was consulted if disagreement persisted.

Data extraction and management

Data extraction was carried out independently by two review authors (LH, Jennifer Holmes (JH)) using a proforma and chief investigators were contacted to provide additional relevant information if necessary.

The following details were extracted from each study.

  1. Study design.

  2. Study setting.

  3. Participant characteristics.

  4. Intervention (advice or provision of fruit and vegetables, personnel, intensity, duration, follow‐up).

  5. Comparison group (no intervention or details of minimal intervention).

  6. Outcome data (outcome assessment, adverse effects).

  7. Methodological quality (randomisation, blinding, attrition).

Disagreements about extracted data were resolved by consensus and a third reviewer (KR) was consulted if disagreement persisted.

Assessment of risk of bias in included studies

Risk of bias was assessed independently by two review authors (LH, JH) by examining the quality of the random sequence generation and allocation concealment, description of drop‐outs and withdrawals (including intention‐to‐treat analysis), blinding (participant, personnel and outcome assessment) and selective outcome reporting (Higgins 2011).

Measures of treatment effect

Data was processed in accordance with the Cochrane Handbook for Systematic Reviews of Interventions (Higgins 2011). For continuous outcomes net changes were compared (i.e. intervention group minus control group differences) and a mean difference (MD) and 95% confidence intervals (CI's) calculated for each study.

Assessment of heterogeneity

For each outcome, tests of heterogeneity were conducted (using Chi2 test of heterogeneity and I² statistic). If no heterogeneity was present a fixed‐effect meta‐analysis was performed. If there was substantial heterogeneity (Igreater than 50%) the review authors looked for possible explanations for this (e.g. intervention and participants). If the heterogeneity could not be explained, we considered the following options:

  1. provide a narrative overview and not aggregate the studies at all;

  2. use a random‐effects model with appropriate cautious interpretation.

Subgroup analysis and investigation of heterogeneity

Results were stratified by i) advice to increase fruit and vegetable consumption and ii) the provision of fruit and vegetables to increase consumption. Trials could not be stratified by baseline risk and the effects of intensity and duration of the intervention due to the small number of trials included in the review.

Sensitivity analysis

We performed sensitivity analysis excluding studies at high risk of bias (e.g. those with loss to follow‐up more than 20% without intention‐to‐treat analysis). We intended to examine the effects of "time and attention" given to participants in the intervention and control groups as potential confounders, and the effects of publication bias using funnel plots and tests of asymmetry (Egger 1997), but these could not be carried out due to the small number of trials included in the review.

Results

Description of studies

Results of the search

The electronic searches generated 7283 hits after duplicates were removed. Screening of titles and abstracts identified 298 papers to go forward for formal inclusion and exclusion. Of these, 10 RCTs met the inclusion criteria. We also identified one ongoing trial from trial registers. Details of the flow of studies through the review are shown in the PRISMA flow diagram in Figure 1.


Study flow diagram.

Study flow diagram.

Included studies

Details of the studies included in the review are shown in the Characteristics of included studies table. Ten trials with 1730 participants met the inclusion criteria. Four of the 10 trials recruited only female participants (Dichi 2011; Djuric 2006; Gravel 2009; Maskarinec 1999). Six trials were conducted in the U.S.A (Djuric 2006; Finley 2007; Fujioka 2006; Gardner 2007; Maskarinec 1999; Smith‐Warner 2000), one trial in Canada (Gravel 2009), one in Brazil (Dichi 2011), and two in the UK (John 2002; Thies 2012).

None of the included studies had interventions that provided fruit and vegetables and gave advice. Six of the 10 trials examined the effects of providing fruit and vegetables to increase consumption (Dichi 2011; Finley 2007; Fujioka 2006; Gardner 2007; Gravel 2009; Thies 2012) and four examined the effects of dietary advice to increase fruit and vegetable intake (Djuric 2006; John 2002; Maskarinec 1999; Smith‐Warner 2000). For those studies examining the effects of provision of fruit and vegetables there was variability in the types of fruit and vegetables provided and the portion size. Furthermore, five of the six provision trials only provided one fruit or vegetable. One study looked at the provision of 25 g/day of soy (Dichi 2011), one looked at the provision of 130 g of cooked pinto beans daily (Finley 2007), another examined the effects of half a grapefruit three times a day (Fujioka 2006), one study examined the provision of raw garlic on a sandwich (Gardner 2007), one study looked at a high tomato diet (Thies 2012) and one trial looked at the provision of 750 mL of legumes a week (Gravel 2009). Similarly, the type of dietary advice to increase fruit and vegetable consumption also varied between studies. Portions of fruit and vegetables included five or more portions a day (John 2002), at least eight servings daily (Smith‐Warner 2000), and at least nine servings a day (Djuric 2006; Maskarinec 1999). In addition, the modality of the advice provided differed between studies. In two studies, advice was provided by individualised in‐person dietary counselling with monthly group meetings (Djuric 2006; Maskarinec 1999). In another study participants were provided with a portion guide, leaflets on barriers to increasing fruit and vegetable consumption and an action plan to increase fruit and vegetable consumption by a research nurse who also introduced the benefits of increasing fruit and vegetable intake (John 2002). In the remaining study a nutritionist helped participants to formulate a plan to help them increase their fruit and vegetable intake and provided participants with educational materials on this topic. Participants were also taught behavioural modification strategies to identify personal barriers to adherence (Smith‐Warner 2000). The dietary advice interventions took place in health centres (John 2002) and a digestive healthcare unit (Smith‐Warner 2000). The two remaining studies did not state where there interventions took place (Djuric 2006; Maskarinec 1999).

The duration of the intervention and follow‐up periods varied between the included studies. Four of the studies had three to six months follow‐up (Dichi 2011; Finley 2007; Fujioka 2006; Thies 2012), four a follow‐up of six months (Gardner 2007; Gravel 2009; John 2002; Maskarinec 1999), and two studies a follow‐up of one year (Djuric 2006; Smith‐Warner 2000).

Studies were also variable in the types of participants they recruited. Two studies were conducted in women with metabolic syndrome (Dichi 2011; Gravel 2009), one study was conducted in healthy post‐menopausal women with a family history of breast cancer (Djuric 2006), one was conducted in participants with LDL concentrations of 130‐190 mg/dL and triglyceride levels of less than 250 mg/dL (Gardner 2007), one study included participants who were obese (Fujioka 2006), another study was conducted in patients who had colorectal adenomatous polyps in the five years before the study (Smith‐Warner 2000), one study included patients who were pre‐metabolic or healthy (Finley 2007) and three studies were conducted in healthy participants (John 2002; Maskarinec 1999; Thies 2012).

Four studies examining the provision of fruit and vegetables to increase consumption are awaiting classification. Details of these studies are provided in the Characteristics of studies awaiting classification table. The first trial examined fruit and vegetable puree and juice drinks in healthy participants (George 2009). The second trial examined three different diets on serum cholesterol in healthy volunteers (Groen 1952). The third study awaiting classification looked at 45 g/day of blueberries or blackberries in postmenopausal women who smoked (Teeple (2011)), while the forth study examined seven or more portions of fruit and vegetables daily for 12 weeks in overweight participants (Wallace 2012).

One ongoing trial examining the provision of fruit and vegetables to increase consumption was identified (Wang 2011). Details of this study are shown in the Characteristics of ongoing studies table. The study examined an avocado‐rich diet (Wang 2011). The anticipated end date for this study was May 2012 but as of yet, no results have been published.

Excluded studies

Details and reasons for exclusion for the studies that most closely missed the inclusion criteria are provided in the Characteristics of excluded studies table. Reasons for exclusion for the majority of studies were alternative designs (not RCTs), the intervention was not relevant, studies were short term with less than three months follow‐up and the control group did not receive a minimal intervention or no intervention (see Figure 1).

Risk of bias in included studies

Details are presented for each of the included trials in the 'Risk of bias' tables in the Characteristics of included studies and summaries are presented in Figure 2 and Figure 3.


'Risk of bias' summary: review authors' judgements about each risk of bias item for each included study.

'Risk of bias' summary: review authors' judgements about each risk of bias item for each included study.


'Risk of bias' graph: review authors' judgements about each risk of bias item presented as percentages across all included studies.

'Risk of bias' graph: review authors' judgements about each risk of bias item presented as percentages across all included studies.

Allocation

The methods of random sequence generation were unclear in seven of the 10 included studies (Dichi 2011; Djuric 2006; Finley 2007; Gravel 2009; Maskarinec 1999; Smith‐Warner 2000; Thies 2012). In the three studies where the random sequence generation methods were stated, the methods were judged to be of low risk of bias (Fujioka 2006; Gardner 2007; John 2002). The methods of allocation concealment were unclear in nine of the 10 included studies (Dichi 2011; Djuric 2006; Finley 2007; Fujioka 2006; Gravel 2009; John 2002; Maskarinec 1999; Smith‐Warner 2000; Thies 2012). In the one study which stated the method of allocation concealment, the method was judged of low risk of bias (Gardner 2007).

Blinding

Blinding participants and personnel was unclear in three of the 10 included studies. Four trials were of dietary advice where blinding of participants to the intervention was impossible (Djuric 2006; John 2002; Maskarinec 1999; Smith‐Warner 2000) and these were regarded as at high risk of bias. Similarly, it may also difficult to blind participants in trials of the provision of fruit and vegetables. One study stated that it was single‐blind and so was regarded as at high risk of bias (Thies 2012), while two studies stated that they were double‐blind and were regarded as at low risk of bias (Fujioka 2006; Gardner 2007). The blinding of outcome assessors was unclear in five of the included studies (Dichi 2011; Finley 2007; Gravel 2009; Smith‐Warner 2000; Thies 2012) but five studies stated that outcome assessors were blinded (Djuric 2006; Fujioka 2006; Gardner 2007; John 2002; Maskarinec 1999).

Incomplete outcome data

Five of the 10 included studies reported losses to follow‐up, had a similar number of losses between the intervention and control arms, and/or stated the reasons for losses to follow‐up (Fujioka 2006; Gardner 2007; John 2002; Smith‐Warner 2000; Thies 2012).These studies were considered to be at low risk of bias. In another five trials, the reporting of incomplete outcome data was judged as unclear as they either did not report losses to follow‐up (Dichi 2011; Gravel 2009) or did not report the reasons for losses to follow‐up (Djuric 2006;Finley 2007; Maskarinec 1999).

Selective reporting

For five of the 10 included studies the risk of bias for selective reporting was unclear as there was insufficient information available for a judgement to be made (Dichi 2011; Djuric 2006; Gravel 2009; John 2002; Smith‐Warner 2000). For two studies, the risk of bias was judged as high (Finley 2007; Maskarinec 1999) because lipid levels were reported in graphical form with no usable numbers for meta‐analysis (Finley 2007) or because lipid levels were presented in the analysis but were not stated in the methods as an outcome (Maskarinec 1999). Three of the 10 included studies were judged to be of low risk of bias as the studies clearly stated primary and secondary outcomes and reported their results (Fujioka 2006; Gardner 2007; Thies 2012).

Other potential sources of bias

For all included studies there was insufficient information to judge the risk of bias from other potential sources.

Effects of interventions

Advice to increase the consumption of fruit and vegetables

Four trials examined dietary advice to increase fruit and vegetable consumption with follow‐up periods of over six months (Djuric 2006; John 2002; Maskarinec 1999; Smith‐Warner 2000). No trials were found with a follow‐up of three to six months.

Clinical Events

None of the included studies provided clinical event data.

Cardiovascular risk factors
Blood pressure

Two of the four studies that examined dietary advice to increase the consumption of fruit and vegetables measured blood pressure (John 2002; Smith‐Warner 2000). In one study, this was at six months (John 2002) and in the other study at 12 months (Smith‐Warner 2000). From the pooled analysis, advice to eat fruit and vegetables significantly reduced systolic blood pressure (mean difference (MD) ‐3.0 mmHg (95% confidence interval (CI) ‐4.92 to ‐1.09)) (Analysis 1.1) (891 participants) but the reduction in diastolic blood pressure was not statistically significant (MD ‐0.90 mmHg (95% CI ‐2.03 to 0.24)) (Analysis 1.2) (891 participants). No heterogeneity was found between trials (I2 = 0%).

Lipid levels

Four studies measured total cholesterol (Djuric 2006; John 2002; Maskarinec 1999; Smith‐Warner 2000). Two studies measured total cholesterol at six months (John 2002; Maskarinec 1999) and two studies measured this at 12 months (Djuric 2006; Smith‐Warner 2000). The pooled analysis showed no effect of the intervention on total cholesterol levels (MD ‐0.01 mmol/L (95% CI ‐0.11 to 0.09)) (Analysis 1.3) (970 participants). No heterogeneity was found between trials (I2 = 0%).

Two trials examined the effects of dietary advice on LDL cholesterol (Djuric 2006; Smith‐Warner 2000); both at 12 months. Both trials could be pooled statistically and showed a reduction in LDL cholesterol but this did not reach statistical significance (MD ‐0.17 mmol/L (95% CI ‐0.38 to 0.03)) (Analysis 1.4) (251 participants). No heterogeneity was found between trials (I2 = 0%).

Two studies also measured HDL cholesterol (Djuric 2006; Smith‐Warner 2000) at 12 months and the pooled data for these studies showed no effect of the intervention on HDL cholesterol levels (MD ‐0.01 (95% CI ‐0.10 to 0.08)) (Analysis 1.5) (251 participants). No heterogeneity was found between trials (I2 = 0%).

Three studies measured triglycerides (Djuric 2006; Maskarinec 1999; Smith‐Warner 2000) and data were pooled from all three. Two trials measured triglycerides at 12 months (Djuric 2006; Smith‐Warner 2000) and one study at six months (Maskarinec 1999). Overall, there was a tendency for triglyceride levels to increase with the intervention, but this did not reach statistical significance (MD 0.10 mmol/L (95% CI ‐0.06 to 0.27)) (Analysis 1.6) (280 participants). Furthermore, no heterogeneity was found between trials (I2 = 0%).

Provision of fruit and vegetables to increase consumption

Six trials examined the effects of provision of fruit and vegetables, four had a follow‐up period of three months (Dichi 2011; Finley 2007; Fujioka 2006; Thies 2012), and two a follow‐up period of over six months (Gardner 2007; Gravel 2009).

Clinical Events

None of the included studies provided clinical event data.

Cardiovascular risk factors
Blood pressure

Four of the five included studies measured blood pressure (Dichi 2011; Fujioka 2006; Gravel 2009; Thies 2012). One study reported medians and interquartile ranges suggesting the data were skewed (Dichi 2011), and authors of two studies were contacted for information on mean changes and variance but this was not forthcoming (Fujioka 2006; Gravel 2009). Two studies also did not provide information on effect size or statistical significance (Fujioka 2006; Gravel 2009)

Differences were seen for diastolic blood pressure in women with metabolic syndrome in both the intervention and control group (P < 0.05) (Dichi 2011) (30 participants) at 90 days. One study reported no effects on systolic (MD 1.00 mmHg, 95% CI 0.45 to 1.55) (Analysis 2.1) or diastolic blood pressure (MD 1.50 mmHg, 95% CI 1.18 to 1.82) (Analysis 2.2) with the provision of fruit and vegetables to increase consumption (Thies 2012) (157 participants) at three months. The remaining two studies also reported no effects on blood pressure with the provision of fruit and vegetables to increase consumption (Fujioka 2006; Gravel 2009) (180 participants) at three months (Fujioka 2006) and six months (Gravel 2009).

Lipid levels

Three trials measured total cholesterol (Dichi 2011; Finley 2007; Thies 2012). One study measured this at 90 days (Dichi 2011) while the other two studies measured total cholesterol at three months (Finley 2007; Thies 2012). One study reported data in graphical form and found a statistically significant reduction in total cholesterol (P < 0.014) for those who ate pinto beans (the intervention) compared with those who ate chicken soup (the comparison group) (Finley 2007) (80 participants) at three months. For the pooled analysis (187 participants), moderate heterogeneity was found between studies (I2 = 51%) so a random‐effects meta‐analysis was performed. From the pooled analysis, fruit and vegetable provision was found to lower total cholesterol slightly (MD ‐0.10 mmol/L, 95% CI ‐0.24 to 0.04) but this was not statistically significant (Analysis 2.3). Results were similar for the fixed‐effect model but the random‐effects results were reported as the effect estimate is more conservative with wider confidence intervals.

Four trials measured LDL cholesterol (Dichi 2011; Finley 2007; Gardner 2007; Thies 2012). One study reported the data in graphical form and found a reduction in LDL cholesterol with the intervention (P < 0.5, Finley 2007) (80 participants) at three months. The other three studies could not be combined as there was substantial heterogeneity between trials (I2 =59%) (Analysis 2.4) (284 participants). One study showed a significant reduction in LDL cholesterol with the intervention (MD ‐0.09 mmol/L, 95% CI ‐0.12 to ‐0.06) (Thies 2012) at three months while the two remaining studies found fruit and vegetable provision to have no effect on LDL cholesterol (Dichi 2011; Gardner 2007) at 90 days (Dichi 2011) and at six months (Gardner 2007).

All six studies examined the effects of provision of fruit and vegetables on HDL cholesterol. Usable data were not available for three studies, two reported that they found no significant effects of the intervention on HDL cholesterol levels (Fujioka 2006; Gravel 2009) at three months (Fujioka 2006) and six months (Gravel 2009), whereas the third study found significantly reduced HDL cholesterol levels (Finley 2007) at three months. Data for the remaining three studies could not be pooled as there was significant heterogeneity present (I2 = 90%) ( (Analysis 2.5) (284 participants). One study showed a significant increase in HDL cholesterol with soy (MD 0.17, 95% CI 0.02 to 0.32) (Dichi 2011) at 90 days and the second study with raw garlic (MD 0.08 mmol/L, 95% CI 0.00 to 0.16) (Gardner 2007) at six months. The third study showed a significant decrease in HDL cholesterol (MD ‐0.06 mmol/L, 95% CI ‐0.08 to ‐0.04) (Thies 2012) at three months.

Similarly, all six trials measured triglycerides and data were pooled for three trials with useable data (Analysis 2.6). For these three trials, triglycerides were measured at three months (Finley 2007; Fujioka 2006) and six months (Gravel 2009). No heterogeneity was found between trials (I2 = 0%). Overall, there was no effect of the intervention on triglyceride levels (MD ‐0.01 mmol/L (95% CI ‐0.03 to 0.01)) (284 participants). No effects on triglycerides were reported in the remaining three trials that did not contribute to the meta‐analysis (Finley 2007; Fujioka 2006; Gravel 2009).

Adverse effects

Adverse effects of the provision of fruit and vegetables were noted in two of the six included studies (Fujioka 2006; Gardner 2007). One reported that there were few adverse effects over three months (Fujioka 2006). The second study reported that no serious adverse effects occurred over six months (Gardner 2007) but that bad breath and body odour were reported in 57% of those receiving the intervention (raw garlic) and flatulence was reported by three participants in the intervention group and one participant in the control group.

One of the three studies examining the effects of dietary advice to increase fruit and vegetable consumption examined adverse effects (Smith‐Warner 2000).This study reported significantly increased bowel movements from 9.2 to 10.0 a week with the intervention and significantly more flatulence (P = 0.01), but this did not persist after three months.

Costs

None of the included studies provided data on costs.

Discussion

Summary of main results

Ten trials which randomised 1730 participants were identified from the 298 papers screened. None of the trials reported clinical endpoints. Six of these 10 trials examined the provision of fruit and vegetables to increase consumption. From these, there was no strong evidence in favour of the effects of fruit and vegetable provision on CVD risk factors, however, the trials were heterogeneous, and short term.

Four trials examined dietary advice to increase fruit and vegetable consumption. From these trials, there was some evidence of favourable effects of dietary advice to increase fruit and vegetable consumption on blood pressure and to a lesser extent on LDL cholesterol at six months. However, it should be noted that few trials contributed to each analysis.

Overall completeness and applicability of evidence

This review included adult participants who were at varying levels of CVD risk and included both men and women. The majority of trials were conducted in developed countries. None of the included studies examined our primary outcomes as trials were relatively short term and participants were relatively healthy. We were also unable to examine the effects of baseline CVD risk or the intensity of interventions due to the limited number of included studies.

The effectiveness of the provision of fruit and vegetables could not be rigorously assessed since only two trials (229 participants) assessed cardiovascular risk factors at six months.The remaining four were shorter term so it is unclear whether any effects of the intervention could be sustained. In most cases, these trials examined one type of fruit or vegetable so generalisability is limited.

Similarly, few trials were identified examining the effectiveness of dietary advice to increase fruit and vegetable consumption. Three trials were found with six months or more follow‐up with 924 participants randomised.

For both trials of provision of fruit and vegetables and dietary advice to increase consumption of fruit and vegetables there was considerable variability in the interventions, the participants recruited and the outcomes measured. For dietary advice trials, there may have also been differences in the serving sizes recommended within interventions, however, the definition of portion size was not provided in these trials and so it is not possible to tell.

Quality of the evidence

Overall, the studies included in this review were at some risk of bias and results should be treated with some caution. In seven of the 10 included studies the methods of random sequence generation were not stated, while in nine of the included trials details of allocation concealment were not given. Eight of the 10 included studies did not state if the participants and personnel were blinded and five studies did not report the blinding of outcome assessment. Blinding of participants and personnel is difficult if not impossible for behavioural interventions, but outcome assessment can be blinded. Risk of bias due to incomplete outcome data was found to be low in four studies and unclear in six studies, and bias due to selective reporting was regarded as high in two studies, low in three and unclear in the remainder. In all studies there was insufficient information to judge the risk of other biases.

Potential biases in the review process

We conducted a comprehensive search across major databases for interventions to increase fruit and vegetable consumption. We also screened systematic review reference lists and contacted trial authors where necessary. However, from corresponding with authors we did not receive further unreported data from two trials which limited our analyses. Screening, inclusion and exclusion and data abstraction were conducted in duplicate by two review authors independently. Data entry and analyses were carried out by two review authors .

Our decision to restrict this review to interventions only investigating fruit and vegetables avoided the potential confounding effects of other behavioural interventions on our outcomes e.g. those involving other dietary interventions, exercise or weight loss, but limited the number of studies eligible for inclusion. By restricting our inclusion criteria in this way, we excluded some large trials, notably the Womens Health Initiative (WHI) trial, which examined also the effects of reducing dietary fat and increasing grain consumption, as well as increasing fruit and vegetable intake (WHI). The WHI trial randomised over 8000 postmenopausal women, follow‐up is reported over eight years and showed no effect of dietary modification including fruit and vegetable intake on cardiovascular disease clinical endpoints. One could argue that assuming reducing dietary fat and increasing grain consumption is not actively harmful, then this trial demonstrates no effect of fruit and vegetable intake on CVD events, at least in this population of well nourished, middle‐aged women.

Furthermore, limitations in reporting methodological quality, an unclear risk of bias in most trials and sparse or no data for primary and secondary outcomes mean that the findings of this review should be treated with caution due to the small number of trials on which they are based.

Agreements and disagreements with other studies or reviews

To our knowledge, no other systematic review involving only randomised controlled trials has been conducted solely to examine the effects of increasing fruit and vegetable consumption in adults for the primary prevention of CVD. Other systematic reviews have looked at dietary advice for the primary prevention of CVD that includes increasing fruit and vegetable consumption, but also other dietary modifications (Brunner 2007). Dietary advice was found to be effective at increasing fruit and vegetable consumption in the review by Brunner et al, but we cannot directly compare the effects on CVD risk factors between the two reviews as changes may be due to other dietary modifications such as decreasing fat, salt or increasing dietary fibre. All of the trials of dietary advice to increase consumption of fruit and vegetables are included in both reviews. CVD risk factors were not measured in the review by Pomerleau et al so again we are unable to compare our findings (Pomerleau 2005). These authors showed that interventions designed to increase fruit and vegetable consumption increased fruit and vegetable intake by ~0.1 to 1.4 servings per day. Provision of fruit and vegetables is more difficult to compare with other studies as most of the studies we found focus on one particular fruit or vegetable, thereby limiting the findings. Other systematic reviews have looked at increasing fruit and vegetable consumption in children (Wolfenden 2012). The findings showed that there were few effective interventions aimed at improving fruit and vegetable consumption in children aged five years and under. Other systematic reviews are ongoing in different populations (Ganann 2010).

The current systematic review found few trials on interventions focused solely on increasing the consumption of fruit and vegetables in the absence of other dietary modifications, which limits the findings. In the four trials we found on dietary advice to increase fruit and vegetable consumption, favourable effects were seen on blood pressure and to a lesser extent lipid levels.

Study flow diagram.

Figures and Tables -
Figure 1

Study flow diagram.

'Risk of bias' summary: review authors' judgements about each risk of bias item for each included study.

Figures and Tables -
Figure 2

'Risk of bias' summary: review authors' judgements about each risk of bias item for each included study.

'Risk of bias' graph: review authors' judgements about each risk of bias item presented as percentages across all included studies.

Figures and Tables -
Figure 3

'Risk of bias' graph: review authors' judgements about each risk of bias item presented as percentages across all included studies.

Comparison 1: Advice to eat fruit and vegetables, Outcome 1: Systolic blood pressure, change from baseline (mmHg)

Figures and Tables -
Analysis 1.1

Comparison 1: Advice to eat fruit and vegetables, Outcome 1: Systolic blood pressure, change from baseline (mmHg)

Comparison 1: Advice to eat fruit and vegetables, Outcome 2: Diastolic blood pressure, change from baseline (mmHg)

Figures and Tables -
Analysis 1.2

Comparison 1: Advice to eat fruit and vegetables, Outcome 2: Diastolic blood pressure, change from baseline (mmHg)

Comparison 1: Advice to eat fruit and vegetables, Outcome 3: Total cholesterol, change from baseline (mmol/l)

Figures and Tables -
Analysis 1.3

Comparison 1: Advice to eat fruit and vegetables, Outcome 3: Total cholesterol, change from baseline (mmol/l)

Comparison 1: Advice to eat fruit and vegetables, Outcome 4: LDL cholesterol, change from baseline (mmol/l)

Figures and Tables -
Analysis 1.4

Comparison 1: Advice to eat fruit and vegetables, Outcome 4: LDL cholesterol, change from baseline (mmol/l)

Comparison 1: Advice to eat fruit and vegetables, Outcome 5: HDL cholesterol, change from baseline (mmol/l)

Figures and Tables -
Analysis 1.5

Comparison 1: Advice to eat fruit and vegetables, Outcome 5: HDL cholesterol, change from baseline (mmol/l)

Comparison 1: Advice to eat fruit and vegetables, Outcome 6: Triglycerides, change from baseline (mmol/l)

Figures and Tables -
Analysis 1.6

Comparison 1: Advice to eat fruit and vegetables, Outcome 6: Triglycerides, change from baseline (mmol/l)

Comparison 2: Provision of fruit and vegetables, Outcome 1: Systolic blood pressure, change from baseline (mmHg)

Figures and Tables -
Analysis 2.1

Comparison 2: Provision of fruit and vegetables, Outcome 1: Systolic blood pressure, change from baseline (mmHg)

Comparison 2: Provision of fruit and vegetables, Outcome 2: Diastolic blood pressure, change from baseline (mmHg)

Figures and Tables -
Analysis 2.2

Comparison 2: Provision of fruit and vegetables, Outcome 2: Diastolic blood pressure, change from baseline (mmHg)

Comparison 2: Provision of fruit and vegetables, Outcome 3: Total cholesterol, change from baseline (mmol/l)

Figures and Tables -
Analysis 2.3

Comparison 2: Provision of fruit and vegetables, Outcome 3: Total cholesterol, change from baseline (mmol/l)

Comparison 2: Provision of fruit and vegetables, Outcome 4: LDL cholesterol, change from baseline (mmol/l)

Figures and Tables -
Analysis 2.4

Comparison 2: Provision of fruit and vegetables, Outcome 4: LDL cholesterol, change from baseline (mmol/l)

Comparison 2: Provision of fruit and vegetables, Outcome 5: HDL cholesterol, change from baseline (mmol/l)

Figures and Tables -
Analysis 2.5

Comparison 2: Provision of fruit and vegetables, Outcome 5: HDL cholesterol, change from baseline (mmol/l)

Comparison 2: Provision of fruit and vegetables, Outcome 6: Trigylcerides, change from baseline (mmol/l)

Figures and Tables -
Analysis 2.6

Comparison 2: Provision of fruit and vegetables, Outcome 6: Trigylcerides, change from baseline (mmol/l)

Comparison 1. Advice to eat fruit and vegetables

Outcome or subgroup title

No. of studies

No. of participants

Statistical method

Effect size

1.1 Systolic blood pressure, change from baseline (mmHg) Show forest plot

2

891

Mean Difference (IV, Fixed, 95% CI)

‐3.00 [‐4.92, ‐1.09]

1.2 Diastolic blood pressure, change from baseline (mmHg) Show forest plot

2

891

Mean Difference (IV, Fixed, 95% CI)

‐0.90 [‐2.03, 0.24]

1.3 Total cholesterol, change from baseline (mmol/l) Show forest plot

4

970

Mean Difference (IV, Fixed, 95% CI)

‐0.01 [‐0.11, 0.09]

1.4 LDL cholesterol, change from baseline (mmol/l) Show forest plot

2

251

Mean Difference (IV, Fixed, 95% CI)

‐0.17 [‐0.38, 0.03]

1.5 HDL cholesterol, change from baseline (mmol/l) Show forest plot

2

251

Mean Difference (IV, Fixed, 95% CI)

‐0.01 [‐0.10, 0.08]

1.6 Triglycerides, change from baseline (mmol/l) Show forest plot

3

280

Mean Difference (IV, Fixed, 95% CI)

0.10 [‐0.06, 0.27]

Figures and Tables -
Comparison 1. Advice to eat fruit and vegetables
Comparison 2. Provision of fruit and vegetables

Outcome or subgroup title

No. of studies

No. of participants

Statistical method

Effect size

2.1 Systolic blood pressure, change from baseline (mmHg) Show forest plot

1

157

Mean Difference (IV, Fixed, 95% CI)

1.00 [0.45, 1.55]

2.2 Diastolic blood pressure, change from baseline (mmHg) Show forest plot

1

157

Mean Difference (IV, Fixed, 95% CI)

1.50 [1.18, 1.82]

2.3 Total cholesterol, change from baseline (mmol/l) Show forest plot

2

187

Mean Difference (IV, Random, 95% CI)

‐0.10 [‐0.24, 0.04]

2.4 LDL cholesterol, change from baseline (mmol/l) Show forest plot

3

Mean Difference (IV, Fixed, 95% CI)

Totals not selected

2.5 HDL cholesterol, change from baseline (mmol/l) Show forest plot

3

Mean Difference (IV, Fixed, 95% CI)

Totals not selected

2.6 Trigylcerides, change from baseline (mmol/l) Show forest plot

3

284

Mean Difference (IV, Fixed, 95% CI)

‐0.01 [‐0.03, 0.01]

Figures and Tables -
Comparison 2. Provision of fruit and vegetables