The role of diet and physical activity in breast, colorectal, and prostate cancer survivorship: a review of the literature
Identifieur interne : 002C74 ( Pmc/Checkpoint ); précédent : 002C73; suivant : 002C75The role of diet and physical activity in breast, colorectal, and prostate cancer survivorship: a review of the literature
Auteurs : N J Davies [Royaume-Uni] ; L. Batehup [Royaume-Uni] ; R. Thomas [Royaume-Uni]Source :
- British Journal of Cancer [ 0007-0920 ] ; 2011.
Abstract
Evidence for the role of diet and physical activity in cancer incidence is well documented, but owing to increased cancer survivorship, an understanding of these lifestyle factors after a cancer diagnosis is of crucial importance. The purpose of this review was to update the literature in a review undertaken for the National Cancer Survivorship Initiative and to include observational studies that were not included in the WCRF survivorship systematic review.
Evidence was initially gathered from pre-defined searches of the Cochrane Library Database and PubMed from March 2006 to February 2010. After a comprehensive review regarding lifestyle and cancer, for the purpose of this article, any studies not related to diet and physical activity, prognostic outcomes, and breast, colorectal or prostate cancers were excluded. Another search of 2011 literature was conducted to update the evidence.
A total of 43 records were included in this review. Evidence from observational studies suggests that a low-fat, high-fibre diet might be protective against cancer recurrence and progression. However, there is a paucity of RCTs substantiating this. There is more support for physical activity, with a dose response for better outcomes. When synthesized with findings from the World Cancer Research Fund review of RCTs investigating the effect of diet and physical activity interventions on cancer survival, evidence suggests that the mechanism of benefit from diet and physical activity pertains to body weight, with excess body weight being a risk factor, which is modifiable through lifestyle.
Cancer survivors would like to have a more active role in their health care and to know how to look after themselves after diagnosis, including what diet and lifestyle changes they should make. The challenge is in integrating lifestyle support into standardised models of aftercare.
Url:
DOI: 10.1038/bjc.2011.423
PubMed: 22048034
PubMed Central: 3251953
Affiliations:
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PMC:3251953Le document en format XML
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<front><div type="abstract" xml:lang="en"><sec><title>Background:</title>
<p>Evidence for the role of diet and physical activity in cancer incidence is well documented, but owing to increased cancer survivorship, an understanding of these lifestyle factors after a cancer diagnosis is of crucial importance. The purpose of this review was to update the literature in a review undertaken for the National Cancer Survivorship Initiative and to include observational studies that were not included in the WCRF survivorship systematic review.</p>
</sec>
<sec><title>Methods:</title>
<p>Evidence was initially gathered from pre-defined searches of the Cochrane Library Database and PubMed from March 2006 to February 2010. After a comprehensive review regarding lifestyle and cancer, for the purpose of this article, any studies not related to diet and physical activity, prognostic outcomes, and breast, colorectal or prostate cancers were excluded. Another search of 2011 literature was conducted to update the evidence.</p>
</sec>
<sec><title>Results:</title>
<p>A total of 43 records were included in this review. Evidence from observational studies suggests that a low-fat, high-fibre diet might be protective against cancer recurrence and progression. However, there is a paucity of RCTs substantiating this. There is more support for physical activity, with a dose response for better outcomes. When synthesized with findings from the World Cancer Research Fund review of RCTs investigating the effect of diet and physical activity interventions on cancer survival, evidence suggests that the mechanism of benefit from diet and physical activity pertains to body weight, with excess body weight being a risk factor, which is modifiable through lifestyle.</p>
</sec>
<sec><title>Implications:</title>
<p>Cancer survivors would like to have a more active role in their health care and to know how to look after themselves after diagnosis, including what diet and lifestyle changes they should make. The challenge is in integrating lifestyle support into standardised models of aftercare.</p>
</sec>
</div>
</front>
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</TEI>
<pmc article-type="research-article"><pmc-dir>properties open_access</pmc-dir>
<front><journal-meta><journal-id journal-id-type="nlm-ta">Br J Cancer</journal-id>
<journal-id journal-id-type="iso-abbrev">Br. J. Cancer</journal-id>
<journal-title-group><journal-title>British Journal of Cancer</journal-title>
</journal-title-group>
<issn pub-type="ppub">0007-0920</issn>
<issn pub-type="epub">1532-1827</issn>
<publisher><publisher-name>Nature Publishing Group</publisher-name>
</publisher>
</journal-meta>
<article-meta><article-id pub-id-type="pmid">22048034</article-id>
<article-id pub-id-type="pmc">3251953</article-id>
<article-id pub-id-type="pii">bjc2011423</article-id>
<article-id pub-id-type="doi">10.1038/bjc.2011.423</article-id>
<article-categories><subj-group subj-group-type="heading"><subject>Full Paper</subject>
</subj-group>
</article-categories>
<title-group><article-title>The role of diet and physical activity in breast, colorectal, and prostate cancer survivorship: a review of the literature</article-title>
<alt-title alt-title-type="running">Role of diet and physical activity in cancer survivorship</alt-title>
</title-group>
<contrib-group><contrib contrib-type="author"><name><surname>Davies</surname>
<given-names>N J</given-names>
</name>
<xref ref-type="aff" rid="aff1">1</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Batehup</surname>
<given-names>L</given-names>
</name>
<xref ref-type="aff" rid="aff1">1</xref>
<xref ref-type="corresp" rid="caf1">*</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Thomas</surname>
<given-names>R</given-names>
</name>
<xref ref-type="aff" rid="aff2">2</xref>
</contrib>
<aff id="aff1"><label>1</label>
<institution>Self-Management Support Programme, National Cancer Survivorship Initiative, Macmillan Cancer Support</institution>
, 89 Albert Embankment, London SE1 7UQ,<country>UK</country>
</aff>
<aff id="aff2"><label>2</label>
<institution>Bedford Hospital and Addenbrooke's Hospital Cambridge University NHS Trusts, c/o The Primrose Unit, Bedford Hospital</institution>
, Bedford MK42 9DJ,<country>UK</country>
</aff>
</contrib-group>
<author-notes><corresp id="caf1"><label>*</label>
E-mail: <email>LBatehup@macmillan.org.uk</email>
</corresp>
</author-notes>
<pub-date pub-type="ppub"><day>08</day>
<month>11</month>
<year>2011</year>
</pub-date>
<pub-date pub-type="epub"><day>03</day>
<month>11</month>
<year>2011</year>
</pub-date>
<pub-date pub-type="pmc-release"><day>8</day>
<month>11</month>
<year>2011</year>
</pub-date>
<volume>105</volume>
<issue>Suppl 1</issue>
<fpage>S52</fpage>
<lpage>S73</lpage>
<permissions><copyright-statement>Copyright © 2011 Cancer Research UK</copyright-statement>
<copyright-year>2011</copyright-year>
<copyright-holder>Cancer Research UK</copyright-holder>
<license license-type="open-access" xlink:href="http://creativecommons.org/licenses/by-nc-sa/3.0/"><pmc-comment>author-paid</pmc-comment>
<license-p>This work is licensed under the Creative Commons Attribution-NonCommercial-Share Alike 3.0 Unported License. To view a copy of this license, visit http://creativecommons.org/licenses/by-nc-sa/3.0/</license-p>
</license>
</permissions>
<abstract><sec><title>Background:</title>
<p>Evidence for the role of diet and physical activity in cancer incidence is well documented, but owing to increased cancer survivorship, an understanding of these lifestyle factors after a cancer diagnosis is of crucial importance. The purpose of this review was to update the literature in a review undertaken for the National Cancer Survivorship Initiative and to include observational studies that were not included in the WCRF survivorship systematic review.</p>
</sec>
<sec><title>Methods:</title>
<p>Evidence was initially gathered from pre-defined searches of the Cochrane Library Database and PubMed from March 2006 to February 2010. After a comprehensive review regarding lifestyle and cancer, for the purpose of this article, any studies not related to diet and physical activity, prognostic outcomes, and breast, colorectal or prostate cancers were excluded. Another search of 2011 literature was conducted to update the evidence.</p>
</sec>
<sec><title>Results:</title>
<p>A total of 43 records were included in this review. Evidence from observational studies suggests that a low-fat, high-fibre diet might be protective against cancer recurrence and progression. However, there is a paucity of RCTs substantiating this. There is more support for physical activity, with a dose response for better outcomes. When synthesized with findings from the World Cancer Research Fund review of RCTs investigating the effect of diet and physical activity interventions on cancer survival, evidence suggests that the mechanism of benefit from diet and physical activity pertains to body weight, with excess body weight being a risk factor, which is modifiable through lifestyle.</p>
</sec>
<sec><title>Implications:</title>
<p>Cancer survivors would like to have a more active role in their health care and to know how to look after themselves after diagnosis, including what diet and lifestyle changes they should make. The challenge is in integrating lifestyle support into standardised models of aftercare.</p>
</sec>
</abstract>
<kwd-group><kwd>diet</kwd>
<kwd>lifestyle</kwd>
<kwd>physical activity</kwd>
<kwd>weight</kwd>
</kwd-group>
</article-meta>
</front>
<floats-group><fig id="fig1"><label>Figure 1</label>
<caption><p>Flow of information.</p>
</caption>
<graphic xlink:href="bjc2011423f1"></graphic>
</fig>
<table-wrap id="tbl1"><label>Table 1</label>
<caption><title>Guidelines: Food, Nutrition, Physical Activity, and the Prevention of Cancer: A Global Perspective, World Cancer Research Fund/American Institute for Cancer Research</title>
</caption>
<table frame="hsides" rules="groups" border="1"><colgroup><col align="left"></col>
<col align="left"></col>
<col align="left"></col>
<col align="left"></col>
</colgroup>
<thead valign="bottom"><tr><th align="left" valign="top" charoff="50"><bold>World Cancer Research Fund/American Institute for Cancer Research (2007)</bold>
</th>
<th align="left" valign="top" charoff="50"><bold>British Association of Sport and Exercise Sciences (2011)</bold>
</th>
<th align="left" valign="top" charoff="50"><bold>Department of Health, Physical Activity, Health Improvement, and Protection (UK) (2011)</bold>
</th>
<th align="left" valign="top" charoff="50"><bold>American College of Sports Medicine Roundtable on Exercise Guidelines for Cancer Survivors (2010)</bold>
</th>
</tr>
</thead>
<tbody valign="top"><tr><td align="left" valign="top" charoff="50"><italic>Body fatness</italic>
:
Be as lean as possible within the normal range of body weight
• Ensure that body weight through childhood and adolescent growth projects towards the lower end of the normal BMI range at age 21 years
• Maintain body weight within the normal range from age 21 years
• Avoid weight gain and increase in waist circumference throughout adulthood.
<italic>Physical activity</italic>
:
Be physically active as part of everyday life.
• Be moderately physically active, equivalent to brisk walking for at least 30 min a day.
• As fitness improves, aim for ⩾60 min of moderate or ⩾30 min of vigorous physical activity every day.
• Limit sedentary habits such as watching television.
Limit consumption of energy-dense foods. Avoid sugary drinks
• Consume energy-dense foods sparingly
• Avoid sugary drinks
• Consume ‘fast foods' sparingly if at all.
<italic>Eat mostly foods of plant origin</italic>
:
• Eat at least 5 portions (at least 400 g or 140 z) of various non-starchy vegetables and fruit a day
• Eat relatively unprocessed cereals(grains) and/or pulses(legumes) with every meal
• Limit refined starchy foods
<italic>Limit intake of red meat and avoid processed meat:</italic>
• People who eat red meat to consume <500 g (180 z) a week, very little if any to be processed.
<italic>Limit consumption of salt. Avoid mouldy cereals (grains) or pulses (legumes)</italic>
:
• Avoid salt-preserved, salted or salty foods; preserve foods without using salt.
• Limit consumption of processed foods with added salt to ensure an intake of <6 g (2.4 g sodium) a day.
• Do not eat mouldy cereals or pulses</td>
<td align="left" valign="top" charoff="50">Follow health-related physical activity guidelines provided for the general UK population
Avoid being sedentary</td>
<td align="left" valign="top" charoff="50"><italic>Adults – 19–64 years</italic>
• Aim to be active daily
• Over a week, activity should add up to 150 min (2.5 h) of moderate-intensity activity in bouts of ⩾10 min – one way to approach this is to do 30 min on at least 5 days a week
• Alternately, comparable benefits can be achieved through 75 min of vigorous-intensity activity spread across the week or a combination of moderate- and vigorous-intensity activity
• Undertake physical activity to improve muscle strength on at least 2 days a week
• Minimise the amount of time spent being sedentary (sitting) for extended periods.
<italic>Older adults</italic>
– <italic>65</italic>
+ <italic>years</italic>
• Older adults who participate in any amount of physical activity gain some health benefits, including maintenance of good physical and cognitive function. Some physical activity is better than none, and more physical activity provides greater health benefits
• Be active daily. Over a week, activity should add up to 150 min (2.5 h) of moderate-intensity activity in bouts of ⩾10 min – one way to approach this is to do 30 min on at least 5 days a week
• For those who are already regularly active at moderate intensity, comparable benefit can be achieved through 75 min of vigorous-intensity activity spread across the week or a combination of moderate and vigorous activity
• Undertake physical activity to improve muscle strength on at least 2 days a week
• Older adults at risk of falls should incorporate physical activity to improve balance on at least 2 days a week
• Minimise the amount of time spent being sedentary (sitting) for extended periods</td>
<td align="left" valign="top" charoff="50">• US DHHS (2008) guidelines on aerobic activity, strength training and flexibility are generally appropriate for cancer survivors
• Improve body composition through fat loss for survivors who are obese or overweight
• Avoid inactivity and return to normal daily activities as soon as possible after surgery and during adjuvant cancer treatments
• The age-appropriate guidelines for aerobic activity are appropriate for cancer survivors; to note a few cancer site-specific elevated risk of skeletal fractures and infection among specific survivors who receive particular treatments</td>
</tr>
</tbody>
</table>
<table-wrap-foot><fn id="t1-fn1"><p>Abbreviation: BMI=body mass index.</p>
</fn>
<fn id="t1-fn2"><p>Recommendations for the Prevention of Cancer, 2007; British Association of Sport and Exercise Sciences, The BASES Statement on Exercise and Cancer Survivorship, first published in Sport and Exercise Sciences, 28, Summer 2011. Start Active, Stay Active. A report on physical activity for health from the four home countries' Chief Medical Officers; American College of Sports medicine Roundtable on Exercise Guidelines for Cancer Survivors, 2010.</p>
</fn>
</table-wrap-foot>
</table-wrap>
<table-wrap id="tbl2"><label>Table 2</label>
<caption><title>WINS and WHELs evidence</title>
</caption>
<table frame="hsides" rules="groups" border="1"><colgroup><col align="left"></col>
<col align="left"></col>
<col align="left"></col>
<col align="left"></col>
<col align="left"></col>
<col align="left"></col>
</colgroup>
<thead valign="bottom"><tr><th align="left" valign="top" charoff="50"><bold>Author</bold>
</th>
<th align="left" valign="top" charoff="50"><bold>Study design/intervention</bold>
</th>
<th align="left" valign="top" charoff="50"><bold>Sample/inclusion</bold>
</th>
<th align="left" valign="top" charoff="50"><bold>Follow-up period</bold>
</th>
<th align="left" valign="top" charoff="50"><bold>Primary outcome</bold>
</th>
<th align="left" valign="top" charoff="50"><bold>Results</bold>
</th>
</tr>
</thead>
<tbody valign="top"><tr><td colspan="6" align="left" valign="top" charoff="50"><italic>WINS</italic>
</td>
</tr>
<tr><td align="left" valign="top" charoff="50"><xref ref-type="bibr" rid="bib17">Chlebowski <italic>et al</italic>
(2006)</xref>
</td>
<td align="left" valign="top" charoff="50">Interim analysis of a randomised, prospective, multicentre clinical trial (WINS) to test the effect of a dietary intervention designed to reduce fat intake. Randomisation was to:
(1) <italic>Dietary intervention</italic>
: reduce percentage of calories from fat to 15%. The low-fat eating plan was initiated during 8 biweekly individual, in-person counselling sessions, each lasting 1λh. Dietician 3 monthly, with optional monthly dietary group sessions.
(2) <italic>Control group</italic>
: one baseline dietician visit and contacts every 3 months thereafter. Written information provided on general dietary guidelines and counselling on nutritional adequacy for vitamin and mineral intake only</td>
<td align="left" valign="top" charoff="50">Breast cancer patients (<italic>n</italic>
=2437)</td>
<td align="left" valign="top" charoff="50">Mean=60 months (5 years)</td>
<td align="left" valign="top" charoff="50">Relapse-free survival;
overall survival</td>
<td align="left" valign="top" charoff="50">A total of 277 relapse events have been reported in 96 of 975 (9.8%) women in the dietary group and 181 of 1462 (12.4%) women in the control group. The HR of relapse events in the intervention group compared with the control group was 0.76 (95% CI=0.60–0.98, <italic>P</italic>
=0.077 for stratified log rank and <italic>P</italic>
=0.034 for adjusted Cox model analysis)</td>
</tr>
<tr><td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
</tr>
<tr><td align="left" valign="top" charoff="50"><xref ref-type="bibr" rid="bib16">Chlebowski <italic>et al</italic>
(2008)</xref>
</td>
<td align="left" valign="top" charoff="50">A protocol-mandated survival analysis update to the interim analysis of WINS</td>
<td align="left" valign="top" charoff="50">Breast cancer patients (<italic>n</italic>
=2437)</td>
<td align="left" valign="top" charoff="50">7 years</td>
<td align="left" valign="top" charoff="50">Overall survival</td>
<td align="left" valign="top" charoff="50">Although fewer deaths were seen in the intervention group, this was not statistically significant. In 362 women with ER and (progesterone receptor) PR disease, a significant overall survival benefit was seen in the intervention group (7.5 <italic>vs</italic>
18.1%, cumulative mortality)</td>
</tr>
<tr><td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
</tr>
<tr><td align="left" valign="top" charoff="50"><xref ref-type="bibr" rid="bib25">Dwyer <italic>et al</italic>
(2008)</xref>
</td>
<td align="left" valign="top" charoff="50">A subanalysis of participants in the WINS trial to determine whether differences existed in dietary intakes of flavonoids among WINS women who had been randomised to the very-low-fat diet after they modified their eating habits to achieve their goals. Comparisons were made between the intervention and control groups on intakes of total flavonoids and six flavonoid classes (isoflavones, flavones, flavanones, flavonols, flavan-3-ols and anthocyanins) using the US Department of Agriculture food flavonoid database and a flavonoid dietary supplement database on three 24-h dietary recalls at baseline and 12 months after randomisation</td>
<td align="left" valign="top" charoff="50">Randomly selected breast cancer patients (<italic>n</italic>
=550; 218 from the dietary intervention and 332 from the control group)</td>
<td align="left" valign="top" charoff="50">12 months of intervention</td>
<td align="left" valign="top" charoff="50">Disease-free survival</td>
<td align="left" valign="top" charoff="50">After 12 months of intervention, with 39 participants lost to follow-up, flavonoid intakes remained similar in both groups (201±252 s.d. mg per day, <italic>n</italic>
=316 in the usual diet group <italic>vs</italic>
235±425 s.d. mg per day, <italic>n</italic>
=195 in the very-low-fat group; <italic>P</italic>
=NS). In this random sample of WINS participants, neither total flavonoid intakes nor intakes of subclasses of flavonoids differed between those who had dramatically decreased their fat intakes and those who had not. Flavonoid intakes are therefore unlikely to account for WINS results</td>
</tr>
<tr><td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
</tr>
<tr><td align="left" valign="top" charoff="50"><xref ref-type="bibr" rid="bib52">Khaodhiar <italic>et al</italic>
(2003)</xref>
</td>
<td align="left" valign="top" charoff="50">Subgroup analysis of WINS participants (<xref ref-type="bibr" rid="bib17">Chlebowski <italic>et al</italic>
, 2006</xref>
), examining relationships between dietary intake and insulin resistance</td>
<td align="left" valign="top" charoff="50">53 women from 3 clinical sites</td>
<td align="left" valign="top" charoff="50">2 years after commencing intervention</td>
<td align="left" valign="top" charoff="50">Insulin resistance</td>
<td align="left" valign="top" charoff="50">Of those women with initial insulin resistance, after 1 year, women in the intervention group saw their fasting insulin decrease by 18±34 <italic>μ</italic>
U ml<sup>−1</sup>
; in comparison, fasting insulin of women in the control group decreased by only 13.8±47 <italic>μ</italic>
U ml<sup>−1</sup>
. Although not quite statistically significant, these results predict that elevated insulin concentrations may be influenced by dietary fat reduction</td>
</tr>
<tr><td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
</tr>
<tr><td colspan="6" align="left" valign="top" charoff="50"><italic>WHEL</italic>
</td>
</tr>
<tr><td align="left" valign="top" charoff="50"><xref ref-type="bibr" rid="bib76">Pierce <italic>et al</italic>
(2007)</xref>
</td>
<td align="left" valign="top" charoff="50">The multicentre WHEL RCT. Participants randomised to:
(1) <italic>An intensive telephone counselling intervention</italic>
: promoting a daily dietary intake of 5 vegetable servings, 16 oz of vegetable juice, 3 fruit servings, 30 g fibre and 15–20% of energy from fat.
(2) <italic>Control group</italic>
: received printed materials (but no counselling) promoting the five-a-day guidelines of daily intakes of 5 servings of fruit and vegetables, >20 g of fibre and <30% of energy from fat</td>
<td align="left" valign="top" charoff="50">Breast cancer (<italic>n</italic>
=3088)</td>
<td align="left" valign="top" charoff="50">After 7 years of intervention</td>
<td align="left" valign="top" charoff="50">Invasive breast cancer incidence or recurrence; death from any cause</td>
<td align="left" valign="top" charoff="50">There were no additional health benefits of dramatically increasing intake of nutrient-rich plant-based foods, relative to the comparison group</td>
</tr>
<tr><td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
</tr>
<tr><td align="left" valign="top" charoff="50"><xref ref-type="bibr" rid="bib87">Thomson <italic>et al</italic>
(2007)</xref>
</td>
<td align="left" valign="top" charoff="50">Subanalysis of a purposive sample of participants in the WHEL RCT (see <xref ref-type="bibr" rid="bib35">Gold <italic>et al</italic>
, 2009</xref>
in this table)</td>
<td align="left" valign="top" charoff="50">Breast cancer patients (<italic>n</italic>
=207)</td>
<td align="left" valign="top" charoff="50">Not reported</td>
<td align="left" valign="top" charoff="50">Oxidative stress</td>
<td align="left" valign="top" charoff="50">Dietary carotenoid levels were not significantly associated with oxidative, stress indicators, although dietary lycopene and lutein/zeaxanthin were modestly associated with 8-OHdG levels (<italic><italic><italic><italic>P</italic>
</italic>
</italic>
</italic>
=0.054 and 0.088, respectively). Key findings include a significant inverse association between total plasma carotenoid concentrations and oxidative stress as measured by urinary 8-OHdG and a moderately significant inverse association with 8-iso-PGF2<italic>α</italic>
, a protective association that was not shown for dietary carotenoid intake</td>
</tr>
<tr><td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
</tr>
<tr><td align="left" valign="top" charoff="50"><xref ref-type="bibr" rid="bib35">Gold <italic>et al</italic>
(2009)</xref>
</td>
<td align="left" valign="top" charoff="50">Secondary analysis of a purposive sample of WHEL participants, to determine whether a low-fat diet high in vegetables, fruit and fibre affects prognosis in breast cancer survivors with or without HFs after treatment</td>
<td align="left" valign="top" charoff="50">2967 women whose baseline HF severity report in the previous 4 weeks was available</td>
<td align="left" valign="top" charoff="50">7.3 years into the intervention</td>
<td align="left" valign="top" charoff="50">Additional breast cancer events and death from any cause</td>
<td align="left" valign="top" charoff="50">HF-negative women in the intervention had a 31% lower event rate than did HF-negative women in the comparison group over 7.3 years of follow-up; among HF-negative post-menopausal women, the intervention effect was even stronger, with a 47% reduction in risk compared with HF-negative women assigned to the comparison group. Compared with HF-negative women in the comparison group, women with baseline HFs had a lower risk of additional breast cancer events, regardless of whether they were randomly assigned to the dietary intervention group or to the comparison group</td>
</tr>
<tr><td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
</tr>
<tr><td align="left" valign="top" charoff="50"><xref ref-type="bibr" rid="bib11">Caan <italic>et al</italic>
(2011)</xref>
</td>
<td align="left" valign="top" charoff="50">Examination of data from the WHEL study, to explore the effect of soy intake on breast cancer prognosis. Isoflavone intakes were measured after diagnosis by using a food-frequency questionnaire. Women self-reported new outcome events semi-annually, which were then verified by medical records and/or death certificates</td>
<td align="left" valign="top" charoff="50">3088 breast cancer survivors, diagnosed between 1991 and 2000 with early-stage breast cancer</td>
<td align="left" valign="top" charoff="50">Median of 7.3 years</td>
<td align="left" valign="top" charoff="50">Breast cancer-related mortality</td>
<td align="left" valign="top" charoff="50">As isoflavone intake increased, risk of death decreased (<italic><italic><italic><italic>P</italic>
</italic>
</italic>
</italic>
for trend=0.02). Women at the highest levels of isoflavone intake (>16.3 mg isoflavones) had a non-significant 54% reduction in risk of death</td>
</tr>
</tbody>
</table>
<table-wrap-foot><fn id="t2-fn1"><p>Abbreviations: CI=confidence interval; ER=oestrogen receptor; HF=hot flush; HR=hazard ratio; NS=non-significant; RCT=randomised controlled study; WHEL=Women's Healthy Eating and Living; WINS=Women's Intervention Nutrition Study.</p>
</fn>
</table-wrap-foot>
</table-wrap>
<table-wrap id="tbl3"><label>Table 3</label>
<caption><title>Diet evidence</title>
</caption>
<table frame="hsides" rules="groups" border="1"><colgroup><col align="left"></col>
<col align="left"></col>
<col align="left"></col>
<col align="left"></col>
<col align="left"></col>
<col align="left"></col>
</colgroup>
<thead valign="bottom"><tr><th align="left" valign="top" charoff="50"><bold>Author</bold>
</th>
<th align="left" valign="top" charoff="50"><bold>Study design/intervention</bold>
</th>
<th align="left" valign="top" charoff="50"><bold>Sample/inclusion</bold>
</th>
<th align="left" valign="top" charoff="50"><bold>Follow-up period</bold>
</th>
<th align="left" valign="top" charoff="50"><bold>Primary outcome</bold>
</th>
<th align="left" valign="top" charoff="50"><bold>Results</bold>
</th>
</tr>
</thead>
<tbody valign="top"><tr><td colspan="6" align="left" valign="top" charoff="50"><italic>DIET</italic>
</td>
</tr>
<tr><td align="left" valign="top" charoff="50">Breast</td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
</tr>
<tr><td align="left" valign="top" charoff="50"><xref ref-type="bibr" rid="bib6">Belle <italic>et al</italic>
(2011)</xref>
</td>
<td align="left" valign="top" charoff="50">Health, Eating, Activity, and Lifestyle (HEAL) study: Investigation into the associations of dietary fibre, carbohydrates, glycaemic index (GI) and glycaemic load (GL) with breast cancer prognosis. Usual diet was assessed with a food-frequency questionnaire. Cox proportional hazards regression estimated multivariate-adjusted hazard ratios and 95% confidence intervals (95% CI)</td>
<td align="left" valign="top" charoff="50"><italic>n</italic>
=688 stage 0 to IIIA breast cancer survivors</td>
<td align="left" valign="top" charoff="50">Median of 6.7 years after diagnosis</td>
<td align="left" valign="top" charoff="50">Total mortality, breast cancer mortality, non-fatal recurrence and second-occurrence data were obtained from SEER (Surveillance, Epidemiology, and End Results) registries and medical records</td>
<td align="left" valign="top" charoff="50">There was an inverse association between fibre intake and mortality. Multivariate-adjusted hazard rate ratios (HRR) comparing high with low intake were 0.53 (95% CI=0.23–1.23) and 0.75 (95% CI=0.43–1.31). A threshold effect was observed whereby no additional benefit was observed for intakes of ⩾9 g per day. Fibre intake was inversely associated with breast cancer-specific mortality (HRR=0.68, 95% CI=0.27–1.70) and risk of non-fatal recurrence or second occurrence (HRR=0.68, 95% CI=0.27–1.70), but results were not statistically significant</td>
</tr>
<tr><td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
</tr>
<tr><td align="left" valign="top" charoff="50"><xref ref-type="bibr" rid="bib10">Boyapati <italic>et al</italic>
(2005)</xref>
</td>
<td align="left" valign="top" charoff="50">The Shanghai Breast Cancer Cohort Study, examining associations between soy and breast cancer survival</td>
<td align="left" valign="top" charoff="50">1459 breast cancer patients</td>
<td align="left" valign="top" charoff="50">5.2 years</td>
<td align="left" valign="top" charoff="50">Disease-free survival</td>
<td align="left" valign="top" charoff="50">Soy intake pre-diagnosis was unrelated to disease-free breast cancer survival (HR=0.99, 95% CI=0.73–1.33 for the highest tertile compared with the lowest tertile)</td>
</tr>
<tr><td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
</tr>
<tr><td align="left" valign="top" charoff="50"><xref ref-type="bibr" rid="bib18">Cho <italic>et al</italic>
(2003)</xref>
</td>
<td align="left" valign="top" charoff="50">A prospective analysis of the relationship between dietary fat intake and breast cancer risk among pre-menopausal women (Nurses' Health Study)</td>
<td align="left" valign="top" charoff="50">Pre-menopausal women (<italic>n</italic>
=90 655) aged between 26 and 46 years when recruited in 1991</td>
<td align="left" valign="top" charoff="50">8 years after recruitment (1991–1999)</td>
<td align="left" valign="top" charoff="50">Fat intake was assessed with a food-frequency questionnaire at baseline in 1991 and again in 1995</td>
<td align="left" valign="top" charoff="50">Relative to women in the lowest quintile of fat intake, women in the highest quintile of intake had a slightly increased risk of breast cancer (RR=1.25, 95% CI=0.98–1.59; <italic>P</italic>
<sub>trend</sub>
=0.06). The increase was associated with intake of animal fat but not vegetable fat; RRs for the increasing quintiles of animal fat intake were 1.00 (referent), 1.28, 1.37, 1.54 and 1.33 (95% CI=1.02–1.73; <italic>P</italic>
<sub>trend</sub>
=0.002)</td>
</tr>
<tr><td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
</tr>
<tr><td align="left" valign="top" charoff="50"><xref ref-type="bibr" rid="bib36">Goodwin <italic>et al</italic>
(2009)</xref>
</td>
<td align="left" valign="top" charoff="50">Prospective cohort study examining the influence of vitamin D on breast cancer prognosis</td>
<td align="left" valign="top" charoff="50">512 women with early breast cancer</td>
<td align="left" valign="top" charoff="50">Mean=11.6 years</td>
<td align="left" valign="top" charoff="50">Cancer recurrence and mortality</td>
<td align="left" valign="top" charoff="50">Women with deficient vitamin D levels had an increased risk of distant recurrence (HR=1.94; 95% CI=1.16–3.25) and death (HR=1.73; 95% CI=1.05–2.86) compared with those with sufficient levels</td>
</tr>
<tr><td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
</tr>
<tr><td align="left" valign="top" charoff="50">Holm <italic>et al</italic>
(1993)</td>
<td align="left" valign="top" charoff="50">Interviews regarding diet history, to determine whether dietary habits are associated with disease-free survival in patients with breast cancer who have undergone treatment</td>
<td align="left" valign="top" charoff="50">240 women with stage I–II breast cancer (50–65 years)</td>
<td align="left" valign="top" charoff="50">4 years</td>
<td align="left" valign="top" charoff="50">Disease-free survival</td>
<td align="left" valign="top" charoff="50">The multiple odds ratio (OR) for treatment failure in women with E-rich tumours was 1.08 for each 1% increment in percentage of total energy (E%) from total fat. For treatment failure within the first 2 years, the OR was 1.19 for each 1-mg increase in vitamin E intake per 10 MJ of energy. No association between dietary habits and treatment failure was found for women with ER-poor cancers</td>
</tr>
<tr><td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
</tr>
<tr><td align="left" valign="top" charoff="50"><xref ref-type="bibr" rid="bib46">Ingram, (1994)</xref>
</td>
<td align="left" valign="top" charoff="50">Cohort study evaluating the role of vitamins in breast cancer mortality</td>
<td align="left" valign="top" charoff="50">103 women 3 months after operation</td>
<td align="left" valign="top" charoff="50">Mean=81 months</td>
<td align="left" valign="top" charoff="50">Mortality from breast cancer</td>
<td align="left" valign="top" charoff="50">At high levels of consumption, there were significantly fewer deaths from breast cancer: only 1 in the group of highest <italic>β</italic>
-carotene consumers compared with 8 in the intermediate group and 12 in the lowest group (trend <italic>P</italic>
=0.0012). Equivalent figures for vitamin C were 3, 7 and 11 deaths for the highest, intermediate and lowest consumption groups, respectively (trend <italic>P</italic>
=0.0286)</td>
</tr>
<tr><td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
</tr>
<tr><td align="left" valign="top" charoff="50"><xref ref-type="bibr" rid="bib60">McEligot <italic>et al</italic>
(2006)</xref>
</td>
<td align="left" valign="top" charoff="50">Retrospective study into the influence of diet on overall survival in women with breast cancer</td>
<td align="left" valign="top" charoff="50">Post-menopausal breast cancer survivors (<italic>n</italic>
=516)</td>
<td align="left" valign="top" charoff="50">Mean=80 months after diagnosis</td>
<td align="left" valign="top" charoff="50">Death due to any cause</td>
<td align="left" valign="top" charoff="50">The HR and 95% CI of death in the highest tertile compared with the lowest tertile of total fat, fibre, vegetable and fruit intake was 3.12 (95% CI=1.79–5.44), 0.48 (95% CI=0.27–0.86), 0.57 (95% CI=0.35–0.94) and 0.63 (95% CI=0.38–1.05), respectively (<italic>P</italic>
⩽0.05 for trend, except for fruit intake). Intakes of other nutrients, including folate, vitamin C and carotenoids, were also significantly associated with reduced mortality (<italic>P</italic>
⩽0.05 for trend)</td>
</tr>
<tr><td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
</tr>
<tr><td align="left" valign="top" charoff="50"><xref ref-type="bibr" rid="bib74">Patterson <italic>et al</italic>
(2010)</xref>
</td>
<td align="left" valign="top" charoff="50">A review of the published epidemiological research on lifestyle and breast cancer outcomes. Research included RCTs, cohort studies or case–control studies of breast cancer outcomes. Included studies had been published in the previous 10 years (1999–2009), as well as a few large studies published >10 years ago.
Papers were included only if there were at least 500 participants. Studies of exposure biomarkers such as serum nutrient concentrations were not included, nor were studies with intermediate markers of breast cancer (e.g., mammographic density) or non-invasive lesions (e.g., ductal carcinoma <italic>in situ</italic>
)</td>
<td align="left" valign="top" charoff="50">Breast cancer</td>
<td align="left" valign="top" charoff="50">Not reported</td>
<td align="left" valign="top" charoff="50">The primary outcomes were additional breast cancer events and mortality. An additional breast cancer event was defined as a recurrence from the original cancer or developing a new invasive breast cancer</td>
<td align="left" valign="top" charoff="50">One study was identified comparing prudent <italic>vs</italic>
Western dietary pattern (<xref ref-type="bibr" rid="bib54">Kwan <italic>et al</italic>
, 2009</xref>
). Overall, there were 12 studies of macronutrients and dietary patterns with mortality as an outcome, 4 of which meet the inclusion criteria of the current review but were not identified by the search strategy (<xref ref-type="bibr" rid="bib8">Borugian <italic>et al</italic>
, 2004</xref>
; <xref ref-type="bibr" rid="bib4">Barnett <italic>et al</italic>
, 2008</xref>
; <xref ref-type="bibr" rid="bib19">Dal Maso <italic>et al</italic>
, 2008</xref>
). For the 3 studies on carbohydrates (<xref ref-type="bibr" rid="bib43">Holmes <italic>et al</italic>
, 1999</xref>
; <xref ref-type="bibr" rid="bib8">Borugian <italic>et al</italic>
, 2004</xref>
; <xref ref-type="bibr" rid="bib60">McEligot <italic>et al</italic>
, 2006</xref>
) findings were mixed, with 1 report of a statistically significant protective effect (<xref ref-type="bibr" rid="bib60">McEligot <italic>et al</italic>
, 2006</xref>
): the weighted average was 0.74. For the 5 studies on dietary fat (<xref ref-type="bibr" rid="bib49">Jain <italic>et al</italic>
, 1994</xref>
; <xref ref-type="bibr" rid="bib90">Zhang <italic>et al</italic>
, 1995</xref>
; <xref ref-type="bibr" rid="bib8">Borugian <italic>et al</italic>
, 2004</xref>
; <xref ref-type="bibr" rid="bib60">McEligot <italic>et al</italic>
, 2006</xref>
; <xref ref-type="bibr" rid="bib19">Dal Maso <italic>et al</italic>
, 2008</xref>
), 4 HRs showed a trend towards increased risk, although only one had a statistically significant finding (<xref ref-type="bibr" rid="bib60">McEligot <italic>et al</italic>
, 2006</xref>
): the weighted HR was 1.53. The 3 studies of dietary fibre showed a trend towards being protective (<xref ref-type="bibr" rid="bib43">Holmes <italic>et al</italic>
, 1999</xref>
; <xref ref-type="bibr" rid="bib8">Borugian <italic>et al</italic>
, 2004</xref>
; <xref ref-type="bibr" rid="bib60">McEligot <italic>et al</italic>
, 2006</xref>
) and 2 were statistically significant (<xref ref-type="bibr" rid="bib43">Holmes <italic>et al</italic>
, 1999</xref>
; <xref ref-type="bibr" rid="bib60">McEligot <italic>et al</italic>
, 2006</xref>
): the weighted average was 0.63. Of the 4 studies that reported on protein (<xref ref-type="bibr" rid="bib43">Holmes <italic>et al</italic>
, 1999</xref>
; <xref ref-type="bibr" rid="bib8">Borugian <italic>et al</italic>
, 2004</xref>
; <xref ref-type="bibr" rid="bib60">McEligot <italic>et al</italic>
, 2006</xref>
; <xref ref-type="bibr" rid="bib19">Dal Maso <italic>et al</italic>
, 2008</xref>
), 2 found a statistically significantly protective association (<xref ref-type="bibr" rid="bib43">Holmes <italic>et al</italic>
, 1999</xref>
; <xref ref-type="bibr" rid="bib8">Borugian <italic>et al</italic>
, 2004</xref>
): the weighted average was 0.72. A prudent dietary pattern (characterised by high intakes of fruit, vegetables, whole grains, legumes, poultry and fish) appeared to be protective (<xref ref-type="bibr" rid="bib53">Kroenke <italic>et al</italic>
, 2005</xref>
; <xref ref-type="bibr" rid="bib54">Kwan <italic>et al</italic>
, 2009</xref>
), with one statistically significant finding (<xref ref-type="bibr" rid="bib54">Kwan <italic>et al</italic>
, 2009</xref>
). Conversely, the Western dietary pattern (characterised by high intakes of refined grains, processed and red meats, desserts, high-fat dairy products and French fries) was associated with a non-significant increase in risk (<xref ref-type="bibr" rid="bib53">Kroenke <italic>et al</italic>
, 2005</xref>
; <xref ref-type="bibr" rid="bib54">Kwan <italic>et al</italic>
, 2009</xref>
)</td>
</tr>
<tr><td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
</tr>
<tr><td align="left" valign="top" charoff="50">Colorectal</td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
</tr>
<tr><td align="left" valign="top" charoff="50"><xref ref-type="bibr" rid="bib64">Meyerhardt <italic>et al</italic>
(2007)</xref>
</td>
<td align="left" valign="top" charoff="50">Prospective observational study to determine the association of dietary patterns with cancer recurrences and mortality of colon cancer survivors</td>
<td align="left" valign="top" charoff="50">1009 patients with stage III colon cancer who were enrolled in an adjuvant chemotherapy RCT between April 1999 and May 2001</td>
<td align="left" valign="top" charoff="50">Median=5.3 years. Patients were followed up for cancer recurrence or death</td>
<td align="left" valign="top" charoff="50">Disease-free survival, recurrence-free survival and overall survival by dietary pattern</td>
<td align="left" valign="top" charoff="50">324 patients had cancer recurrence, 223 patients died with cancer recurrence and 28 died without documented cancer recurrence. Two major dietary patterns, prudent and Western, were identified by factor analysis. The prudent pattern was characterised by high intakes of fruit and vegetables, poultry and fish; the Western pattern was characterised by high intakes of meat, fat, refined grains and dessert. A higher intake of a Western dietary pattern after cancer diagnosis was associated with a significantly worse disease-free survival (colon cancer recurrences or death). Compared with patients in the lowest quintile of Western dietary pattern, those in the highest quintile experienced an adjusted hazard ratio (AHR) for disease-free survival of 3.25 (95% CI=2.04–5.19; <italic><italic><italic><italic>P</italic>
</italic>
</italic>
</italic>
for trend <0.001). The Western dietary pattern was associated with a similar detriment in recurrence-free survival (AHR=2.85; 95% CI=1.75–4.63) and overall survival (AHR=2.32; 95% CI=1.36–3.96), comparing highest with lowest quintiles (both with <italic><italic><italic><italic>P</italic>
</italic>
</italic>
</italic>
for trend <0.001). The reduction in disease-free survival with a Western dietary pattern was not significantly modified by sex, age, nodal stage, body mass index, physical activity level, baseline performance status or treatment group. In contrast, the prudent dietary pattern was not significantly associated with cancer recurrence or mortality</td>
</tr>
<tr><td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
</tr>
<tr><td align="left" valign="top" charoff="50">Prostate</td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
</tr>
<tr><td align="left" valign="top" charoff="50"><xref ref-type="bibr" rid="bib3">Aronson <italic>et al</italic>
(2010)</xref>
</td>
<td align="left" valign="top" charoff="50">An RCT with participants being randomised to a 4-week low-fat diet group or a Western diet group. Feeding study with the low-fat diet defined as <15% of total energy from fat and the Western diet defined as 40% of energy coming from fat</td>
<td align="left" valign="top" charoff="50">18 men diagnosed with prostate cancer within the past 2 years and on active surveillance (mean age=64 years)</td>
<td align="left" valign="top" charoff="50">Immediately after the 4-week intervention</td>
<td align="left" valign="top" charoff="50">Fasting serum was collected at baseline and after the intervention to measure prostate-specific antigen, sex hormones, insulin, insulin-like growth factor I and II, insulin-like growth factor-binding proteins, lipids and fatty acids. LNCaP cells (ATCC(R)) were cultured in medium containing pre-intervention and post-intervention human serum to assess the <italic>in vitro</italic>
effect of the diet on prostate cancer cell proliferation</td>
<td align="left" valign="top" charoff="50">Serum from men in the low-fat group significantly decreased the growth of LNCaP cells relative to Western diet serum (<italic>P</italic>
=0.03). There were no significant between-group changes in serum prostate-specific antigen, sex hormones, insulin, insulin-like growth factor I and II, and insulin-like growth factor-binding proteins. Serum triglyceride and linoleic acid (omega-6) levels were decreased in the low-fat group (<italic>P</italic>
=0.034 and <italic>P</italic>
=0.005, respectively). Correlation analysis revealed that decreased omega-6 and increased omega-3 fatty acid correlated with decreased serum stimulated LNCaP cell growth (<italic>r</italic>
=0.64, <italic>P</italic>
=0.004, and <italic>r</italic>
=−0.49, <italic>P</italic>
=0.04, respectively)</td>
</tr>
<tr><td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
</tr>
<tr><td align="left" valign="top" charoff="50"><xref ref-type="bibr" rid="bib40">Heymach <italic>et al</italic>
(2011)</xref>
</td>
<td align="left" valign="top" charoff="50">Exploration of the effect of diet on angiogenesis and inflammation, which are central to tumour growth and progression. Changes in 50 plasma cytokines and angiogenic factors (CAFs) were explored in prostate cancer patients enrolled in a pre-operative, randomised controlled phase II trial with four arms: control (usual diet); low-fat (LF) diet; flaxseed-supplemented (FS) diet; and flaxseed-supplemented, low-fat diet. The mean duration of dietary intervention was 30–31 days</td>
<td align="left" valign="top" charoff="50">145 men with prostate cancer</td>
<td align="left" valign="top" charoff="50">N/A</td>
<td align="left" valign="top" charoff="50">Changes in CAFs</td>
<td align="left" valign="top" charoff="50">Compared with the control arm, 6 CAFs including pro-angiogenic factors (stromal-cell derived-1-<italic>α</italic>
and myeloid factors (granulocyte colony-stimulating factor, macrophage colony-stimulating factor) all decreased in the LF arm compared with controls; 3 and 4 CAFs changed in the FS and FS+LF arms, respectively. These results suggest that a low-fat diet without flaxseed may reduce levels of specific inflammatory cytokines and angiogenic factors and suggests that the NF-<italic>κ</italic>
B pathway may be a mediator of these changes</td>
</tr>
<tr><td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
</tr>
<tr><td align="left" valign="top" charoff="50">Hori <italic>et al</italic>
(2011)</td>
<td align="left" valign="top" charoff="50">A review exploring the current evidence for the role of different dietary components and its effect on prostate cancer prevention and progression. A literature search was conducted using PubMed to identify key studies. RCTs were favoured over observational studies. Results from systematic reviews or a meta-analysis of RCTs/observational studies were given preference to quoting individual studies</td>
<td align="left" valign="top" charoff="50">Prostate cancer</td>
<td align="left" valign="top" charoff="50">N/A</td>
<td align="left" valign="top" charoff="50">Prevention and progression</td>
<td align="left" valign="top" charoff="50">There was some evidence suggesting green tea, isoflavone, lycopene, cruciferous vegetable and omega-3 polyunsaturated fatty acid intake to be beneficial in the prevention and/or progression of prostate cancer. There was also evidence suggesting that a high total fat, meat (especially well-cooked) and multivitamin intake may be associated with an increased risk of developing prostate cancer; more research is required to establish its effect on progression</td>
</tr>
<tr><td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
</tr>
<tr><td align="left" valign="top" charoff="50"><xref ref-type="bibr" rid="bib73">Parsons <italic>et al</italic>
(2008)</xref>
</td>
<td align="left" valign="top" charoff="50">Part of the Men's Eating and Living (MEAL) Study (a multicentre pilot trial of a diet-based intervention for prostate cancer). A theory-based telephone counselling intervention <italic>vs</italic>
standardised written materials. The intervention group were counselled to consume at least seven servings of vegetables per day (two cruciferous, two tomato products and three others), two servings a day of whole grains and one serving a day of beans/legumes. Telephone counselling comprised 13 (25–50 min) sessions over 6 months</td>
<td align="left" valign="top" charoff="50">43 prostate cancer survivors on active surveillance (mean age=64 years)</td>
<td align="left" valign="top" charoff="50">6 months</td>
<td align="left" valign="top" charoff="50">Dietary intakes and plasma carotenoid levels were assessed at baseline and after 6 months</td>
<td align="left" valign="top" charoff="50">In the intervention group, the mean daily intakes of total vegetables, crucifers and tomato products increased by 71%, 180% and 265%, respectively (<italic><italic><italic><italic>P</italic>
</italic>
</italic>
</italic>
<0.05); in the control group, there were no significant changes in mean intakes of these components. Similarly, in the intervention arm, mean plasma levels of <italic>α</italic>
-carotene, <italic>β</italic>
-carotene, lutein, lycopene and total carotenoids increased by 37%, 32%, 23%, 30% and 25%, respectively (<italic><italic><italic><italic>P</italic>
</italic>
</italic>
</italic>
<0.05); in the control group, there were no significant changes in plasma levels of these components. There were no significant changes in either group in whole grain, beans/legumes or fat intake</td>
</tr>
<tr><td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
</tr>
<tr><td align="left" valign="top" charoff="50"><xref ref-type="bibr" rid="bib77">Richman <italic>et al</italic>
(2010)</xref>
</td>
<td align="left" valign="top" charoff="50">A prospective study of the association between post-diagnostic consumption of processed and unprocessed red meat, fish, poultry and eggs, and the risk of prostate cancer recurrence or progression</td>
<td align="left" valign="top" charoff="50">1294 men with prostate cancer, without recurrence or progression as of 2004–2005, who were participating in the Cancer of the Prostate Strategic Urologic Research Endeavour</td>
<td align="left" valign="top" charoff="50">Mean=2 years</td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50">Intakes of processed and unprocessed red meat, fish, total poultry and skinless poultry were not associated with prostate cancer recurrence or progression. Greater consumption of eggs and poultry with skin was associated with twofold increases in risk in a comparison of extreme quantiles: eggs (HR=2.02; 95% CI=1.10–3.72; <italic><italic><italic><italic>P</italic>
</italic>
</italic>
</italic>
for trend=0.05) and poultry with skin (HR=2.26; 95% CI=1.36–3.76; <italic><italic><italic><italic>P</italic>
</italic>
</italic>
</italic>
for trend=0.003). An interaction was observed between prognostic risk at diagnosis and poultry. Men with high prognostic risk and a high poultry intake had a fourfold increased risk of recurrence or progression compared with men with low/intermediate prognostic risk and a low poultry intake (<italic><italic><italic><italic>P</italic>
</italic>
</italic>
</italic>
for interaction=0.003). The findings suggest that the post-diagnostic consumption of processed or unprocessed red meat, fish or skinless poultry is not associated with prostate cancer recurrence or progression, whereas consumption of eggs and poultry with skin may increase the risk</td>
</tr>
</tbody>
</table>
<table-wrap-foot><fn id="t3-fn1"><p>Abbreviations: CI=confidence interval; ER=oestrogen receptor; HR=hazard ratio; N/A=not applicable; RCT=randomised controlled trial; RR=relative risk.</p>
</fn>
</table-wrap-foot>
</table-wrap>
<table-wrap id="tbl4"><label>Table 4</label>
<caption><title>Dietary supplements evidence</title>
</caption>
<table frame="hsides" rules="groups" border="1"><colgroup><col align="left"></col>
<col align="left"></col>
<col align="left"></col>
<col align="left"></col>
<col align="left"></col>
<col align="left"></col>
</colgroup>
<thead valign="bottom"><tr><th align="left" valign="top" charoff="50"><bold>Author</bold>
</th>
<th align="left" valign="top" charoff="50"><bold>Study design/intervention</bold>
</th>
<th align="left" valign="top" charoff="50"><bold>Sample/inclusion</bold>
</th>
<th align="left" valign="top" charoff="50"><bold>Follow-up period</bold>
</th>
<th align="left" valign="top" charoff="50"><bold>Primary outcome</bold>
</th>
<th align="left" valign="top" charoff="50"><bold>Results</bold>
</th>
</tr>
</thead>
<tbody valign="top"><tr><td colspan="6" align="left" valign="top" charoff="50"><italic>Supplements</italic>
</td>
</tr>
<tr><td align="left" valign="top" charoff="50">Breast</td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
</tr>
<tr><td align="left" valign="top" charoff="50"><xref ref-type="bibr" rid="bib31">Fleischauer <italic>et al</italic>
(2003)</xref>
</td>
<td align="left" valign="top" charoff="50">Case–control study testing the hypothesis that antioxidant supplements may reduce the risk of breast cancer recurrence or mortality</td>
<td align="left" valign="top" charoff="50">385 post-menopausal women with breast cancer</td>
<td align="left" valign="top" charoff="50">12–14 years</td>
<td align="left" valign="top" charoff="50">Breast cancer recurrence or death</td>
<td align="left" valign="top" charoff="50">Antioxidant supplement users compared with non-users were less likely to have a breast cancer recurrence or breast cancer-related death (OR=0.54, 95% CI=0.27–1.04). Vitamin E supplements showed a modest protective effect when used for >3 years (OR=0.33, 95% CI=0.10–1.07). Risks of recurrence and disease-related mortality were reduced among women using vitamin C and vitamin E supplements for >3 years</td>
</tr>
<tr><td align="left" valign="top" charoff="50"><xref ref-type="bibr" rid="bib74">Patterson <italic>et al</italic>
(2010)</xref>
</td>
<td align="left" valign="top" charoff="50">A review of the published epidemiological research on lifestyle and breast cancer outcomes. Research included RCTs, cohort studies, or case–control studies of breast cancer outcomes. Included studies had been published in the previous 10 years (1999–2009), as well as a few large studies published >10 years ago.
Papers were included only if there were at least 500 participants. Studies of exposure biomarkers such as serum nutrient concentrations were not included, nor were studies with intermediate markers of breast cancer (e.g., mammographic density) or non-invasive lesions (e.g., ductal carcinoma <italic>in situ</italic>
)</td>
<td align="left" valign="top" charoff="50">Breast cancer</td>
<td align="left" valign="top" charoff="50">Not reported</td>
<td align="left" valign="top" charoff="50">Additional breast cancer events and mortality</td>
<td align="left" valign="top" charoff="50">There were only four studies of micronutrients and/or fruit and vegetables with mortality (<xref ref-type="bibr" rid="bib49">Jain <italic>et al</italic>
, 1994</xref>
; <xref ref-type="bibr" rid="bib43">Holmes <italic>et al</italic>
, 1999</xref>
; <xref ref-type="bibr" rid="bib60">McEligot <italic>et al</italic>
, 2006</xref>
; <xref ref-type="bibr" rid="bib19">Dal Maso <italic>et al</italic>
, 2008</xref>
), although these publications typically included many exposures. For example, Holmes <italic>et al</italic>
reported on 93 dietary exposures in relation to all-cause mortality (of which 17 were statistically significant). Overall, the HRs showed a trend towards being protective. Among the vitamins, minerals, fruit, and vegetables in this review; statistically significant protective associations were seen for higher intakes of calcium (<xref ref-type="bibr" rid="bib43">Holmes <italic>et al</italic>
, 1999</xref>
), vitamin C (<xref ref-type="bibr" rid="bib49">Jain <italic>et al</italic>
, 1994</xref>
), and vegetable consumption (<xref ref-type="bibr" rid="bib60">McEligot <italic>et al</italic>
, 2006</xref>
). Given the limited number of total studies and the multiplicity of dietary exposures reported in each study, it was not considered appropriate to calculate a weighted average for the exposures presented in the review</td>
</tr>
<tr><td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
</tr>
<tr><td align="left" valign="top" charoff="50">Colorectal</td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
</tr>
<tr><td align="left" valign="top" charoff="50"><xref ref-type="bibr" rid="bib69">Ng <italic>et al</italic>
(2008)</xref>
</td>
<td align="left" valign="top" charoff="50">Nurses' Health Study prospective examination of the association between pre-diagnosis 25(OH)D levels and mortality in colorectal cancer patients</td>
<td align="left" valign="top" charoff="50">304 colorectal cancer patients</td>
<td align="left" valign="top" charoff="50">Mean=78 months</td>
<td align="left" valign="top" charoff="50">Colorectal cancer mortality</td>
<td align="left" valign="top" charoff="50">Higher plasma 25(OH) D levels were associated with a significant reduction in overall mortality (<italic>P</italic>
for trend=0.02). Compared with the lowest quartile, participants in the highest quartile had an adjusted HR of 0.52 (95% CI=0.29–0.94) for overall mortality. A trend towards improved colorectal cancer-specific mortality was also seen (HR=0.61; 95% CI=0.31–1.19)</td>
</tr>
<tr><td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
</tr>
<tr><td align="left" valign="top" charoff="50"><xref ref-type="bibr" rid="bib68">Ng <italic>et al</italic>
(2010)</xref>
</td>
<td align="left" valign="top" charoff="50">A prospective, observational study. Patients reported on multivitamin use during and 6 months after adjuvant chemotherapy. Patients were observed until March 2009 for disease recurrence and death. To minimise bias by occult recurrence, patients who had a recurrence or died within 90 days of their multivitamin assessment were excluded</td>
<td align="left" valign="top" charoff="50">1038 patients with stage III colon cancer enrolled in a randomised adjuvant chemotherapy trial</td>
<td align="left" valign="top" charoff="50">6 months after adjuvant chemotherapy</td>
<td align="left" valign="top" charoff="50">Cancer-specific and overall mortality</td>
<td align="left" valign="top" charoff="50">Among 1038 patients, 518 (49.9%) reported multivitamin use during adjuvant chemotherapy. Compared with non-users, the multivariate HR for disease-free survival was 0.94 (95% CI=0.77–1.15) for patients who used multivitamins. Similarly, multivitamin use during adjuvant chemotherapy was not significantly associated with recurrence-free survival (multivariate HR=0.93; 95% CI=0.75–1.15) or overall survival (multivariate HR=0.92; 95% CI=0.74–1.16). Neither an increasing number of tablets nor increasing duration of use before cancer diagnosis was associated with cancer recurrence or mortality. Multivitamin use also did not improve the rates of grade 3 and higher GI toxicity</td>
</tr>
<tr><td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
</tr>
<tr><td align="left" valign="top" charoff="50">Prostate</td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
</tr>
<tr><td align="left" valign="top" charoff="50"><xref ref-type="bibr" rid="bib21">Demark-Wahnefried <italic>et al</italic>
(2008)</xref>
</td>
<td align="left" valign="top" charoff="50">Phase II trial testing the comparative effects of flaxseed supplementation with and without a low-fat diet. Controls continued usual diet. The flaxseed group received 30 g per day of ground flaxseed. The low-fat group received instructions on a diet of <20% of kcal from fat. The study was conducted for a mean of 30 days</td>
<td align="left" valign="top" charoff="50">161 men with operable prostate cancer scheduled for prostatectomy (mean age=59.2 years)</td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50">Urine analysed for presence of lignans to confirm flaxseed consumption</td>
<td align="left" valign="top" charoff="50">Proliferation rates were significantly lower (<italic>P</italic>
<0.002) among men in the flaxseed group. Men in the low-fat group had a significant decrease in serum cholesterol (<italic>P</italic>
=0.048)</td>
</tr>
<tr><td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
</tr>
<tr><td align="left" valign="top" charoff="50"><xref ref-type="bibr" rid="bib28">Epstein <italic>et al</italic>
(2011)</xref>
</td>
<td align="left" valign="top" charoff="50">Swedish population-based cohort study examining whether dietary zinc assessed near the time of prostate cancer diagnosis is associated with improved disease-specific survival</td>
<td align="left" valign="top" charoff="50">525 men aged <80 years with a diagnosis of prostate cancer made between 1989 and 1994</td>
<td align="left" valign="top" charoff="50">Median follow-up of 6.4 years</td>
<td align="left" valign="top" charoff="50">Study participants completed self-administered food-frequency questionnaires, and zinc intake was derived from nutrient databases</td>
<td align="left" valign="top" charoff="50">High dietary zinc intake was associated with a reduced risk of prostate cancer-specific mortality (HR<sub>Q4 <italic>vs</italic>
Q1</sub>
=0.64; 95% CI=0.44–0.94; <italic><italic><italic><italic>P</italic>
</italic>
</italic>
</italic>
for trend=0.05) in the study population. The association was stronger in men with localised tumours (HR=0.24; 95% CI=0.09–0.66; <italic><italic><italic><italic>P</italic>
</italic>
</italic>
</italic>
for trend=0.005). Zinc intake was not associated with mortality from other causes</td>
</tr>
<tr><td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
</tr>
<tr><td align="left" valign="top" charoff="50"><xref ref-type="bibr" rid="bib61">McLarty <italic>et al</italic>
(2009)</xref>
</td>
<td align="left" valign="top" charoff="50">An investigation into the effects of short-term supplementation with the active compounds in green tea on serum biomarkers in patients with prostate cancer</td>
<td align="left" valign="top" charoff="50">26 men with prostate cancer</td>
<td align="left" valign="top" charoff="50">Not reported</td>
<td align="left" valign="top" charoff="50">PSA levels</td>
<td align="left" valign="top" charoff="50">Biomarkers of prostate cancer decreased significantly, including total protein, albumin, aspartate aminotransferase, alkaline phosphatase and amylase</td>
</tr>
<tr><td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
</tr>
<tr><td align="left" valign="top" charoff="50"><xref ref-type="bibr" rid="bib71">Ornish <italic>et al</italic>
(2005)</xref>
</td>
<td align="left" valign="top" charoff="50">RCT exploring lifestyle changes including a vegan diet supplemented with soy, vitamin E, fish oils, selenium and vitamin C, together with a moderate physical activity programme and stress management techniques</td>
<td align="left" valign="top" charoff="50">Men with early prostate cancer (<italic>n</italic>
=93)</td>
<td align="left" valign="top" charoff="50">12 months into the intervention</td>
<td align="left" valign="top" charoff="50">PSA and serum stimulated LNCaP cell growth</td>
<td align="left" valign="top" charoff="50">PSA levels decreased by 4% at 12 months in the intervention group, but increased by 6% in the control group; this was statistically significant and strongly correlated with the degree of lifestyle change. The growth of LNCaP prostate cancer cells was inhibited almost 8 times more by serum from the intervention group compared with the control group (70 <italic>vs</italic>
9%, <italic>P</italic>
<0.001)</td>
</tr>
<tr><td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
</tr>
<tr><td align="left" valign="top" charoff="50"><xref ref-type="bibr" rid="bib72">Pantuck <italic>et al</italic>
(2006)</xref>
</td>
<td align="left" valign="top" charoff="50">Phase II, two-stage clinical trial to determine the effects of pomegranate juice on PSA levels</td>
<td align="left" valign="top" charoff="50">46 men with increasing PSA levels, post-treatment (surgery or radiotherapy)</td>
<td align="left" valign="top" charoff="50">Every 3 months for 54 months</td>
<td align="left" valign="top" charoff="50">PSA levels</td>
<td align="left" valign="top" charoff="50">Mean PSA doubling time significantly increased with treatment from a mean of 15 months at baseline to 54 months after treatment (<italic>P</italic>
<0.001). <italic>In vitro</italic>
assays comparing pre-treatment and post-treatment patient serum on the growth of LNCaP showed a 12% decrease in cell proliferation and a 17% increase in apoptosis (<italic>P</italic>
=0.0048 and 0.0004, respectively), a 23% increase in serum nitric oxide (<italic>P</italic>
=0.0085) and significant (<italic>P</italic>
<0.02) reductions in oxidative state and sensitivity to oxidation of serum lipids after <italic>vs</italic>
before pomegranate juice</td>
</tr>
</tbody>
</table>
<table-wrap-foot><fn id="t4-fn1"><p>Abbreviations: CI=confidence interval; HR=hazard ratio; GI=gastrointestinal; OR=odds ratio; RCT=randomised controlled trial.</p>
</fn>
</table-wrap-foot>
</table-wrap>
<table-wrap id="tbl5"><label>Table 5</label>
<caption><title>Physical activity evidence</title>
</caption>
<table frame="hsides" rules="groups" border="1"><colgroup><col align="left"></col>
<col align="left"></col>
<col align="left"></col>
<col align="left"></col>
<col align="left"></col>
<col align="left"></col>
</colgroup>
<thead valign="bottom"><tr><th align="left" valign="top" charoff="50"><bold>Author</bold>
</th>
<th align="left" valign="top" charoff="50"><bold>Study design/intervention</bold>
</th>
<th align="left" valign="top" charoff="50"><bold>Sample/inclusion</bold>
</th>
<th align="left" valign="top" charoff="50"><bold>Follow-up period</bold>
</th>
<th align="left" valign="top" charoff="50"><bold>Primary outcome</bold>
</th>
<th align="left" valign="top" charoff="50"><bold>Results</bold>
</th>
</tr>
</thead>
<tbody valign="top"><tr><td colspan="6" align="left" valign="top" charoff="50"><italic>Physical activity</italic>
</td>
</tr>
<tr><td align="left" valign="top" charoff="50">Breast</td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
</tr>
<tr><td align="left" valign="top" charoff="50"><xref ref-type="bibr" rid="bib15">Chen <italic>et al</italic>
(2011)</xref>
</td>
<td align="left" valign="top" charoff="50">An evaluation of any associations of exercise after breast cancer diagnosis with total mortality and recurrence/disease-specific mortality after accounting for conditions that restrict exercise participation</td>
<td align="left" valign="top" charoff="50">4826 women with stage I–III breast cancer identified 6 months after diagnosis through the population-based Shanghai Cancer Registry and recruited into the study between 2002 and 2006</td>
<td align="left" valign="top" charoff="50">Median follow-up of 4.3 years</td>
<td align="left" valign="top" charoff="50">Exercise was assessed ∼6, 18 and 36 months after diagnosis MET scores were derived</td>
<td align="left" valign="top" charoff="50">After adjustment for QoL, clinical prognostic factors and other covariates, exercise during the first 36 months after diagnosis was inversely associated with total mortality and recurrence/disease-specific mortality, with hazard ratios of 0.70 (95% confidence interval (95% CI)=0.56–0.88) and 0.60 (95% CI=0.47–0.76), respectively. Significant dose–response relationships between total and recurrence/disease-specific mortality rates and exercise duration and MET scores were observed (all <italic>P</italic>
trend <0.05). The exercise–mortality associations were not modified by menopausal status, comorbidity, QoL or body size, assessed ∼6 months after diagnosis</td>
</tr>
<tr><td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
</tr>
<tr><td align="left" valign="top" charoff="50"><xref ref-type="bibr" rid="bib41">Holick <italic>et al</italic>
(2008)</xref>
</td>
<td align="left" valign="top" charoff="50">Prospective cohort study examining the relationship between post-diagnosis recreational physical activity and risk of breast cancer death</td>
<td align="left" valign="top" charoff="50">Women with a history of invasive breast cancer, diagnosed between the ages of 20 and 79 years (<italic>n</italic>
=4482)</td>
<td align="left" valign="top" charoff="50">Maximum of 6 years post-diagnosis (median=5.6 years post-diagnosis)</td>
<td align="left" valign="top" charoff="50">Mortality from breast cancer; mortality from any cause</td>
<td align="left" valign="top" charoff="50">Women who engaged in greater levels of activity had a significantly lower risk of dying from breast cancer (HR=0.65; 95% CI=0.39–1.08 for 2.8–7.9 MET-h per week; HR=0.59; 95% CI=0.35–1.01 for 8.0–20.9 MET-h per week; and HR=0.51; 95% CI=0.29–0.89 for ⩾21.0 MET-h per week; <italic>P</italic>
for trend=0.05)</td>
</tr>
<tr><td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
</tr>
<tr><td align="left" valign="top" charoff="50"><xref ref-type="bibr" rid="bib42">Holmes <italic>et al</italic>
(2005)</xref>
</td>
<td align="left" valign="top" charoff="50">Prospective observational study (Nurses' Health Study) to determine whether physical activity among women with breast cancer decreases their risk of death from breast cancer</td>
<td align="left" valign="top" charoff="50">2987 female registered nurses, diagnosed with stage I, II or III breast cancer</td>
<td align="left" valign="top" charoff="50">Women were diagnosed between 1984 and 1998 and followed until death or June 2002</td>
<td align="left" valign="top" charoff="50">Breast cancer mortality risk</td>
<td align="left" valign="top" charoff="50">Compared with women who engaged in <3 MET-h per week of physical activity, the adjusted relative risk (RR) of death from breast cancer was 0.80 (95% CI=0.60–1.06) for 3–8.9 MET-h per week; 0.50 (95% CI=0.31–0.82) for 9–14.9 MET-h per week; 0.56 (95% CI=0.38–0.84) for 15–23.9 MET-h per week; and 0.60 (95% CI=0.40–0.89) for ⩾24 MET-h per week (<italic>P</italic>
for trend=0.004)</td>
</tr>
<tr><td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
</tr>
<tr><td align="left" valign="top" charoff="50"><xref ref-type="bibr" rid="bib45">Ibrahim and Al-Homaidh (2011)</xref>
</td>
<td align="left" valign="top" charoff="50">Meta-analysis of physical activity and survival after breast cancer diagnosis. A comprehensive literature search identified six studies. The search was limited to randomised, case–control, cohort or observational peer-reviewed clinical studies and reviews in English language</td>
<td align="left" valign="top" charoff="50">2108 patients with breast cancer</td>
<td align="left" valign="top" charoff="50">N/A</td>
<td align="left" valign="top" charoff="50">Breast cancer survival</td>
<td align="left" valign="top" charoff="50">Pre-diagnosis PA reduced all-cause mortality by 18% but had no effect on breast cancer deaths. Post-diagnosis PA reduced breast cancer deaths by 34% (HR=0.66, 95% CI=0.57–0.77, <italic>P</italic>
<0.00001), all-cause mortality by 41% (HR=0.59, 95% CI=0.53–0.65, <italic>P</italic>
<0.00001) and disease recurrence by 24% (HR=0.76, 95% CI=0.66–0.87, <italic>P</italic>
=0.00001). Breast cancer mortality was reduced by pre-diagnosis PA in women with body mass index (BMI) <25 kg m<sup>2</sup>
, whereas post-diagnosis PA reduced that risk among those with BMI ⩾25 kg m<sup>2</sup>
. On the other hand, post-diagnosis PA reduced all-cause mortality regardless of the BMI. The analysis showed that post-diagnosis PA reduced breast cancer deaths (HR=0.50, 95% CI=0.34–0.74, <italic>P</italic>
=0.0005) and all-cause mortality (HR=0.36, 95% CI=0.12–1.03, <italic>P</italic>
=0.06) among patients with oestrogen receptor (ER)-positive tumour, whereas women with ER-negative disease showed no gain</td>
</tr>
<tr><td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
</tr>
<tr><td align="left" valign="top" charoff="50"><xref ref-type="bibr" rid="bib47">Irwin <italic>et al</italic>
(2008)</xref>
</td>
<td align="left" valign="top" charoff="50">The Health, Eating, Activity, and Lifestyle Study (HEAL): Prospective observational study investigating the association between pre- and post-diagnosis physical activity and mortality among women with breast cancer</td>
<td align="left" valign="top" charoff="50">933 women diagnosed with local or regional breast cancer</td>
<td align="left" valign="top" charoff="50">5–8 years from diagnosis (median=6 years)</td>
<td align="left" valign="top" charoff="50">Mortality from breast cancer; mortality from any cause</td>
<td align="left" valign="top" charoff="50">Compared with inactive women, the multivariable HRs for total deaths for women expending at least 9 MET-h per week were 0.69 (95% CI=0.45–1.06; <italic>P</italic>
=0.045) for those active in the year before diagnosis and 0.33 (95% CI=0.15–0.73; <italic>P</italic>
=0.046) for those active 2 years after diagnosis. Compared with women who were inactive both before and after diagnosis, women who increased physical activity after diagnosis had a 45% lower risk of death (HR=0.55; 95% CI=0.22–1.38), and women who decreased physical activity after diagnosis had a four-fold greater risk of death (HR=3.95; 95% CI=1.45–10.50)</td>
</tr>
<tr><td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
</tr>
<tr><td align="left" valign="top" charoff="50"><xref ref-type="bibr" rid="bib48">Irwin <italic>et al</italic>
(2009)</xref>
</td>
<td align="left" valign="top" charoff="50">RCT – Post-menopausal breast cancer survivors were identified from the Yale-New Haven Hospital Tumour Registry and randomly assigned to an exercise (<italic>n</italic>
=37) or usual care (<italic>n</italic>
=38) group. The exercise group participated in 150 min per week of moderate-intensity aerobic exercise. The usual care group was instructed to maintain their current physical activity level</td>
<td align="left" valign="top" charoff="50">75 post-menopausal breast cancer survivors</td>
<td align="left" valign="top" charoff="50">6 months</td>
<td align="left" valign="top" charoff="50">A fasting blood sample was collected on each study participant at baseline and 6 months. Blood levels of insulin and IGF were measured with ELISA</td>
<td align="left" valign="top" charoff="50">On average, exercisers increased aerobic exercise by 129 min per week compared with 45 min per week among usual-care participants (<italic><italic><italic><italic>P</italic>
</italic>
</italic>
</italic>
<0.001). Women randomised to exercise experienced decreases in insulin, IGF-I and IGFBP-3, whereas women randomised to usual care had increases in these hormones. Between-group differences in insulin, IGF-I and IGFBP-3 were 20.7% (<italic>P</italic>
=0.089), 8.9% (<italic>P</italic>
=0.026) and 7.9% (<italic>P</italic>
=0.006), respectively</td>
</tr>
<tr><td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
</tr>
<tr><td align="left" valign="top" charoff="50"><xref ref-type="bibr" rid="bib57">Ligibel <italic>et al</italic>
(2008</xref>
, <xref ref-type="bibr" rid="bib58">2009</xref>
)</td>
<td align="left" valign="top" charoff="50">RCT examining the impact of physical activity on insulin levels in participants randomly assigned to:
(1) <italic>Physical activity intervention:</italic>
a 16-week supervised strength training and home-based cardiovascular training protocol (two supervised 50-min strength training sessions per week and 90λmin of home-based aerobic physical activity weekly)
(2) <italic>Control group:</italic>
routine care for 16 weeks</td>
<td align="left" valign="top" charoff="50">101 sedentary, overweight breast cancer survivors (stage I–III) who had completed chemotherapy and/or radiation therapy 3 months previously (mean age=53 years)</td>
<td align="left" valign="top" charoff="50">On completion of the 16-week intervention</td>
<td align="left" valign="top" charoff="50">Fasting insulin and glucose levels</td>
<td align="left" valign="top" charoff="50">There were significant post-treatment decreases in insulin levels for the exercise group but not for the control group. Fasting insulin concentrations decreased by an average of 2.86 <italic>μ</italic>
U ml in the exercise group (<italic>P</italic>
=0.03), with no significant change in the control group (decrease of 0.27 <italic>μ</italic>
U ml, <italic>P</italic>
=0.65) (<italic>P</italic>
=0.07)</td>
</tr>
<tr><td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
</tr>
<tr><td align="left" valign="top" charoff="50"><xref ref-type="bibr" rid="bib74">Patterson <italic>et al</italic>
(2010)</xref>
</td>
<td align="left" valign="top" charoff="50">A review of the published epidemiological research on lifestyle and breast cancer outcomes. Research included RCTs, cohort studies or case–control studies of breast cancer outcomes. Included studies had been published in the previous 10 years (1999–2009), as well as a few large studies published >10 years ago.
Papers were included only if there were at least 500 participants. Studies of exposure biomarkers such as serum nutrient concentrations were not included, nor were studies with intermediate markers of breast cancer (e.g., mammographic density) or non-invasive lesions (e.g., ductal carcinoma <italic>in situ</italic>
)</td>
<td align="left" valign="top" charoff="50">Breast cancer</td>
<td align="left" valign="top" charoff="50">Not reported</td>
<td align="left" valign="top" charoff="50">Additional breast cancer events and mortality</td>
<td align="left" valign="top" charoff="50">Four studies of physical activity and additional breast cancer events were identified, two of which were not identified in the current search strategy (<xref ref-type="bibr" rid="bib32">Friedenrich, 2009</xref>
; <xref ref-type="bibr" rid="bib83">Sternfeld, 2009</xref>
). None of these studies found a statistically significant association, although there was a trend towards a protective effect: the weighted average was 0.86. Nine studies of physical activity and breast cancer mortality were identified, four of which were not identified through the current search strategy (<xref ref-type="bibr" rid="bib8">Borugian <italic>et al</italic>
, 2004</xref>
; <xref ref-type="bibr" rid="bib19">Dal Maso <italic>et al</italic>
, 2008</xref>
; <xref ref-type="bibr" rid="bib32">Friedenrich, 2009</xref>
; <xref ref-type="bibr" rid="bib83">Sternfeld, 2009</xref>
), of which three showed a statistically significant protective effect (<xref ref-type="bibr" rid="bib42">Holmes <italic>et al</italic>
, 2005</xref>
; <xref ref-type="bibr" rid="bib41">Holick <italic>et al</italic>
, 2008</xref>
; <xref ref-type="bibr" rid="bib47">Irwin <italic>et al</italic>
, 2008</xref>
). The weighted average for the association of lifetime, at diagnosis or post-diagnosis physical activity with mortality was 0.71</td>
</tr>
<tr><td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
</tr>
<tr><td align="left" valign="top" charoff="50"><xref ref-type="bibr" rid="bib75">Pekmezi and Demark-Wahnefried (2011)</xref>
</td>
<td align="left" valign="top" charoff="50">Literature review designed to synthesise recent progress in lifestyle interventions in light of current guidelines put forth by the ACS, WCRF/AICR, and ACSM.
The PubMed database was searched for terms of cancer survivor(s) or neoplasms/survivor, cross-referenced with MeSH terms of lifestyle, health behaviour, physical activity, exercise, body weight, obesity, weight loss, diet, nutrition. Only intervention studies and RCTs with retention rates exceeding 75% were included</td>
<td align="left" valign="top" charoff="50">All cancer survivors, but primarily breast cancer</td>
<td align="left" valign="top" charoff="50">N/A</td>
<td align="left" valign="top" charoff="50">Fitness, strength, physical function and cancer-related psychosocial variables, whereas dietary interventions improve diet quality, nutrition-related biomarkers and body weight</td>
<td align="left" valign="top" charoff="50">There has been an increase in the number and methodological rigour of the studies in this area, with 21 RCTs identified in the past 3 years. Results suggest that physical activity interventions are safe for cancer survivors and produce improvements in fitness, strength, physical function and cancer-related psychosocial variables, whereas dietary interventions improve diet quality, nutrition-related biomarkers and body weight. Preliminary evidence also suggests that diet and exercise may positively influence biomarkers associated with progressive disease and overall survival (e.g., insulin levels, oxidative DNA damage and tumour proliferation rates)</td>
</tr>
<tr><td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
</tr>
<tr><td align="left" valign="top" charoff="50">Colorectal</td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
</tr>
<tr><td align="left" valign="top" charoff="50"><xref ref-type="bibr" rid="bib2">Allgayer <italic>et al</italic>
(2008)</xref>
</td>
<td align="left" valign="top" charoff="50">Prospective, randomised trial exploring the impact of exercise on oxidative DNA damage. Patients were allocated to a moderate intensity (MI) exercise group following primary therapy, or to a high-intensity exercise group</td>
<td align="left" valign="top" charoff="50">48 colorectal cancer patients following primary therapy (mean age=59 years)</td>
<td align="left" valign="top" charoff="50">Concentrations were determined immediately before and after completion of the exercise programmes</td>
<td align="left" valign="top" charoff="50">Urinary 8-oxo-dG excretion concentration was determined by a highly sensitive detection method using high-performance liquid chromatography coupled to electrospray ionisation mass spectrometry (HPLC-ESI-MS)</td>
<td align="left" valign="top" charoff="50">MI exercise significantly reduced urinary 8-oxo-dG excretion levels from 8.47±1.99 to 5.81±1.45 (ng mg<sup>−1</sup>
creatinine, mean±s.e., <italic>P</italic>
=0.02), whereas HI exercise resulted in a non-significant increase from 5.00±1.31 to 7.11±1.63 (ng mg<sup>−1</sup>
creatinine, <italic>P</italic>
=0.18). Clinical characteristics (gender, age, body mass index (BMI), diet, chemotherapy/irradiation) were not associated/correlated with urinary 8-oxo-dG levels</td>
</tr>
<tr><td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
</tr>
<tr><td align="left" valign="top" charoff="50"><xref ref-type="bibr" rid="bib38">Haydon <italic>et al</italic>
(2006)</xref>
</td>
<td align="left" valign="top" charoff="50">Melbourne Collaborative Cohort Study, examining colorectal cancer incidence against self-reported physical activity</td>
<td align="left" valign="top" charoff="50">526 Australians with colorectal cancer</td>
<td align="left" valign="top" charoff="50">Median=5.5 years</td>
<td align="left" valign="top" charoff="50">Disease-specific survival</td>
<td align="left" valign="top" charoff="50">Exercisers had an improved disease-specific survival (HR=0.73; 95% CI=0.54–1.00). The benefit of exercise was largely confined to stage II–III tumours (HR=0.49; 95% CI=0.30–0.79). Increasing percentage body fat resulted in an increase in disease-specific deaths (HR=1.33 per 10 kg; 95% CI=1.04–1.71)</td>
</tr>
<tr><td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
</tr>
<tr><td align="left" valign="top" charoff="50"><xref ref-type="bibr" rid="bib63">Meyerhardt <italic>et al</italic>
(2005)</xref>
</td>
<td align="left" valign="top" charoff="50">Prospective study of recreational physical activity and prognosis among stage III colon cancer patients enrolled in an RCT of post-operative adjuvant chemotherapy</td>
<td align="left" valign="top" charoff="50">816 patients with stage III colon cancer</td>
<td align="left" valign="top" charoff="50">6 months post-therapy</td>
<td align="left" valign="top" charoff="50">Disease-free survival</td>
<td align="left" valign="top" charoff="50">Levels of physical activity were associated with significantly improved disease-free survival among patients with stage III colon cancer. The HR for DFS for individuals in the highest quintile (>25 MET-h per week) was 0.65 (95% CI=0.38–1.11; <italic>P</italic>
for trend=0.02) compared with those in the lowest quintile of PA. This relationship varied by gender, with a HR=0.33 (95% CI=0.11–0.99) for women (<italic>P</italic>
for trend=0.046) and a HR=0.89 (95% CI=0.44–1.78) for men (<italic>P</italic>
for trend=0.3)</td>
</tr>
<tr><td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
</tr>
<tr><td align="left" valign="top" charoff="50">Prostate</td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
</tr>
<tr><td align="left" valign="top" charoff="50"><xref ref-type="bibr" rid="bib9">Bourke <italic>et al</italic>
(2011)</xref>
</td>
<td align="left" valign="top" charoff="50">Participants were randomised to a 12-week lifestyle programme comprising aerobic and resistance exercise, plus dietary advice or standard care</td>
<td align="left" valign="top" charoff="50">50 (25 per group) advanced prostate cancer patients receiving androgen suppression therapy (AST) for a minimum of 6 months</td>
<td align="left" valign="top" charoff="50">Baseline, after the intervention and at 6 months</td>
<td align="left" valign="top" charoff="50">Exercise behaviour, dietary macronutrient intake, quality of life, fatigue, functional fitness and biomarkers associated with disease progression</td>
<td align="left" valign="top" charoff="50">The lifestyle group showed improvements in exercise behaviour (<italic><italic><italic><italic>P</italic>
</italic>
</italic>
</italic>
<0.001), dietary fat intake (<italic>P</italic>
=0.001), total energy intake (<italic>P</italic>
=0.005), fatigue (<italic>P</italic>
=0.002), aerobic exercise tolerance (<italic><italic><italic><italic>P</italic>
</italic>
</italic>
</italic>
<0.001) and muscle strength (<italic>P</italic>
=0.033) compared with standard care controls. No effects on clinical prostate cancer disease markers were observed</td>
</tr>
<tr><td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
<td align="left" valign="top" charoff="50"> </td>
</tr>
<tr><td align="left" valign="top" charoff="50"><xref ref-type="bibr" rid="bib51">Kenfield (2010)</xref>
</td>
<td align="left" valign="top" charoff="50">Prospective study (Health Professionals Follow-up Study) assessing the relationship of physical activity, and duration and pace of walking, with total and prostate cancer-specific mortality</td>
<td align="left" valign="top" charoff="50">2686 men with prostate cancer</td>
<td align="left" valign="top" charoff="50">4 years</td>
<td align="left" valign="top" charoff="50">Prostate cancer mortality</td>
<td align="left" valign="top" charoff="50">Men who were physically active, especially those engaging in ⩾3 MET-h of total activity, had a 35% lower risk of death from any cause (HR=0.65; 95% CI=0.52–0.82) and a modest non-significant reduction in risk of prostate cancer death (HR=0.88; 95% CI=0.52–1.49), after adjustment for other risk factors for PCa mortality and pre-diagnosis physical activity. Although no benefit from walking was observed for PCa mortality, men who walked ⩾4λh per week <italic>vs</italic>
those who walked <20 min per week had a 23% lower risk of all-cause mortality (95% CI=0.61–0.97; <italic>P</italic>
-trend=0.01). In addition, compared with men who walked <90 min at an easy walking pace, those who walked ⩾90λmin at a normal to very brisk pace had a 51% lower risk of all-cause mortality (95% CI=0.37–0.64). More vigorous activity, and longer duration of activity, was associated with significant further reductions in risk for all-cause mortality. More vigorous activity was associated with a borderline-significant reduction in risk for PCa mortality</td>
</tr>
</tbody>
</table>
<table-wrap-foot><fn id="t5-fn1"><p>Abbreviations: ACSM=American College of Sports Medicine; AICR=American Institute for Cancer Research; CI=confidence interval; DFS=disease-free survival; ELISA=enzyme-linked immunosorbent assay; FS=flaxseed-supplemented; HI=high intensity; HR=hazard ratio; IGFBP-3=insulin-like growth factor-binding protein 3; IGF=insulin-like growth factor; LF=low-fat; MET=metabolic equivalent tasks; MI=moderate inetnsity; N/A=not available; PA=physical activity; PCa=prostate cancer; PSA=prostate-specific antigen; QoL=quality of life; RCT=randomised controlled trial; WCRF=World Cancer Research Fund.</p>
</fn>
</table-wrap-foot>
</table-wrap>
</floats-group>
</pmc>
<affiliations><list><country><li>Royaume-Uni</li>
</country>
</list>
<tree><country name="Royaume-Uni"><noRegion><name sortKey="Davies, N J" sort="Davies, N J" uniqKey="Davies N" first="N J" last="Davies">N J Davies</name>
</noRegion>
<name sortKey="Batehup, L" sort="Batehup, L" uniqKey="Batehup L" first="L" last="Batehup">L. Batehup</name>
<name sortKey="Thomas, R" sort="Thomas, R" uniqKey="Thomas R" first="R" last="Thomas">R. Thomas</name>
</country>
</tree>
</affiliations>
</record>
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