text:
In the United States, an estimated 45% of men and 38% of women will
develop cancer in their lifetimes (1). Only 10% to 15% of
cancers are due to an inherited genetic predisposition, and the remainder is
thought to be due to lifestyle or environmental factors (2). The International Agency for Research on Cancer (IARC)
estimates that 25% of cancer cases worldwide are due to overweight and obesity
and a sedentary lifestyle (2). The most consistent
associations between increased physical activity and reduced cancer risk have
been observed for colon and breast cancers. Growing evidence supports a reduced
risk of endometrial and lung cancers in physically active versus sedentary
persons. A large number of studies have investigated the association between
physical activity and prostate cancer and, in summary, have found no
association between physical activity and risk of prostate cancer. Few data are
available to determine whether physical activity affects risk of cancer at
other sites.
A total of 1,437,180 new cancer cases and 565,650 deaths from cancers
were projected to occur in the United States in 2008, and cancer is the leading
cause of death for men and women younger than age 80 (1). A
growing body of literature supports a role for physical activity in improving
cancer prognosis and quality of life (3). Therefore, it is
imperative to identify lifestyle factors that could be modified to reduce the
impact of cancer.
This chapter addresses 3 specific questions:
This chapter reviews the available epidemiologic data on associations
between physical activity and risks of specific cancers, the intervention study
data on physical activity in cancer survivors, and the human experimental data
on mechanisms that might explain the links between physical activity and
cancer. The Cancer subcommittee began its literature review with the
Physical Activity Guidelines for Americans Scientific Database, which
includes publications since 1995 (see Part F: Scientific Literature Search
Methodology, for a full description of the Database). This
search was augmented with MEDLINE searches of English-language articles using
the terms "physical activity," "exercise," and "cancer." In addition, the
subcommittee used several comprehensive literature reviews (2;4-8).
Because all of the studies that examined the association of physical
activity with risk of cancer are observational epidemiologic studies, causality
cannot be inferred. However, chance is unlikely as an alternate explanation
because many of the results were statistically significant, particularly for
colon and breast cancer.
A large body of epidemiologic data exists on the association between
physical activity and the risk of developing various types of cancer. Although
the direct evidence of these associations derives only from observational
studies, randomized controlled trials (RCTs) have provided indirect evidence by
examining the association of physical activity with markers of cancer risk,
such as circulating levels of sex hormones, insulin, and cytokines.
The observational data are clearest for colon and breast cancer, with
case-control and cohort studies supporting a moderate, inverse relation between
physical activity and the development of these cancers. Individuals engaging in
aerobic physical activity for approximately 3 to 4 hours per week at moderate
or greater levels of intensity have on average a 30% reduction in colon cancer
risk and a 20% to 40% lower risk of breast cancer, compared with those who are
sedentary. A dose-response relation also is apparent, with risk decreasing at
higher levels of physical activity. However, little information is available
regarding what additional amounts and intensity of physical activity are
associated with additional risk reductions; it also is unclear what the
magnitude of the additional decrements in risk may be. The available evidence
suggests that at least 30 to 60 minutes per day of moderate to vigorous
intensity physical activity is required to significantly lower the risk of
colon and breast cancer.
Compared with sedentary people, the available epidemiologic data suggest
that active people have approximate reductions in risk of lung, endometrial,
and ovarian cancers of 20%, 30%, and 20%, respectively. The data overall do not
support associations of physical activity with prostate or rectal cancers. Too
few data exist regarding the other site-specific cancers to make reasonable
More than two dozen prospective cohort studies (9-34), and an even greater number of population-based
case-control studies (35-71) have examined the relation
between physical activity and breast cancer risk. These studies have primarily
assessed the role of recreational physical activity on breast cancer risk.
Overall, most studies suggest that physically active women have a lower risk of
developing breast cancer than sedentary women. The majority of reported cohort
studies (10-15;17;18;20-22;24;27;29;31-34) have reported a reduction in risk with physical
activity ranging from 20% to 80%, and a number of population-based case-control
studies (35-37;41-49;51;53;54;56;69-71) have reported reduction in
risk ranging from 20% to 70%. In a meta-analysis of 23 studies focused on
physical activity in adolescence and young adulthood, a summary relative risk
(RR) estimate of breast cancer for highest versus lowest category of physical
activity was 0.81 (95% CI 0.73-0.89), and each 1-hour increase of recreational
physical activity per week was associated with a 3% (95% CI 0%-6%) risk
reduction (72). A more extensive systematic review of
recreational activity and breast cancer risk included 19 cohort and 29
case-control studies (73). The review concluded that
evidence was strong that physical activity reduced risk of postmenopausal
breast cancer by 20% to 80%, and that each additional hour of physical activity
per week reduced risk for breast cancer by 6% (95% CI 3%-8%). They further
concluded that the effect of physical activity on premenopausal breast cancer
risk was a more modest 15% to 20% reduction.
The relevant lifetime periods for the effects of physical activity on
breast cancer risk are not established. Lifetime recreational physical activity
(35;51;54;64), adolescent physical activity (15;17;24;35;42;45;47), and
physical activity at various life points (10-14;17;18;22;24;37;47;49;51;60) have been
associated with lower breast cancer risk in several studies. Studies examining
risk more broadly for specific decades of life also have observed an inverse
association with some or all examined time periods (24;45;58;59).
Furthermore, physical activity after menopause has been found to reduce breast
cancer risk (12;22;24). Other studies that specifically looked at physical
activity at various life periods have not found a reduced breast cancer risk
with physical activity at any time (25).
Within the United States, associations between increased physical
activity and decreased breast cancer risk have been observed in multiethnic
populations (24;70;71). These observations also hold true for specific racial
and ethnic populations, including black (46;70), Hispanic (49;71), and Asian American women (56).
Results from some studies with sufficient numbers in subgroup
populations suggest that the association with physical activity may be stronger
in women without a family history of breast cancer than in those with a family
history (22;34;51;69), although other large studies
have found that women with as well as women without a family history of breast
cancer had reduced risk of breast cancer with increasing physical activity (24;32). Several previous studies
reported a greater reduction in risk with increasing physical activity among
parous compared to nulliparous women (34;35). However, other studies have either observed the opposite
finding with risk reduction greater in nulliparous women (32;44), or have found no effect
modification of parity (24). One study found that physical
activity may be more strongly associated with reduced risk of postmenopausal
breast cancer in women who do not use menopausal hormones (22;71), though other studies found that
physical activity effect did not change according to menopausal hormone use (16;24;32;40;64).
In 4 studies, researchers examined effect modification by adult weight
gain (14;17;45;74), and 1 study reported a greater
reduction in risk among women who had less than a 17% increase in adult weight
(74). Several studies documented a greater reduction in
risk among leaner women compared to heavier women (11;24;44;51), although
other studies found that physical activity reduced risk of breast cancer in
women with all levels of body mass index (BMI) (32;34).
Two cohort studies have addressed the effect of physical activity on
breast cancer within the context of other variables related to energy balance,
specifically adiposity and dietary energy intake. One study found evidence that
premenopausal women who did not participate in vigorous activity, were
overweight or obese (BMI greater than 25 kg/m2), and had a
relatively high calorie intake (more than 1,970 kilocalories per day, as
determined from a food frequency questionnaire), had a statistically
significant 60% increased risk of breast cancer compared with active, normal
weight women with lower calorie intake (26). Another
cohort study found that women with the highest quartile of energy intake, were
obese, and participated in less than 4 hours per week of vigorous physical
activity, had a RR of 2.1 (95% CI 1.27-3.45) compared with normal or
overweight, active women who had the lowest quartile of calorie intake (31).
In hypothesizing about the reasons for the effects of energy balance on
breast cancer risk, investigators speculate that, in addition to the potential
role of obesity as an effect modifier, obesity possibly may be on the causal
pathway between physical activity and postmenopausal breast cancer development.
Specifically, physical activity reduces levels of adiposity, and subsequently
reduces adipose tissue production of estrogen and testosterone, both of which
can promote breast carcinogenesis or progression. However, most studies of
physical activity and breast cancer have adjusted for BMI as a proxy for
adiposity, and an inverse association between physical activity and breast
cancer risk persisted. Thus, it is likely that physical activity may have some
effect on breast cancer risk independent of their mutual relation with
Several studies have tried to quantify the level of physical activity
required for a decreased risk of breast cancer. Investigators have reported
statistically significantly lower rates of breast cancer among women exercising
at least 1 hour per week (14); exercising at least 3.8
hours per week (primarily vigorous exercise) (35);
exercising to keep fit at least 4 hours per week (11); and
exercising vigorously at least 7 hours per week (46).
Other investigators have observed significantly lower rates among women
expending at least 1,500 kilocalories per week (18)
(approximately 4 hours per week of moderate-intensity activity); at least 15.3
metabolic equivalent (MET)-hours per week (approximately 4 hours per week of
moderate-intensity activity) (41); and at least 17.6
MET-hours per week (4 to 5 hours per week of moderate-intensity activity) (74). Two reports from the same study found significantly
lower rates of breast cancer only among women who exercised vigorously on a
daily basis during the ages to 14 to 22 years (45;68). Finally, in a study where total physical activity over
the lifetime was assessed, significantly lower breast cancer rates were seen in
women who expended at least 47.5 MET-hours per week per year in total activity
(48). The impact of these various levels of activity on
reducing risk has varied from 20% to 40%. However, other studies that
specifically looked at dose-response have had not found an effect of any dose
of exercise on breast cancer risk (28;30). Overall, it appears that at least 4 to 7 hours per week
of moderate to vigorous intensity physical activity is required to produce a
statistically significant reduction in risk, although some evidence suggests
greater reduction in risk with greater amount of activity, such that 1 hour per
day of moderate or vigorous activity produces greater reduction in risk
compared with the Surgeon General recommendation of 30 minutes per day on most
days of the week (4).
The incidence of in situ breast cancer is largely influenced by
prevalence of screening, and therefore it is important to examine the effects
of physical activity on invasive breast cancer separately from that on in
situ breast cancer. Furthermore, breast cancers consist of distinct
biological subtypes that are strongly related to prognosis and that may differ
in etiology including tumor responsiveness to hormones (i.e., estrogen and
progesterone receptor [ER/PR] status positive or negative), and other tumor
characteristics (e.g., Her2neu receptor status, and other proliferative
indices). A few studies have separately examined the association between
physical activity and in situ versus invasive breast cancer, however,
very few have examined physical activity effects separately in hormone receptor
positive or negative tumors, and none has considered other tumor
characteristics. In one study, researchers examined the association between
physical activity and breast cancer stratified by stage of disease and found
risk reduction to be greater for localized invasive disease compared to either
in situ or regional/distant breast cancer (54). A
recent large cohort study found a greater risk reduction for in situ
(RR 0.69, P for trend 0.04) than for invasive breast cancer (RR 0.80,
P for trend 0.02) (34). One case-control study
focused specifically on in situ breast cancer, and found that risk of
this stage of breast cancer was approximately 35% lower in women reporting any
lifetime exercise activity compared with sedentary women (54). Two studies also reported risk ratios separately for
ER/PR positive and negative tumors, but neither found a difference in risk by
ER/PR subtype (18;75). A recent
cohort study found that women who reported high versus low levels of physical
activity at enrollment had a 13%, 33%, and 20% decreased risk of developing
ER+/PR+, ER+/PR−, and ER−/PR− breast cancer, respectively (29). Another large cohort study found the greatest risk
reduction from increased physical activity for ER−/PR− breast
cancer (34). Most other studies have included too few
women with hormone receptor negative disease to be able to assess the
association of physical activity with risk of this subtype of breast
An association of sedentary occupations with increased risk of breast
cancer has been documented in reports from some (11;17;27) but not other (76) prospective cohort studies. Published reports from some
(43;47;48;53;61;77) but not
other (41;44;52;55;56)
population-based case-control studies also document an inverse association
between occupational physical activity and breast cancer risk.
The effect of low-intensity activity (such as household activities,
gardening, dancing, leisurely walking, or other activities with a MET score
below 4) on breast cancer risk is still unclear, but may be of importance,
particularly for postmenopausal breast cancer, as a large portion of activity
among postmenopausal and elderly women is not vigorous. Although previous
studies have examined the association between leisure-time physical activity,
such as walking, biking, swimming, and aerobics, few studies have included the
effects of other low-intensity activities, such as gardening, housework, or
shopping, in their calculation of leisure-time physical activity. This may lead
to an underestimation of true energy expenditure, especially among groups of
women who do not have access to recreational or sports activity. In support of
the importance of household activity, a recent large European cohort study
found that for women in the highest versus lowest household activity quartile,
risks for postmenopausal and premenopausal breast cancer were reduced by 19%
(P for trend 0.0001) and 29% (P for trend 0.0003),
respectively (33).
A number of epidemiologic studies have examined physical activity and
prostate cancer risk (28;78-123),
including 25 cohort studies (28;78;80-82;87-89;91-102;117;119-121;123) and 14 case-control
studies (104-116;118). Several of
the cohort studies (78;80;81;94;117)
included prostate cancer mortality or advanced or metastatic prostate cancer as
at least one endpoint. One study (91) also examined the
association between cardiopulmonary fitness and risk of prostate cancer.
Of these studies, 19 found some suggestion for an inverse relation
between physical activity and prostate cancer (80;81;87;89;91;93;94;96;97;101;102;104;105;109;112;113; 117;120;123).
No overall association between physical activity and prostate cancer was found
in 14 studies (28;82;88;95;98-100;106;108;110;114;115;119;121), and an increased risk of prostate cancer among
physically active men was found in some studies (78;92;107;111). The
size of the association ranged from an 80% reduction in prostate cancer risk
for the highest physical activity levels (113) to a 220%
increased risk in one study (111).
No consistent subgroup effects have been defined for demographic or
health factors such as age, race/ethnicity, or BMI. A recent study found that,
among men with a family history of prostate cancer, risk for those in the
highest quartile of physical activity was reduced by 52%, compared to that for
those in the lowest quartile of physical activity. Those without a family
history had no risk reduction (115).
Several studies have attempted to quantitate a dose-response association
of prostate cancer risk with levels of physical activity (82;87;88;91-96;98;100-102;104-106;108-110;112-118;120;121). A statistically significant
trend toward decreasing prostate cancer risk with increasing physical activity
level was observed in several studies (87;93;94;102;104;105;113;118;120), although this was limited to
advanced disease in two studies (120;124). In one study, a 74% reduction in prostate cancer risk
was found in the highest compared to the lowest quartile of fitness level (91).
Occupational activity was associated with a decreased risk of prostate
cancer in several studies (80;81;93;97;105;113;116) and recreational activity
decreased risk of either overall or advanced prostate cancer in several
additional studies (91;93;94;96;101;104;115;117). In
one study, non-significant risk decreases were found for occupational and
recreational activity but an increased risk was observed for household activity
(115). No study differentiated between types of
recreational activity, such as aerobic or resistance exercise, or to their
subtypes such as jogging versus walking. Rather, activities were combined into
measures of MET-hours per week, or to measures of frequency or total duration
of activity per week.
One consideration for prostate cancer is the effect of screening.
Prostate-specific antigen (PSA) screening for early detection became widespread
in the United States in the 1990s. If physically active men also are more
health conscious (i.e., they are more likely to be screened for prostate
cancer), it may result in higher observed rates of prostate cancer among these
men because of increased detection. This notion is supported by several cohort
studies (94;117;120), which identified a reduction in risk of aggressive,
metastatic, or fatal prostate cancer with increased physical activity level. In
contrast, an investigation of physical activity and prostate cancer, diagnosed
in 1988 or earlier (before widespread PSA screening was available), among
Harvard University alumni found an almost halving of prostate cancer incidence
rates among men aged 70 years or older who expended at least 4,000 kilocalories
per week in physical activity, compared with those expending less than 1,000
kilocalories per week (84). However, an updated analysis
of these men, examining prostate cancer diagnosed after 1988, did not support
the earlier observations (100). These inconsistent
findings may have been due to bias arising from increased screening for
prostate cancer among the most active men.
To examine the association between physical activity and colon cancer,
the Cancer subcommittee searched the Physical Activity Guidelines for
Americans Scientific Database. Because the association of physical
activity with colon and rectal cancer appears different (see rectal cancer below), we did not include studies where
colorectal cancer was the outcome of interest, as the relation between physical
activity and colon cancer likely would be diluted. The search yielded 23
publications eligible for inclusion in the present report.
The 23 publications reviewed represented 12 prospective cohort studies
and 8 case-control studies (134-140). Four of these
publications (137-140) pertained to different aspects of
the same case-control study. The database represented by the 23 studies was
large, including a total of 9,747 cases of colon cancer with approximately
equal distribution between the sexes (4,933 in men and 4,814 in women). The
studies were conducted in the United States (124-126;129;131;132;137-142), Europe (Denmark (28), Finland
(99;127), Italy (143), Norway (133), Sweden (128) and Switzerland (136)), and Asia
(China (134), Japan (130;135), and Taiwan (144)).
Overall, the studies consistently show an inverse association between
physical activity and the risk of developing colon cancer, with 9 of the 12
cohort studies and 5 of the 8 case-control studies indicating significant,
inverse associations with at least one domain of physical activity (e.g.,
occupational versus leisure-time) and/or in one sex. Across all the studies,
the median RR, comparing most with least active subjects, was 0.7. More
specifically, results were similar across the cohort studies (median RR = 0.8)
and the case-control studies (median RR = 0.7), as well as for men and women
(median RR in both sexes = 0.7). These findings, encompassing studies published
in 1995 and later in the Physical Activity Guidelines for Americans
Scientific Database, are comparable with findings from a recent review of the
literature on physical activity and colon cancer risk that also included
studies published before 1995 (145). In this recent
review, the median RR, comparing most with least active subjects across all
studies, also was 0.7 (median RR for men, 0.7; for women, 0.6).
For the prospective cohort studies, bias due to recall of physical
activity is unlikely because physical activity was assessed before the
development of colon cancer. Thus, any misclassification of physical activity
is likely to be random, diluting associations rather than causing spurious
inverse relations. The results also do not appear to be confounded by other
factors associated with colon cancer risk because many studies adjusted their
findings for several factors, including BMI, smoking, alcohol, diet (e.g.,
energy intake, intake of calcium and folate intake of fiber, vegetables, and
meat), use of aspirin, screening, menopausal status and use of menopausal
hormone therapy, and family history of colon cancer. In particular, the
findings appear independent of BMI, with most cohort studies (9 of 12) (28;124;125;127-130;132;133)
adjusting for this factor, and continuing to observe significant inverse
associations. However, fewer than half the case-control studies (3 of 8)
adjusted for BMI. Finally, the inverse associations observed are supported by
plausible biologic mechanisms. Thus, although the data on physical activity and
risk of developing colon cancer are based on observational epidemiologic
studies, the inverse associations indicated by these studies are likely to be
Several studies have examined whether the association between physical
activity and decreased colon cancer risk varies, depending on use of menopausal
hormone therapy (125;131), various
aspects of diet (125;139), or BMI
(125;128;130;134;138;142). The findings have been inconsistent, with the most
consistent being the suggestion that the adverse impact of high BMI on colon
cancer risk may be ameliorated by higher levels of physical activity (134;138;142).
Several studies also have examined whether physical activity has a
different association with colon cancers occurring at different subsites of the
colon. The data have been equivocal, with some studies suggesting a larger
magnitude of association for cancers occurring in the proximal colon (130;136;142),
while others have reported greater associations for cancers of the distal colon
(128;132). Most studies, however,
have observed equivalent associations or unclear differences across proximal
and distal sites of the colon (125;126;131;133;135;140;143).
All but one (99) of the studies classified subjects
according to at least 3 levels of physical activity, allowing investigators to
assess dose-response. In the cohort studies, 7 of 11 studies with at least 3
physical activity levels reported significant, inverse trends between physical
activity and colon cancer risk (124;126-128;130;132;133). For the case-control
studies, 4 of 8 also observed significant, inverse trends between activity
level and colon cancer risk (134;136;143;144). As
discussed above, because of the many different methods used to assess and
classify physical activity in these studies, it is difficult to ascertain the
shape of the dose-response curve, apart from noting that a dose-response
relation appears likely.
Most studies have assessed leisure-time and/or occupational physical
activity only, with one study also assessing active commuting, in the form of
walking or bicycling to work (134). Because of the
different questionnaires used to assess physical activity and the different
categories used to group subjects in the studies, it is difficult to integrate
the findings across the studies. Further, most studies presented their findings
according to overall volume of energy expended, and data are sparse on specific
kinds of activity associated with decreased colon cancer risk.
However, significantly lower risks of colon cancer have been observed
with leisure-time physical activity (ordered in approximately ascending doses
of physical activity) of at least twice a week for at least 10 minutes'
duration (142), at least 4 hours per week of
moderate-to-vigorous intensity recreational activity (131), at least 20 MET-hours per week of leisure-time
activity (144), more than 21 MET-hours per week of
leisure-time activity (132), 7 or more hours per week of
recreational activities including walking (126) a median
of 35.25 MET-hours per week of overall activity (130), a
median of 46.8 MET-hours per week of leisure-time activity (124), and more than 94.3 MET-hours per week of active
commuting (134). Additionally, the case-control study by
Slattery and colleagues suggests that physical activity needs to be vigorous in
intensity (137-140) to reduce colon cancer risk. Overall,
these data suggest that 30 to 60 minutes per day of moderate-to-vigorous
intensity physical activity may be needed to significantly lower the risk of
developing colon cancer.
In contrast to the associations observed between physical activity and
colon cancer, the data on physical activity and risk of developing rectal
cancer are far more mixed. More than half of the studies have reported no
significant associations (99;126;130;133;143;144;146), with the remaining studies
observing significantly lower risks (or of borderline significance) with higher
levels of physical activity (127;128;135;136;140). In a recent review of the literature on physical
activity and rectal cancer risk, the median relative risk, comparing most with
least active subjects across all studies, was 1.0, indicating little
association (130).
The available evidence for an association of physical activity with
reduced risk of lung, endometrial, ovarian, pancreatic, and other cancers is
less complete than that for breast, prostate, colon, and rectal cancers.
Therefore, the following sections present a general overview.
A review of the association of physical activity and lung cancer risk
was included within a recently published book chapter (145). At the time of that review, 15 cohort studies and 6
case-control studies had been published, overall indicating a median of 20%
reduced risk for lung cancer in the most versus the least active subjects. This
present review focused on studies published between 1996 and 2006. Results
indicate a 24% median reduction of lung cancer risk for the most versus least
active subjects (101;147-156). As
with the prior review, the reduction of risk was more obvious with case-control
(median RR over 2 studies = 0.61) (154;156) than with cohort studies (median RR over 8 studies =
0.77) (101;147-153). The inverse
relation of physical activity with lung cancer risk is similar for men (0.74, 8
studies since 1996) (101;147;149-153;156) and women (0.75, 6
studies since 1996) (147-149;152;154;156).
Most of the studies on the association of physical activity and lung
cancer adjust for cigarette smoking. However, even with this adjustment, the
potential for residual confounding is quite high. Three studies have reported
risk reductions specifically for current smokers, former smokers, or never
smokers (148;150;155). The risk reduction in these studies is more similar
for current and former smokers (median RR of 0.61 (148;150;155) and 0.59 (148;150), respectively) than for never
smokers (median RR of 1.03 for 2 studies reporting for this subgroup) (148;155). As yet, evidence is too
sparse to conclude that the reduction of lung cancer risk by physical activity
is isolated to current and former smokers.
The question of whether the association of physical activity with lung
cancer is due to residual confounding by smoking has been addressed in 2 ways:
examining consistency of association across histologic subtypes of lung cancer
and exploring the association in never smokers. Smoking is more clearly
established as a risk factor for some histologic subtypes of lung cancer than
others. Evidence links smoking more closely to small cell and squamous cell
lung cancers than to adenocarcinoma of the lung. Therefore, one indirect
approach to the question of whether the association of physical activity with
reduced risk for lung cancer is due to residual confounding by smoking status
is to evaluate whether the association is present for all histologic subtypes,
including adenocarcinoma. Three studies to date have examined whether the
association of physical activity is similar across most lung cancer histologic
subtypes, as well as within sex. In men, the median relative risks for lung
cancer for those who are most versus least active are 0.59, 0.96, 0.80, and
0.73 for small cell, squamous cell, adenocarcinoma, and other/nonspecified
histologic types, respectively (147;149;156). In women, the median RR
values for most versus least active among the same subtypes are 0.81, 0.77,
0.86, and 0.56, respectively (147;148;156). This evidence suggests that
the physical activity association is present across histologic subtypes,
including adenocarcinoma. Another approach to determining whether the overall
association of physical activity and lung cancer is due to residual confounding
by smoking is to study non-smokers. The RR (or odds radio) for non-smokers was
1.32 and 0.74 in the one cohort and one case-control study to report an
association specifically for non-smokers (148;155). It also should be noted that the 39% risk reduction
for most versus least active current smokers pales in comparison to the
reduction of risk from quitting smoking. Smoking cessation remains the most
important means to reduce lung cancer risk among smokers. That stated, it would
be of interest to understand better the potential mechanisms by which physical
activity may assist in marginally reducing lung cancer risk among current and
former smokers. To our knowledge, no research has directly addressed this
A review of the association of physical activity and endometrial cancer
risk was included within a recently published book chapter (145). At the time of that review, 4 cohort studies and 11
case control studies had been published, overall indicating a median relative
risk of 0.70 for the most versus the least active subjects. An update of that
review, focusing on studies published since 1996 reported a similar median RR
(0.70) for the 15 most recently published studies, which included 7 cohort
studies and 8 case-control studies (157-171). Of these
more recent studies, 5 include relative risks that are adjusted for multiple
variables but not for BMI (157-160;171). The median RR of 0.73 for these studies is similar to
the results after adjustment for BMI, which was 0.70. This is important because
the effect of physical activity on body weight has been hypothesized to mediate
the purported association of physical activity with reduction of risk of
endometrial cancer.
Another factor that should be accounted for in analyses is menopausal
hormone therapy, given the potential causal link between use of unopposed
estrogen therapy and increased risk of endometrial cancer. For example, the
median RR from the 3 case-control studies that adjusted for menopausal hormone
therapy was 0.70 (165;168;170) (no cohort studies published to date have adjusted for
this factor) compared to a median RR of 0.68 for the 10 case-control and cohort
studies that did not adjust for menopausal hormone therapy (157-164;169;171).
Overall, evidence indicates an inverse association between physical
activity and incidence of endometrial cancer. Further, the lack of change in
the median relative risks for studies that did versus did not adjust for BMI or
menopausal hormone therapy may indicate that the association is not mediated
through obesity or the generally healthy lifestyle commonly associated with
exogenous hormonal exposure.
The association of physical activity with incidence of ovarian cancer
was explored in a meta-analysis and systematic review published late in 2007
(172). This review concluded that a modest inverse
association exists, with a weighted pooled RR of 0.81 (95% confidence interval
was 0.72-0.92). Sensitivity analyses indicated no difference of findings when
summarized studies did versus did not adjust for BMI (which may be on the
causal pathway) and for exogenous hormone use (e.g., oral contraceptives).
A total of 8 cohort studies (173-180) and 2
case-control studies (181;182) have
examined whether physical activity may reduce incidence of pancreatic cancer.
Case-control studies may be particularly biased for pancreatic cancer, given
that at diagnosis most patients have advanced disease, are symptomatic, and
often have recent weight loss. Four of the 10 cited case-control studies of
pancreatic cancer adjusted for BMI in multivariate models. In the 5 cohort
studies that did not adjust for BMI (173-177), the median
relative risk for the association of physical activity with pancreatic cancer
incidence was 1.21. One of the case-control studies provided an odds ratio (OR
= 0.78) for men that was not adjusted for BMI (182). Both
of the case-control studies provided odds ratios for women that were not
adjusted for BMI; the average of these was 0.82 (181;182). In spite of this inconsistent evidence, when taken in
combination with the observation of a weak positive association with BMI (177;183), it remains possible that a
level of physical activity sufficient for weight control would be associated
with reduced incidence of pancreatic cancer.
The potential for physical activity to reduce incidence of other cancers
(e.g., thyroid, kidney, bladder, and hematopoietic) also has been studied.
Reviews of these cancers are not included here because the data are too sparse
to allow any conclusions regarding a potential relation with physical
inactivity. Readers are referred to other reviews for an overview of results
from these studies (2;145).
A common definition of "cancer survivor" is any individual who has had a
diagnosis of cancer, from the point of diagnosis and for the balance of life.
Cancer survivors are a subset of the US adult population that is expected to
grow substantively in the coming decades. As such, the role of physical
activity in improving outcomes for cancer survivors is likely to increase in
importance as well. Recently, data have been published regarding the effects of
physical activity on health outcomes among persons who already have cancer.
These studies suggest that physically active individuals with breast or colon
cancer may have improved prognosis (i.e., fewer recurrences and deaths),
compared with sedentary survivors. In addition, physical activity may play an
important role in preventing, attenuating, or rehabilitating late and long-term
effects of cancer treatment. Walking is a commonly prescribed form of exercise
in the studies reviewed here and appears to have benefits on muscular strength
and endurance, as well as quality of life. Dose-response effects and long-term
outcomes are unknown for any outcomes from physical activity interventions in
cancer survivors at this time.
More than 10 million people in the United States are cancer survivors,
and more than 16% of adults older than age 65 years are cancer survivors (184). The increasing success of cancer treatments has
required a shift in focus toward new outcomes, such as preventing recurrence
and mortality, and accommodating the unique medical and psychosocial needs of
cancer survivors.
Cancer treatment typically includes some combination of surgery,
radiation therapy, or chemotherapy, and may also include hormonal therapies,
steroid treatment, immunotherapies, or monoclonal antibody treatment. Each of
these therapies is associated with acute as well as late and long-term adverse
physiologic and psychological effects. The terms "late effects" or "long-term
effects" (185) are distinct in the timing of their onset.
Late effects are side effects or complications that are absent or subclinical
at the end of therapy but that emerge after compensatory systems fail or some
second insult (e.g., deconditioning) occurs that results in a clinically
significant diagnosis that can be traced back to effects of treatment. An
example of a late effect would be the diagnosis of a cardiac arrhythmia years
after treatment with a cardiotoxic chemotherapeutic agent such as adriamyacin
(186). Long-term effects are adverse effects or
complications that appear during treatment and persist long afterward, for
months, years, or the duration of life. Physical activity could be useful for
preventing or attenuating some late and long-term effects of cancer treatments
(Figure G7-1) (187), and may also be useful for
prevention of recurrence or cancer mortality among cancer survivors.
The acute effects of treatment and the potential for positive effects of
physical activity during active cancer treatment are beyond the scope of this
review, but have been reviewed elsewhere (188;189). Also not reviewed here are the late or long-term
effects of childhood cancer treatment, as little research has been conducted in
this area.
Though few studies have been conducted on the role of physical activity
in preventing cancer recurrence or reducing mortality, the consistent findings
of a preventive effect warrants comment. Data from the Nurses' Health Study
were used to explore the dose-response association of physical activity with
overall and breast cancer specific mortality, as well as recurrence, among
2,987 breast cancer survivors over a median of 96 months of follow-up (190). The results indicated a 29% decrease in overall
mortality among women who did at least 3 MET-hours per week of aerobic activity
after diagnosis, with minimal additional protection from greater levels of
physical activity. The decrease in breast cancer-specific mortality and
recurrence were 50% and 43%, respectively, in women who engaged in at least 9
MET-hours per week of physical activity compared with women who did less than
3. Additional benefits were small for activity levels greater than 9 MET-hours
per week, which can be translated to 3 hours per week of walking at 2.5 miles
per hour. Considerable evidence indicates that overweight, obesity, and weight
gain are associated with breast cancer recurrence (191-193). These results are consistent with the hypothesis
that physical activity reduces risk of mortality or recurrence among breast
cancer survivors through weight control.
Evidence for a role of physical activity in colon and colorectal cancer
survivorship comes from 2 recently published observational studies. One of
these, the Nurses' Health Study, observed an inverse dose-response association
of physical activity and overall and colorectal cancer-specific mortality in
554 women who had had a previous diagnosis of colorectal cancer. Women who
engaged in at least 18 MET-hours per week of physical activity after diagnosis
had a 61% and 57% reduced risk of colorectal cancer-specific and overall
mortality, respectively, compared to women who did less than 3 MET-hours per
week (194). A dose-response association of physical
activity and colon cancer disease-free survival also was seen in the cohort of
832 male and female patients who participated in the CALBG trial (195). In this latter cohort, 18 MET-hours per week, or 6
hours of walking per week at 2.5 miles per hour, was associated with a 49%
reduction in risk of recurrence (195).
A number of recent systematic reviews (188;196-205) as well as 2
meta-analyses (188;206) have
recently been conducted on the effects of physical activity interventions on a
variety of outcomes in cancer survivors. Readers interested in an in-depth
discussion of the effects of exercise on cancer survivors are guided to these
reviews. Below, the effects of exercise training on late or long-term effects
is reviewed for outcomes for which there is the greatest amount of evidence and
consensus and that may be most useful in guiding quantitative or qualitative
behavioral recommendations for cancer survivors. Of the 22 controlled clinical
trials published since 1995 and reviewed here, only 1 (207), examined a dose-response pattern of exercise training
on any outcome, and none was noted. For each of the outcomes reviewed below,
effects of walking programs are noted, if such data were available. Most of the
studies reviewed were relatively short in duration (6 months or less);
long-term effects are not yet known.
Cardiorespiratory Fitness. Though the effect of
physical activity on cardiorespiratory fitness has been long established (see
Part G. Section 2: Cardiorespiratory
Health for a detailed discussion of this topic), it is of
particular relevance for cancer survivors given the cardiotoxic effects of
several commonly used cancer treatment drugs and radiation to the chest (186;208). A meta-analysis published in
2005 indicated a strong weighted mean effect size of 0.65 (P=0.003)
for cardiorespiratory fitness based on the 4 exercise interventions that had
assessed this outcome in cancer survivors after treatment (188). Since this meta-analysis, 9 additional RCTs have
assessed whether various of exercise interventions in cancer survivors improve
cardiorespiratory fitness after treatment (209-217). All
13 studies have shown positive effects, and 11 showed statistically significant
improvements on cardiorespiratory function tests ranging from a 6-minute walk
test to maximal treadmill or cycle ergometer tests. All of these studies
included breast cancer survivors, and most included only breast cancer
survivors. Fitness improvements have been demonstrated in a variety of
programs, including walking, yoga, tai chi chuan, exercise at home, and
exercise at fitness facilities. For most of the studies, exercise doses used
were 3 weekly sessions of 20 to 40 minutes in duration at moderate
Muscular Strength and Endurance. Observational evidence
in small convenience-sample studies suggests that muscle mass may decrease and
fat mass may increase after some breast cancer chemotherapy regimens (218). Cancer treatment may result in a decrease in activity
(219), with subsequent deconditioning associated with
muscle disuse. Therefore, it is important to determine whether exercise
training improves muscular strength or endurance in cancer survivors. Six
studies have examined the effects of some form of resistance training, tai chi
chuan, or yoga on muscle strength or endurance (211-213;215;220;221). All of these studies were
conducted in women who had completed breast cancer treatment. Five observed
positive effects of training (211;213;215;220;221) and 4 reported statistically significant improvements
(211;213;215;220) in strength or endurance
Flexibility. Cancer surgeries may result in decreased
range of motion with scarring or tissue trauma, and these changes may result in
altered physical function. Six studies have examined the effects of exercise
training on flexibility. Three assessed effects of aerobic exercise or yoga on
lower body flexibility with the sit-and-reach test in breast and colon cancer
survivors (207;215;222). All 3 showed improvements in flexibility, but only one
(207) observed a statistically significant improvement
comparing changes between treatment and control participants. Three other
studies examined effects of tai chi chuan, dance and movement, or aerobic
exercise and stretching on shoulder range of motion in breast cancer survivors
(211;223;224). All 3 noted improvements, and 2 noted significant
between-group differences in shoulder range of motion (211;223).
Lymphedema. Surgical removal or irradiation of lymph
nodes results in damage to the lymphatic system that can result in an inability
of the affected body part to manage fluid balance and temperature regulation.
This damage may impair immune response and wound healing, as well as response
to trauma or injury. Swelling and pain in the affected body part can develop
immediately after surgery and/or radiation or years later, making lymphedema a
long-term risk among several types of survivors, including those with breast,
head and neck, melanoma, genital cancers, lower gastrointestinal tract and
bladder cancers. Lymphedema is considered a chronic condition, and occurs in 6%
to 50% of breast cancer survivors, depending on number of nodes removed and
intensity of radiation (225-227). Lower-limb lymphedema
also occurs in 20% to 30% of cancer patients who have had lymph node removal or
radiation in the groin or retroperitoneal lymph nodes (228-237). Four studies have examined the risk of lymphedema
onset or worsening among breast cancer survivors by measuring changes in arm
circumferences or symptoms resulting from exercise training (217;221;224;238). None of these studies has noted negative effects of
aerobic or resistance exercise on arm circumferences or symptoms; evidence of
possible benefit to the affected limb has not been examined. No studies of the
safety or efficacy of exercise for cancer survivors with or at risk for
lymphedema for cancer sites other than breast have been conducted.
Weight Change. Some breast cancer patients gain weight
after diagnosis, and the associated changes in body composition may include
decreased muscle mass and increased body fat, as suggested by a few
convenience-sample studies (218). These effects have not
been examined in population-based or clinical trial series of patients, nor in
patients with other cancers. However, it is important to determine the effects
of exercise training on body weight and body composition in survivors who have
had any type of cancer treatment. The results of the 13 identified controlled
trials conducted since 1995 indicate that, as for the general population,
exercise may decrease percent body fat to a small degree, but has little to no
effect on body weight in the absence of concurrent caloric restriction (188;207;210-215;217;222;239-241). (See Part G.
Section 4: Energy Balance, for a detailed discussion of the
association between physical activity, weight loss, and changes in body
Quality of Life. The effect of exercise on
health-related quality of life was examined in a systematic review and
meta-analysis published in 2005 (188). This review
concluded that evidence was strong for a positive effect of physical activity
on quality of life in cancer survivors, though the weighted mean effect size of
0.30 was not statistically significant. Since the publication of that
meta-analysis, an additional 10 studies have examined effects of physical
activity on cancer survivors after treatment (209;213-217;223;224;240;242). Of these, all showed positive effects, and 8 indicated
a statistically significant improvement in at least one quality of life
indicator after a physical activity intervention. Overall, 10 out of 13
identified studies showed statistically significant improvements in quality of
life resulting from a physical activity intervention after cancer
Fatigue. Cancer-related fatigue is distinct from
ordinary types of fatigue in its persistence and severity (243). The effects of physical activity interventions on
fatigue in cancer survivors (primarily breast cancer) have been tested in 8
studies since 1995. Of these 8 trials (207;209;210;214;216;222;239;244), 3 reported statistically significant improvements in
fatigue after a program of aerobic exercise, walking, or cycling. Five other
studies, most of which focused on walking programs among breast cancer
survivors during the time period after treatment, observed improvements, but
not statistically significant improvements. The mechanisms through which
physical activity may improve cancer-related fatigue are not yet fully
understood (243).
A number of plausible mechanisms might explain the associations between
physical activity and cancer risk and prognosis. Increased physical activity
reduces adiposity, which may explain reductions in cancers that are associated
with overweight and obesity, including postmenopausal breast, colon,
endometrial, and other cancers. Increased physical activity is associated with
reduced levels of sex hormones, which may explain a link between physical
activity and hormone-related cancers such as breast and endometrial cancers.
Another possible mechanism is through the effect of physical activity and
inflammation and immune function. Finally, increased physical activity reduces
insulin resistance, which could explain associations with risk for some
cancers, such as colon cancer, that may be increased in individuals with
insulin resistance or hyperinsulinemia.
Physical activity could affect cancer risk or progression through
several plausible mechanisms (245). Many of these
mechanisms may act through the effects of physical activity on obesity, with
resulting changes to circulating levels of adipokines, cytokines, insulin, and
sex hormones. Other mechanisms may involve direct effects on target organs and
tissues. The effects of physical activity on carcinogenesis or prognosis are
likely to be multi-factorial and may be affected by many factors such as age,
sex, and adiposity, in addition to physical activity specific factors such as
type, duration, frequency, and intensity of physical activity.
Several modifiable menstrual factors increase breast cancer risk,
including early age at menarche, frequent ovulation, regular cycles, and late
age at menopause (246). Women with elevated levels of
estrogens and androgens have increased risk of developing breast cancer. In a
combined analysis of 9 large cohort studies, postmenopausal women in the top
quintile for various estrogens or androgens had approximately double the risk
of developing breast cancer compared with women in the lowest quintile (247).
Elevated levels of estradiol or testosterone in premenopausal women increase
risk of breast cancer as well (248;249). Medications that block estrogen receptors or that
prevent estrogen production in peripheral tissues have been a mainstay of
treatment for women with estrogen receptor positive breast cancer (250). Women with elevated estrogen concentrations (unopposed
by progesterone) are at an increased risk for endometrial cancer (251). In men, anti-androgen therapy improves prostate cancer
survival (252) and reduces overall incidence of the
disease when tested as a preventive agent (253). However,
recent evidence suggests that blood levels of androgens or estrogens are not
related to prostate cancer risk (247), suggesting that
only prostatic levels of sex hormones are relevant for prostate carcinogenesis
or progression.
The effect of physical activity on age at menarche, menstrual cycle
function, and level of ovarian-produced sex steroid hormone levels in girls and
young women are potential mechanisms for reduced breast cancer risk (254). Moderate-intensity physical activity may cause small
changes in reproductive hormones in premenopausal women, but high intensity or
volume of exercise sufficient to cause a negative energy balance may be
required to induce menstrual dysfunction (amenorrhea, anovular cycles and
luteal phase deficiency) with significantly decreased production of ovarian
estradiol and progesterone (255-263).
In postmenopausal women, increased physical activity has been associated
with decreased serum concentrations of estradiol, estrone, and androgens (264-266). The positive effect of physical activity is
closely linked to body composition because the primary source of estrogen in
postmenopausal women is from aromatization of androgen precursors in
peripheral, mainly adipose, tissue. In a sub-sample from the Women's Health
Initiative (WHI) Dietary Modification Trial, women with low self-reported
physical activity had higher levels of estrone, estradiol, and free estradiol,
and lower levels of sex-hormone binding globulin (which binds estradiol, making
less available to target tissue) than did active women (265). The highest levels of estrogen were observed in women
who were both below the median level for physical activity (i.e., less than 6.5
MET-hours per week, approximately less than 1.5 hours per week of brisk
walking) and above the median BMI (i.e., at least 29 kg/m2).
In an RCT, 173 overweight, sedentary postmenopausal women were assigned
to a moderate-intensity aerobic exercise, 45 minutes per day, 5 days per week
for 12 months or to a control group. A significant decrease in estradiol,
estrone, and free estradiol was seen from baseline to 3 months in exercisers
versus controls, with an attenuation of the effect at 12 months (267). However, in those women who lost body fat, the
exercise intervention resulted in a statistically significant reduction in
these estrogens at both 3 and 12 months. Similarly, in women who lost body fat,
a statistically significant decrease in testosterone and free testosterone
occurred in exercisers compared with controls (268).
These intervention and observational studies results suggest that both
increased physical activity and reduced body fat will produce the greatest
protection against breast cancer by producing the greatest decrease in serum
sex hormones.
Chronically lowered testosterone concentrations have been reported in
athletes, but this finding may require a threshold amount or intensity of
physical activity to occur (269), and the effects of
moderate-intensity aerobic exercise on sex steroid hormones in men is not
known. In a recent trial, 102 men aged 40 to 75 years were randomly assigned to
a 12-month moderate to vigorous intensity aerobic exercise intervention (60
minutes per day, 6 days per week) or a control group (no change in activity)
(270). Dihydrotestosterone (DHT) increased 14.5% in
exercisers compared to 1.7% in controls at 3 months (P=0.04). At 12
months, DHT remained 8.6% above baseline in exercisers versus a 3.1% decrease
in controls (P=0.03). Sex hormone binding globulin increased 14.3% in
exercisers versus 5.7% in controls at 3 months (P=0.04), while at 12
months it remained 8.9% above baseline in exercisers compared to 4.0% in
controls (P=0.13). No statistically significant differences were
observed for testosterone, free testosterone, 3α-Diol-G, estradiol, or
free estradiol in exercisers versus controls. Therefore, the association of
physical activity with circulating hormone levels in men is still unclear.
Insulin resistance has been linked to increased risk of breast, colon,
pancreas, endometrial and stomach cancers (271). Higher
cancer incidence and mortality also have been noted in those with type 2
diabetes or impaired glucose tolerance (271;272). Insulin can enhance tumor development by stimulating
cell proliferation or inhibiting apoptosis (271). It also
can regulate the synthesis and biological availability of sex steroid hormones,
and inhibit hepatic synthesis of sex hormone binding globulin (271). Acute bouts of physical activity improve insulin
sensitivity and increase glucose uptake by skeletal muscle for up to 12 hours
(273), and chronic exercise training results in prolonged
improvements in insulin sensitivity (274-276). Although
body composition has been strongly associated with insulin sensitivity,
exercise-induced changes in insulin sensitivity can occur from physical
activity, independent of the changes in weight or body composition (273;274;277). An
additive effect of resistance training to improve insulin sensitivity and
glycemic control also has been proposed because skeletal muscle is a primary
site of insulin resistance (273;278).
Women with elevated levels of prolactin are at increased risk of breast
cancer (279), and a recent clinical trial found that
increased physical activity levels as measured by increased VO2max
over 1 year in a moderate-intensity exercise intervention was associated with
statistically significant reductions in prolactin levels in postmenopausal,
overweight women (280).
Elevated levels of pro-inflammatory factors, such as C-reactive protein
(CRP), interleukin (IL)-6, tumor-necrosis factor-α (TNF-α), and
decreased levels of anti-inflammatory factors, such as adiponectin, have been
linked with increased cancer risk (281). Physical
activity may reduce systemic inflammation alone or in combination with body
weight or composition through reducing macrophage or adipose cell production of
inflammatory cytokines in adipose tissue, although exact mechanisms are unknown
Although cross-sectional studies support an association between chronic
physical activity and lower levels of the inflammatory markers CRP, serum
amyloid A (SAA), IL-6 and TNF-α in both men and women, intervention
studies of exercise alone or exercise and diet combined have had inconsistent
results, with some studies but not others showing reductions in these
inflammatory markers (282).
Increases in adiponectin have been seen with physical activity
interventions in the presence of significant weight loss (283). Shorter duration prospective physical activity and
weight loss interventions have failed to alter adiponectin levels despite
modest changes in body weight and body composition (278).
The immune system is thought to play a role in reducing cancer risk by
recognizing and eliminating abnormal cells or through acquired and/or innate
immune system components (284). The role of physical
activity on immune factors related to cancer has been largely untested, but one
hypothesis is that physical activity could improve the number or function of
natural killer cells, which play a role in tumor suppression (282).
Bouts of physical activity have been shown to result in acute increases
in a number of components of immune function (e.g., neutrophils, monocytes,
eosinophils, and lymphocytes), followed by a dip below pre-exercise levels
lasting up to 1 to 3 hours (285). For chronic physical
activity, an inverted J-shaped dose-response relation between intensity of
physical activity and immune function has been shown. Moderate physical
activity results in enhanced immune function, but exhaustive exercise,
overtraining, or high-intensity exercise may lead to immunosuppression, which
may result in increased susceptibility to ailments such as upper respiratory
infections (282). However, the current evidence on
moderate-intensity physical activity from randomized controlled trials is
inconclusive, with differences in components of the innate immune system noted
in some, but not all, cross sectional studies that compare exercisers to
non-exercisers. Randomized controlled trials of moderate physical activity show
little effect on immune function (282).
Physical activity also could mediate cancer risk through additional
mechanisms, such as its effects on other body structures. For example, physical
activity affects colon motility, leading to decreased transit time and,
perhaps, reduced carcinogen exposure in the colon (254).
In addition, physical activity has been hypothesized to affect various tissues
leading to reduced carcinogenic prostaglandin (PG) production (286), although an RCT found no effect of a 12-month aerobic
exercise intervention (1 hour per day, 6 day per week) on colon mucosal
prostaglandins PGE2 or PGF2alpha in 202 men or women aged 40 to 75 years (287).
Increased physical activity is associated with reduced risk of several
cancers. Most evidence for this association is available for breast and colon
cancers, although growing evidence suggests an association between increased
physical activity and reduced risk of endometrial and lung cancers. Overall,
data suggest that 30 to 60 minutes per day of moderate-to-vigorous intensity
physical activity may be needed to significantly lower the risk of developing
breast and colon cancers. The effect of physical activity is larger for colon
cancer (median reduction in risk of 30% across reviewed studies) compared with
breast cancer (median reduction in risk of 20% across studies). A large part of
the effect of physical activity on cancer is likely mediated through obesity
and other hormonal and metabolic mechanisms. Randomized controlled trials have
demonstrated effects of physical activity interventions on cancer risk factors,
which further support a role of physical activity in reducing risk for
Strong evidence links increased physical activity in cancer survivors
with improved quality of life and increased fitness. Less evidence is available
regarding the effect of physical activity on cancer recurrence and survival. A
2006 publication from the American Cancer Society (3)
states that although the current public health guidelines of 30 to 60 minutes
of moderate-intensity aerobic exercise 5 times per week have not been studied
systematically in cancer survivors, there is no reason to think that this would
not also benefit survivors. Overall, results indicate that guidelines for
cardiovascular exercise for cancer survivors who have completed treatment need
not be different from those of the general population, and that particular
physiologic and psychosocial effects of cancer and its treatments are
positively affected by cardiovascular exercise, resistance training, and
flexibility training.
Knowledge about the role of physical activity in reducing the risk of
common cancers would benefit from additional evidence gathered from clinical
trials. In the survivorship setting, clinical trials showing a benefit of
physical activity interventions on reducing deaths, recurrences, and reducing
the impact of late or long-term treatment effects, also would make a valuable
contribution to our understanding of the needs of this growing population.
Other research needs include studies to clarify biological mechanisms
linking physical activity to specific cancers in order to identify associations
with less commonly studied cancers, define the shape of dose-response curve of
the physical activity-cancer relation, determine the effect of low-intensity
activities and accumulated bouts, and assess the effect of physical activity
within specific population subgroups.
Additional observational epidemiologic research to identify the dose,
type, and frequency of physical activity on risk of various cancer sites and
subtypes is needed, in addition to identifying the effect of physical activity
on risk of specific cancers within particular population subgroups including
various race/ethnic, age, sex, and groups at elevated risk of cancer.
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Structural Steel Educational Council
The Structural Steel Educational Council (SSEC) is a nonprofit corporation organized under the laws of the State of California in 1975, for the purpose of producing and distributing educational material. The groups served are educational institutions, public officials, architects, engineers, and other persons or agencies involved with the use of structural steel in construction. This educational material is made available in the publication titled Steel TIPS.
The SSEC also helps sponsor educational seminars and events focused
on assisting design professional and engineering students.
American Institute of Steel Construction (AISC)
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Electroslag Welding Facts for Structural Engineers

subset: commoncrawl


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Date published: 2018-06-09


text:
DEAR DR. FOX: I have two Irish setters, a 7-year-old male and a 12-year-old female. For a few years, they would nose around the backyard grass as if looking for something. I couldn't see anything.
DEAR DR. FOX: I have two Irish setters, a 7-year-old male and a 12-year-old female. For a few years, they would nose around the backyard grass as if looking for something. I couldn't see anything.
Two weeks ago, my husband laid some sod in some bare sections of our yard. Overnight the dogs started pulling it up, eating the dirt and leaving the grass wherever it fell.
I feed them dry Purina mixed with half a can of Pedigree each. What are they lacking — iron? B.A., Alexandria, Va.
DEAR B.A.: You are right that dogs, humans and other animals will eat dirt when they are suffering from anemia. But your dogs are more likely exercising their innate nutritional wisdom, seeking organic trace nutrients and digestive- and immune system-enhancing bacteria in the soil.
Since they are both getting on in life, one of my geriatric suggestions is to provide them with digestive enzymes and probiotics, available in health stores, better pet supply stores and from holistic veterinary practitioners.
The kinds of manufactured pet foods you are giving to your dogs could be improved upon. Try to reduce the grain/cereal content and increase the nutrient value of their food. You can feed them wholly or partially on my home-prepared diet, detailed on DrFoxVet.com.
When they are outdoors, let them eat dirt! ... In moderation.
DEAR DR. FOX: We fed a feral cat for the last six years. Once our elderly indoor cats died, we enticed the feral one indoors. He now sleeps in the house and loves to avoid the cold and bad weather by coming indoors.
The problem will be when we move sometime later this year. What kind of sedative will help a cat "chill out" for a 9� hour car trip? Also, he is used to going outside daily. How do we acclimate him to the new environment? He won't wear a collar, so I am fearful he will disappear. J.D., Belleville, Ill.
DEAR J.D.: I am so glad to hear that you were able to bring this feral cat inside. I would begin to acclimate him to his new environment now by not allowing him outside anymore except in a secure harness. Let him walk you around on the end of an attached leash.
Make indoor life fun with a cat condo and padded window shelves/perches so he can look out. Try installing a few bird feeders for him to gaze at — we call it cat TV for our two ex-feral cats who have never wanted to go back out by themselves again.
If he ever gets out at the new home, he is likely to try to get back to his old home environment. In case he ever does, be sure to have some good ID photos and have him microchipped.
Do not use any sedatives for the long journey, but get him used to sleeping and eating in the carrier. Keep a strip of gauze with a few drops of lavender essential oil in the car, which you can freshen after a few hours on the road.
Some readers have told me that when they take clippings from my column to their veterinarians, they are not always well received. I received flak some years ago when I cited studies from England supporting my contention that dogs, especially smaller ones and those who are not overweight, will gradually heal from torn knee cruciate ligament injuries if physical activity is restricted. My detractors insisted that surgery is the only solution.
Now a study by Dr. K.L. Wucherer and others, published in the Journal of the American Veterinary Medical Association, reports that almost two-thirds of a study group of medium and large-sized, overweight dogs not treated with surgery had successful outcomes when evaluated after a course of treatment including anti-inflammatory medication, weight loss diet and physical therapy.
My advice is to try this approach before costly surgery. If knee surgery is done, follow this same nonsurgical treatment protocol after the operation.
DEAR DR. FOX: I have a standard poodle who is about 7 years old. He developed sores and flaking skin on his nose that wouldn't go away. It seemed to expand to around his nostrils.
I took him to the vet, and he said my dog likely had lupus but could not tell for sure without a biopsy. I was saddened by this preliminary diagnosis. The crustiness would improve and get worse. Home treatment of Vaseline improved the appearance.
After a few months, I took him in for the recommended biopsy, which appeared painful and was also expensive. It turned up nothing but a crusty nose. Since then, I've looked online and found the problem is reported to be a common cosmetic issue. I treat it successfully with Blistex.
Now, I have two questions. Should my vet have been able to diagnose the crusty nose without all the cost and trauma of a biopsy? Also, is crusty nose truly benign and nothing to worry about? J.G., St. Louis
DEAR J.G.: I have seen this kind of condition in standard poodles, and it certainly can be a lupus-like autoimmune disease, which I've seen lead to lesions around the nose, lips and face and broken and bleeding toenails.
Taking a biopsy can help in the diagnosis of autoimmune disease versus a benign skin condition, such as solar dermatitis or allergic contact dermatitis. In many instances, a treatment trial with antihistamine or steroid cream — or my formula of 10 drops each of frankincense, myrrh and helichrysum in 100 drops of olive or almond oil, applied two to three times daily — can be more cost-effective and less distressing for the canine patient. Increasing the amount of omega-3 fatty acids in the daily diet may also help.
Send mail to email@example.com or to Dr. Michael Fox in care of Universal Uclick, 1130 Walnut St., Kansas City, MO 64106. Visit Dr. Fox's website at DrFoxVet.com.


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Baseball is back, and soon Washington Nationals Park will be swarming with fans eager to see their team try to build on the momentum with which they ended last season.
The park itself has undergone some changes since fans saw it last. From new concessions to improved technology, here are a few new things to look out for this season at Nationals Park:
1.) New Restaurants Popping up Everywhere
- G at Nationals Park (Section 136, in partnernship with D.C.-based chef Mike Isabella)
- South Capitol Sushi (Section 129)
- Intentional Wok (Section 233)
- Chesapeake Crab Cake (Section 114)
- Bullpen Burrito (Section 140)
- Kettle Corn (Section 108)
2.) Added Locations and Expanded Menus for Old Favorites
- Two more District Drafts stands added in Sections 118 and 225
- Another Ben's Chili Bowl added on the main concourse behind Section 141
- A second Change Up Chicken added in Section 129
- Expanded menu for first exclusively vegetarian concession stand, Field of Greens (Section 113)
- Third Hard Times Cafe added in Section 310
3.) New Fan Spaces
- Norfolk Southern Club (formerly the Stars and Stripes Club), now including South Capitol Grill
- Gold Glove Club
- Silver Slugger Suite
- Heineken Red Star Bar
- Clubhouse Team Store Ladies' Boutique
4.) Wi-Fi Ugrades
The Nationals are doing everything in their power to improve the park's Wi-Fi network, which was sorely lacking. Kudos on the effort!


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840 Deltona Blvd. St. F-1
Deltona, Florida 32725
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