relative risk for mortality of 25%, 20%, and 12%,
respectively. There were stronger associations for
leukemia/lymphomas and breast cancer, but not
enough studies for other cancers to differentiate
effect sizes (Pinquart and Duberstein, 2010). And as
a generic health effect: across 148 studies, the effect
size was OR = 1.50 (95% CI 1.42 to 1.59), 50%
more likelihood of survival with stronger social
relationships, a finding consistent across age, sex,
initial health status, cause of death, and follow-up
period (Holt-Lunstad, 2010).
On the other hand, there is the question how
effective psycho-social interventions are. There was
initial enthusiasm based on successful interventions
(Spiegel, 1989); (Fawzy, 1993), but larger RCTs
have not been able to replicate these results
(Kissane, 2007). Still, it is interesting that in one
study, both control and treatment groups had half the
mortality risk of those who declined to participate in
the study (Boesen, 2007). And another study showed
that those who reduced their degree of depression in
the first year had improved survival, irrespective of
being in the control or treatment group (Giese-
Davis, 2011). An important complexity in this field
is that seeking support has become very normal, and
cancer patients may do so independent of a formal
support group. For example, even the simple yes/no
answer to the question ‘Do you have someone to talk
to in the 3 months after your diagnosis?’ correlated
with a 30% increase (for ‘yes’) in survival after 7
years (Maunsell, 1995). And a review of the psycho-
oncological literature concluded (Garssen, 2004)
that one of the most consistent findings is that: the
more hopelessness and helplessness are experienced,
the more unfavorable the cancer progression is
(Watson 1999); (Goldberg, 1996); (Schulz 1996).
2.2.2 Stress
A next potential factor is the effect of chronic
stress. Potential pathways run via increased cell
aging and and telomere shortening (Epel, 2004);
(Puterman, 2010), increased DNA damage and
hampered DNA repair (Flint, 2007), reduced
immune function (Segerstrom, 2004), increased
levels of inflammatory cytokines (Bower, 2007), and
stress-induced activation of the sympathetic nervous
system (SNS) and hypothalamic–pituitary–adrenal
(HPA) axis which results in the production of
catecholamines and cortisol, which have direct
effects on epithelial cell growth and tumor
vascularization (McGregor, 2009). Besides, there are
higher order mechanisms like stress-induced
depression (for example, depression raised mortality
in men for melanoma, colon and prostate cancer
with 67%: Almeida 2010), reduced self-efficacy and
self-care (Miller, 2001) or the 90% increased cancer
risk due to low perceived quality of life (Flensborg-
Madsen, 2011). For an overview of biological
mechanisms, see McGregor (2009). Next, one study
found that men who experienced high levels of
stress were more than three times as likely to have
elevated PSA levels (Prostate Specific Antigen) than
were men who experienced low levels of stress
(Stone, 1999). And using the breast/prostate cancer
analogy, another large study showed that African
American women who experienced more emotional
stress due to discrimination (on the job, on the street
and by the police) had a 48% increased risk of
developing cancer after six years (Taylor, 2007).
In terms of interventions, cognitive-behavioral
therapy (Philips, 2008) and well as yoga
(Raghavendra, 2009) and meditation programs
(Biegler, 2009) have resulted in lower cortisol
levels, as well as improved mental health and quality
of life (Nidich, 2009); (Beard, 2011); (Chambers,
2011). Survival impacts are not always clear or
made explicit. When they do appear they seem
dependent on improvements in relation to depression
(Giese-Davis, 2011) hopelessness (Garssen, 2004) or
quality of life (Flensborg-Madsen, 2011); (Spiegel
2011).
2.2.3 Physical Activity
Two different effects exist between physical activity
and cancer. The first effect is that sedentary behavior
increases cancer risk, independent of BMI (Body
Mass Index) or other activity. Sedentary behavior is
associated with adverse cardio-metabolic and cancer
mortality; in a review of 18 cancer studies has been
associated with increased colorectal, endometrial,
ovarian, and prostate cancer risk (Lynch, 2010). The
second effect is that vigorous exercise helps reduce
cancer risk. Already in the College Study, running
for over 40 years and following 50.000+
participants, a more than 30% reduction in cancer
mortality risk due to physical exercise across all
cancers was found, including prostate cancer when
exercise is heavy (Paffenbarger, 1986). As one
hypothesized pathway, heavy exercise decreases
testosterone, which in turn is linked to lower prostate
cancer risk.
The EPIC study found an inverse association
between advanced prostate cancer risk and
occupational physical activity - which is inversely
correlated with inactivity throughout the day - but
not with leisure activity (Johnsen, 2009). A study
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