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Publication of the International Union Against Cancer
Publication de l’Union Internationale Contre le Cancer
Int. J. Cancer: Supplement 10, 13–17 (1997)
r 1997 Wiley-Liss, Inc.
DIET, NUTRITION AND PROSTATE CANCER
Graham GILES* and Paul IRELAND
Cancer Epidemiology Centre, Anti-Cancer Council of Victoria, Carlton South, Victoria, Australia
Although much has been written, little is known about the
causes of prostate cancer. Variations between populations in
the incidence of invasive cancers, together with changes in
the incidence of invasive cancers in migrants, have pointed to
environmental (lifestyle) factors that might be amenable to
intervention. Conversely, there is a lack of international
variation in the prevalence of microscopic tumours, so the
essential question is: what causes only some of the common
microscopic tumours to become aggressive? Dietary factors
hold the most promise in this regard and have been the
subject of recent reviews. The strongest and most consistent
effects are positive associations with animal products such as
red meats, eggs and dairy foods, and possibly by implication,
fat. Evidence of a protective effect of fruit and vegetables is
weak and inconsistent, as is the relationship with vitamin A
and carotenoids, such as b-carotene. There are some interesting leads. Lycopene, the carotenoid found in tomatoes, has
been reported to be protective; a-tocopherol supplementation has shown a protective effect in one intervention study;
and vitamin D has been shown to be protective in a prospective study. Interest is also growing in phytoestrogens and the
extent to which dietary manipulation with these and other
phytochemicals might influence prostate cancer by modifying
male sex hormone levels or actions. There is limited evidence
of associations with obesity. It is not known whether these are
related to a particular dietary pattern or to possible physiological effects on the male’s hormonal milieu. Associations with
lean body mass are likely to be related to the action of
androgens during growth and development. Dietary and
nutritional effects on prostate cancer do not appear to be
strong, but they may be subtle and attenuated by measurement error. To explore these aspects further will require
large prospective studies that include improved (repeated)
dietary measurements and also blood sampling, so that
genetic polymorphisms can be adequately investigated. Such
studies are underway. Int. J. Cancer Suppl. 10:13–17, 1997.
r 1997 Wiley-Liss, Inc.
Prostate cancer is the leading cancer in males of many countries.
Little is known of its causes and nothing can be done to prevent it.
Prostate cancer epidemiology, particularly in regard to diet, presents
interesting challenges. In its microscopic histological form, prostate cancer attains a very high prevalence with increasing age, but
in few men does the small focus of cancer cells become invasive.
Many prostate ‘‘cancers’’ recorded by cancer registries are diagnosed incidentally during treatment for benign enlargement or by
screening using blood PSA levels. The observation that the
microscopic form (often termed ‘‘latent’’) is of equivalent prevalence in both high- and low-risk populations for the invasive form
of the disease supports the probability of a lifestyle exposure being
implicated in progression (Yatani et al., 1982). Further evidence of
environmental causes comes from the observation of marked
international variation and increased incidence in migrant populations from low- to high-risk communities. In Italian migrants to
Australia, for example, the risk of mortality from prostate cancer
increases with duration of residence, but even after more than 30
years remains less than the risk to the Australian-born (Geddes and
Buiatti, 1993).
Of the environmental and lifestyle factors that have been studied,
diet offers the most interesting leads, and has been the subject of
much epidemiological investigation. Ecological studies (Blair and
Fraumeni, 1978; Howell, 1974; Armstrong and Doll, 1975; Rose et
al., 1986) have shown striking correlations between international
prostate cancer mortality and per capita consumption of fat.
Measurement of diet in epidemiological studies at the level of the
individual has been extremely varied, and even the better ‘‘vali-
dated’’ methods perform badly. Because diet is poorly measured,
very large studies are needed to detect statistically meaningful
effects. The earlier generation of studies that examined diet and
prostate cancer were invariably small, used rudimentary dietary
instruments and further, were usually retrospective, relying on
recall. This has resulted in a confused picture of weak and
inconsistent findings.
METHODS
Two recent reviews (Key, 1995; Kolonel, 1996) were used as the
basis of a bibliographical search. Further studies were identified
from computer searches of standard bibliographical databases, but
were limited to reports in English. Studies were restricted to those
that measured dietary intakes or anthropometry; those based solely
on serum micronutrient concentrations were excluded from the
overview. Estimates of risk associated with dietary and anthropometric variables were extracted, with confidence intervals when
available. Care was taken to include null findings that were
reported without formal statistical estimates. Because the odds
ratios (ORs) and relative risks (RRs) were calculated for a variety
of different exposures, used a range of cut points and were often
adjusted for one or more factors, the unadjusted estimates were
usually chosen. Due to the heterogeneity of study design, exposure
measurement and analysis, no formal summary estimate of effect
was attempted. Measures of dietary exposure varied considerably
in scope and quality between studies. For this reason, the measures
were grouped into broad categories: meat, fat, alcohol, vegetables
and fruit. The inclusion of a study was sometimes based on a single
vegetable or meat (beef). The nutritional covariate most commonly
reported was obesity described by body mass index (BMI).
RESULTS
The majority of reports available for overview originated from
36 retrospective and 16 prospective studies. The studies are not
referenced here, but are included in the References. Only 2 of the
36 retrospective studies contained over 400 cases. Of the 16
prospective studies, only 3 contained over 400 cases. Further, the
methods used to collect dietary information were often rudimentary
and/or described in vague terms. Few studies combined adequate
sample size and good dietary assessments. Recently, studies have
begun to address disease status of cases and controls. Many have
included clinically insignificant cancers in their case series and, in
recent times, will have included screen-detected cancers of unknown clinical significance. These factors ensure that a significant
proportion of the findings discussed below will be spurious.
The overview is summarised in Table I. This lists the number of
retrospective and prospective studies separately and gives the
number of positive (OR or RR $ 1.1) and negative (OR or
RR # 0.9) associations reported. The number of statistically significant ORs or RRs is given in parentheses, and the range of
significant ORs and RRs is given to identify the strength of effect.
Because of subgroup analysis, the sum of associations is sometimes
greater than the number of studies.
Fat
Dietary fat appears to be the strongest environmental risk factor
for prostate cancer yet identified. Even so, the evidence is
*Correspondence to: Cancer Epidemiology Centre, 1 Rathdowne Street,
Carlton South, VIC 3053, Australia. Fax: 61-3-9279-1210. e-mail:
ggg@accv.org.au
GILES AND IRELAND
14
TABLE I – SUMMARY OF REPORTED ASSOCIATIONS (ODDS RATIOS/RELATIVE RISKS)
WITH DIETARY INTAKES AND OBESITY
Retrospective studies
Studies
Total fat
Animal fat
Meat
Dairy products
Eggs
Fruit
Vegetables
Vitamin A/retinol
b-carotene
Alcohol
Obesity
14
10
10
7
7
2
7
8
6
9
17
Prospective studies
Associations
Positive1
Negative2
Range3
12 (3)
12 (3)
11 (3)
4 (4)
6 (1)
2 (0)
4 (0)
4 (0)
3 (0)
5 (1)
7 (2)
6 (0)
6 (0)
0 (0)
0 (0)
1 (0)
1 (1)
12 (2)
2 (1)
4 (0)
5 (0)
0 (0)
1.4–1.7
1.7–2.8
1.7–2.6
1.6–3.1
2.1
0.4
0.3–0.5
0.4
1.9
4.0–4.4
Studies
2
3
10
7
5
8
6
1
3
6
10
Associations
Positive1
Negative2
1 (0)
4 (1)
7 (3)
3 (2)
3 (0)
2 (0)
5 (0)
1 (1)
1 (1)
2 (0)
8 (3)
1 (0)
0 (0)
3 (0)
2 (0)
2 (0)
2 (0)
4 (2)
1 (1)
1 (1)
1 (0)
1 (0)
Range3
1.6
1.6–2.6
1.4–2.4
0.6–0.7
0.4–2.8
0.2–1.9
1.3–2.4
ORs/RRs $ 1.1 (numbers in parentheses are statistically
ORs/RRs
#0.9 (numbers in parentheses are statistically significant).–3Range, lowest to highest statistically
significant ORs/RRs.
1Positive,
inconclusive. Fat intake is often implied from certain food sources
that are high in fat, and it is often difficult to discern whether fat per
se or some other property of these foods is the important exposure.
A total of 16 studies reported total fat intake. These yielded 13
OR/RR estimates $1.1 and 6 estimates #0.9. Only 3 were
statistically significant, ranging from 1.4–1.7. Of the 13 studies that
measured fat from animal sources, 16 had OR/RR estimates $1.1
and 6 #0.9. Only 4 estimates were statistically significant, ranging
from 1.6–2.8. Some studies (Kolonel et al., 1983, 1988; West et al.,
1991) reported a different effect of fat with age, with low risks
under age 70 and increased risks over age 70.
Animal foods
Meat is a fairly heterogeneous entity when measured in epidemiological studies. We concentrated on beef in this overview. Its
relationship to cancer risk could include the following: an effect of
meat alone, an effect of the fat contained in meat, or an effect of
carcinogens created in cooking or some other correlate of meat,
e.g., low vegetable intake. There is no convincing evidence to
support any of these hypotheses. Of the 20 studies included, 18
gave OR/RR estimates $1.1 and 3 #0.9. Of these, 6 OR/RR
estimates were statistically significant, ranging from 1.6–2.6. The
highest OR of 2.6 was reported by Bravo et al. (1991). The highest
RR was 2.64 (Giovannucci et al., 1993); after multivariate
adjustment this was reduced to 1.9.
Fourteen studies measured intake of dairy products. These
produced 7 OR/RR estimates $1.1 and 2 #0.9. There were 4 ORs
significantly $1.1 (range, 1.6–3.1) and 2 RRs $1.1 (range,
1.4–2.4). Associations with eggs were reported in 12 studies. Of
these, 9 estimates were $1.1 and 3 were #0.9. Only one OR was
statistically significant at 2.1 (Walker et al., 1992).
Plant foods
Ten studies, 2 retrospective and 8 prospective, reported on fruit
consumption. Of these, 3 were negative and 4 were positively
associated with risk. Only one retrospective study (Negri et al.,
1991) gave a statistically significant OR of 0.4.
Vegetables were measured in various ways in different studies.
Altogether, 13 studies reported on at least one vegetable or
vegetable group. These yielded 9 positive associations and 16
negative associations that included 4 significant OR/RRs. Carrots
were found by Walker et al. (1992) to give an OR of 0.5; green
vegetables were found by Negri et al. (1991) to give an OR of 0.3;
and tomato consumption was found by Mills et al. (1989) and
Giovannucci et al. (1996) to give RRs of 0.6 and 0.65, respectively.
Dietary b-carotene was estimated in 9 studies, 4 of which gave
estimates $1.1 and 5 #0.9. Only one study (Hsing et al., 1990)
significant).–2Negative,
yielded significant results. In this prospective study, men ,75 years
old had increased risk associated with b-carotene, RR 1.9 (1.0–
3.7), and men older than 75 had reduced risk, RR 0.2 (0.1–0.6).
Alcohol
Alcohol consumption appears to have little association with
prostate cancer risk. Of 8 earlier retrospective studies that included
alcohol, none gave an OR that was significantly different from 1.0.
A similar pattern was observed in the 6 prospective studies.
However, Hayes et al. (1996) published an OR of 1.9 (1.3–2.7)
from a large case-control study. This study was unusual in that
elevated risk was observed at very high levels of alcohol consumption.
Obesity
Obesity was reported in most studies as BMI. Of the 17 reports
from retrospective studies, only the study of Talamini et al. (1986)
yielded a statistically elevated OR of 4.0 that increased a little after
adjustment to 4.4. For comparison, there were 10 prospective
studies that reported associations with BMI. Of these, 8 OR/RR
estimates were $1.1 and one was #0.9. Three of the elevated RRs
were statistically significant, the 2 largest being 2.4 and 2.5
(adjusted) from Snowdon et al. (1984).
For a measure that is fairly accurate, the BMI results are fairly
inconsistent. This may be due in part to the failure of BMI to
distinguish between lean and fat mass. Lean mass is related to
androgen supply and may be positively associated with prostate
cancer risk (Severson et al., 1988). On the other hand, fat mass is a
source of androstenedione that can be aromatised to form oestrogens that might be protective against prostate cancer.
Studies that have examined height (Kolonel et al., 1988;
Whittemore et al., 1995; La Vecchia et al., 1990; Severson et al.,
1988) have found no associations. There has been one report of an
association with high birth weight (Tibblin et al., 1995).
Other foods and nutrients
Dietary vitamin A was estimated in various ways in 9 studies, of
which 3 gave negative and 6 gave positive associations. Only 2
studies produced statistically significant estimates. The case control study of Negri et al. (1991) gave an OR of 0.4. Hsing et al.
(1990) in a prospective study showed a similar effect to that for
b-carotene. Men below age 75 had an increased RR of 2.8, and men
older than 75 had reduced RR of 0.4. A protective effect of
a-tocopherol has been observed in one intervention trial (ATBC
Cancer Prevention Group, 1994), suggesting that this micronutrient
might be worth following up in other studies. However, concentrations of vitamin D [1,25-(OH)2 D in serum] shown to be protective
DIET, NUTRITION AND PROSTATE CANCER
in a prospective study (Corder et al., 1993) have not been
confirmed in another (Braun et al., 1995).
In summary, much of the evidence of associations between diet
and prostate cancer is weak and inconsistent. This is related to the
small size and quality of many of the retrospective studies, and
poor dietary measurement in some of the prospective studies. The
data from the better prospective studies suggest that animal
foods/fat and carotenoids are significantly associated with prostate
cancer risk and, further, possibly interact with each other and with
age. These aspects merit further follow-up in prospective cohort
studies that use validated dietary instruments, and that are of a size
to provide sufficient statistical power to examine interactions.
Ideally, research should be performed in populations that demonstrate a wide range in levels of intake.
FUTURE RESEARCH
It is important that the trend towards specifying the nature of
cases of prostate cancer is continued and improved. We are
interested in discovering the causes of clinically significant disease
rather than the cause of common microscopic foci of cancer. To this
end, it might be useful to collect blood and tissue samples against
the day when molecular and genetic markers will be available to
explore this avenue further. We do not know, for example, how
dietary intakes might interact with genetic factors that control the
androgen receptor or 5 a-reductase.
There is probably little to be gained from conducting more small
case-control studies of diet and prostate cancer that measure diet
poorly. When the current generation of case-control studies is
completed, it will be time to plan new research that has newly
refined objectives and methods. There are now several large
prospective cohorts of men that will yield considerable numbers of
prostate cancer over the next 5–10 years. Provided that these
studies have measured diet in a reasonable way, they may offer
more evidence of effects. Better dietary assessment will continue to
be a long-term goal. In cohort settings, advances in dietary
assessment methods can be built fairly easily into repeated
measures made at periodic follow-ups. It is also important that such
studies collect anthropometric measures of lean and fat mass to be
able to qualify our understanding of the risks associated with
obesity.
There remains an important role for ecological studies in
contemporary nutritional epidemiology. While it is true that
ecological studies are most appropriate for generating hypotheses
which then can be tested in case-control and cohort studies, the
extent to which ecological studies are being used for this purpose in
current prostate cancer epidemiology is not evident. Foods that are
only now being recognised as potentially protective for prostate
cancer could have been identified as useful leads from comparison
of high- and low-risk populations several decades ago. Tomato use
15
in southern Europe and soya bean products in Japan are just 2
examples. We need to broaden our horizons when thinking about
diet. While nutrients may be important determinants of cancer risk,
there are many other possibilities in terms of foods, non-nutritive
components of foods and food preparation practices.
Australian contributions
Two studies, a large case-control study and a prospective cohort
study, are underway in Australia that are designed to overcome
some of the shortcomings of previous efforts (Giles, 1990). The
case-control study is being conducted in Melbourne, Sydney and
Perth and will enroll over 2,000 cases and an equal number of
age-frequency-matched population-based controls. Cases are restricted to adenocarcinomas of moderate to poor differentiation,
and we are also collecting staging data and information on the
mode of detection. We are collecting blood from every case and
from a sample of controls. The dietary instrument is a 121-item
FFQ that was developed for the cohort study, and is used in
combination with graded pictures of food portions obtained from
pilot studies of weighed food records from over 900 Melburnians.
This instrument has been validated in a sample of the cohort study
and performs comparatively well (Ireland, 1996). For example, we
have correlated its estimate of protein intake against urinary
nitrogen output and have obtained a Pearson’s R of 0.25 for males
and 0.37 for females. This compares favourably with the correlations for females found when validating the Oxford and Cambridge
dietary instruments used in the EPIC cohort studies (0.24 and 0.15,
respectively) (Bingham et al., 1995).
In our Australian cohort of 17,000 men, we used the dietary
instruments described above and have also measured anthropometric indices, including body impedance, in order to explore the
question of obesity associations being related to lean or fat mass.
The cohort was aged 40–69 at recruitment; they are now 5 years
older. Men of southern European birth (Italy, Greece and Malta),
who were deliberately oversampled to add dietary range to the
study population, represent 28% of the sample. Extensive questionnaire data were collected on lifestyle exposures, tobacco, alcohol,
physical activity and other factors. A blood sample was collected
from each individual, and aliquots were stored in liquid nitrogen
and as dried blots on Guthrie cards. The study centre also runs the
population-based cancer registry and routinely links with the death
register to identify endpoints.
Together, these studies address the issues identified with disease
characterisation, dietary assessment, anthropometry, tissue collection, population sampling and statistical power. In regard to the
ability to further the dietary investigation of some of the newer
micronutrients of interest, they are currently limited by the
availability of food tables for many phytochemicals, including
carotenoids and phytoestrogens.
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