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Epidemiology Branch, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709;
* Nutrition Unit, General Clinical Research Center, Emory University School of Medicine, Atlanta, GA 30322; and
Department of Epidemiology and Population Health, Albert Einstein College of Medicine, Bronx, NY 10461
2To whom correspondence should be addressed. E-mail: terry2{at}niehs.nih.gov.
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ABSTRACT |
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 TOP ABSTRACT LITERATURE CITED |
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KEY WORDS: • (n-3) • (n-6) • breast neoplasms • prostate neoplasms • hormone-dependent
The convincing protective effects of dietary long-chain (n-3) fatty acids on breast and prostate cancers observed in various animal models and mechanistic experiments in vitro have not been supported clearly by the results of epidemiological studies (1,2). Several reasons for this discrepancy have been suggested, including the higher levels of exposure used in the animal and in vitro studies, the occurrence of measurement error in the epidemiological studies, together with other methodological issues (2), and the more general difficulty of extrapolating the results of animal experiments and in vitro studies to free-living humans (1). Nonetheless, an increasing number of epidemiological studies of marine fatty acids intake and cancer have been published in recent years, and these studies have, to various degrees, attempted to address the conceptual and methodological issues identified previously (2). In this review, we update our previous review of marine fatty acids and cancers of the breast and the prostate (2), which included studies before 2003, by including the results of recent epidemiological studies, and we discuss possible biological mechanisms and directions for future research.
Our review includes relevant articles currently available in the MEDLINE and CANCERLIT databases; we used a variety of keywords and terms for the various malignancies. We obtained additional published reports by cross matching the references of relevant articles. Virtually all published reports are in English, and we have restricted our review to those. We excluded studies where levels of long-chain (n-3) fatty acids or fish consumption were reported only in terms of mean intake levels (3–7). Several figures were constructed to summarize the results of epidemiological studies. In rare instances, when several control series were used in comparison with a single case series (a rare occurrence), only the results from analyses using population-based controls are included. In a few instances, we impute CIs for relative risk estimates, for example, when we derive summary estimates from results that were presented only over strata of a third variable. Imputed CIs are marked in the figures by "?".
Eicosapentaenoic acid (EPA)3 and docosahexaenoic acid (DHA) are PUFA found mainly in fatty fish, hence, they are often referred to as marine fatty acids. EPA and DHA can be biosynthesized in humans from 
-linolenic acid, sources of which include green leafy vegetables, flaxseed, canola oil, soybeans, and walnuts. However, the conversion of -linolenic acid by the body to the more active longer-chain metabolites is inefficient: <5–10% for EPA and 2–5% for DHA (8). A common feature of most of the proposed mechanisms by which marine fatty acids might lower cancer risk is the inhibition of eicosanoid production from (n-6) fatty acid precursors (9), which include linoleic acid, found primarily in vegetable oils, and arachidonic acid (AA), found mainly in animal products. Therefore, epidemiological studies increasingly have examined the interrelated effects of marine (n-3) and (n-6) fatty acids on cancer risk.
Breast cancer
Breast cancer is the most commonly diagnosed cancer among women and is the leading cause of female cancer mortality in the world (10,11). The estimated annual incidence is one million cases worldwide, 200,000 cases in the United States, and 320,000 cases in Europe (11–13). A comparison of breast cancer data worldwide shows tremendous variation in both incidence and mortality rates, with greater than 5-fold differences observed between low-risk and high-risk areas (10,14). In the United States, breast cancer incidence rates have been rising slowly for the past 2 decades (15).
Differences in eating patterns across countries suggest several dietary components that could possibly affect breast cancer risk. The focus of this review is on long-chain (n-3) fatty acids, although other dietary factors have been investigated in relation to breast cancer, including consumption of fat, meat, fruits, vegetables, and soy products, among others (16,17). The results of migrant studies suggest that the observed geographic differences in breast cancer incidence are due, at least in part, to differences in environmental exposures. For example, dietary factors are thought to be most responsible for the change in incidence rates among migrants (18), although correlated changes in lifestyle factors, such as obesity and physical activity, may also play important roles.
Recent cohort studies of marine fatty acids intake and breast cancer.
At least 7 cohort studies (19–25) and 6 case-control studies (26–31) of long-chain (n-3) fatty acids or fish consumption and breast cancer risk were published recently. In a prospective cohort study of breast cancer of 35,298 Singapore Chinese women (314 cases), Gago-Dominguez et al. (20) analyzed data from a validated 165-item FFQ that included 14 items on seafood consumption. In contrast with the results of Stripp et al. (23), this study found long-chain (n-3) fatty acid intake was inversely associated with breast cancer, with a 30% reduction in risk among women with the highest intake compared with those with the lowest intake. However, (n-3) fatty acid intake from sources other than fish (e.g., meat, oils) was not clearly associated with risk. An inverse association was also observed with fish or seafood intake of 
40 g/d. The inverse association with fish and marine fatty acids was stronger for breast cancers in advanced stages. Furthermore, although (n-6) intake was not associated with risk overall, a positive association was observed with (n-6) intake among women with low intake of marine fatty acids.
Stripp et al. (23) used information from a validated 192-item FFQ that included 24 specific questions on fish to examine the association of total fish consumption with breast cancer risk in a prospective cohort study of 23,693 postmenopausal women (424 cases) in Denmark. That study, conducted in a country with relatively high per capita marine fatty acids intake (32), found an 
50% increased risk among women with the highest compared with the lowest total fish consumption. The type of fish consumed (fatty vs. lean) had no clear effect modification. However, the positive association with total fish consumption was limited to estrogen-receptor (ER) positive (ER+) tumors. Specifically, high fish consumption was associated with a statistically significant 14% increased risk of ER+ tumors; no association was observed with ER– tumors. An earlier case-control study (33) found an inverse association between fish consumption and ER– tumors but no association with ER+ tumors. Because some environmental contaminants found in fish (e.g., organochlorines) have estrogenic effects, it has been suggested that such contamination may have nullified or exceeded the beneficial effects of the (n-3) fatty acids with respect to the ER+ tumors (23). Although plausible, the majority of epidemiological studies do not clearly support an association between circulating levels of organochlorines (34,35) or other endocrine disrupters and breast cancer risk.
Pala et al. (22) examined erythrocyte DHA and EPA levels in 4052 postmenopausal women (71 cases) in a prospective cohort study in northern Italy. That study found an approximate halving of breast cancer risk among women who were in the 2nd or 3rd tertile of erythrocyte marine fatty acids levels compared with women in the 1st tertile. The inverse association was more pronounced for DHA than for EPA. Italy is a country with relatively low per capita intake of marine fatty acids, similar to that in the United States (32). In a case-control study nested within the New York University Women’s Health Study Cohort (197 cases), serum EPA and DHA levels were not clearly associated with risk nor were other fatty acids that were examined (24). Women in the highest quartile of serum EPA levels had a relative risk of 0.85; 95% CI: 0.44–1.65 compared with those in the lowest quartile level. The corresponding relative risk for DHA was 0.70; 95% CI: 0.35–1.40. Dietary intake of (n-3) relative to (n-6) fatty acids was not examined. The association with fatty acids was not affected by menopausal status. Similarly, in a case-control study nested within the Malmo Diet Cancer Cohort (237 cases), erythrocyte membrane EPA and DHA levels were not associated with risk nor was the ratio of total (n-3) to total (n-6) (25).
Holmes et al. (21) examined fish consumption in the Nurses’ Health Study, a prospective study of 88,647 female nurses followed for 18 y (4107 cases) with 5 assessments of diet by validated FFQ. In this study, total fish consumption was not clearly associated with breast cancer risk (>0.40 vs. 
0.13 servings per day) for premenopausal or postmenopausal women. Similarly, the Pooling Project examined data from validated FFQs in a pooled analysis of 351,041 women (200 cases) participating in 8 prospective cohort studies in North America and Western Europe (19), including two of the studies reviewed above (21,24). In this pooled analysis, no association was observed with total fish, seafood, or shellfish. Other than shellfish, this study did not account for the type of fish consumed.
Recent case-control studies of marine fatty acids intake and breast cancer. Two recent case-control studies of fish consumption were conducted in China and Japan (28,30), countries with relatively high per capita intake of marine fatty acids (32). Dai et al. (30) used a 76 food-item FFQ to assess consumption of fish (total, freshwater, and saltwater) and other dietary factors in a population-based case-control study of breast cancer in China (1459 cases). Higher total fish consumption was associated with increased breast cancer risk, a finding driven by the positive association with freshwater (but not saltwater) fish. The results were not clearly modified by cooking method or doneness, which have been associated with exposure to heterocyclic amines (2). In a population-based case-control study of breast cancer in Japan, Hirose et al. (28) used a 16 food-group FFQ to assess consumption of fish (fresh and dried/salted) (2385 cases). Among postmenopausal women, both fresh and dried/salted fish were inversely associated with risk. Women in the highest quartile level had a 22–25% decreased risk. Among premenopausal women, there was no association with fresh fish and there was a suggestion of increased risk with higher consumption of dried/salted fish.
Three recent case-control studies were conducted in the United States, a country with relatively low per capita intake of marine fatty acids (32). Using data from a 95 food-item FFQ, Shannon et al. (26) examined total fish consumption in a population-based case-control study of postmenopausal breast cancer in western Washington. Risk decreased by 30% for women with the highest (>0.43 servings/d) compared with the lowest consumption levels (0–0.13 servings/d), with a statistically significant trend. However, no information was given on the type of fish consumed. Goodstine et al. (29) examined fish consumption and marine fatty acids in a population-based case-control study of breast cancer in Connecticut using both population-based and hospital-based control series (565 cases). That study found no association with EPA or DHA separately but found an inverse association with increasing ratio of EPA plus DHA to total (n-6), particularly when only population-based controls were used as the comparison group. When examined by menopausal status, the inverse association was observed primarily among premenopausal women. Bagga et al. (31) examined breast adipose tissue levels of (n-3) and (n-6) fatty acids in a case-control study using cases and controls (women undergoing reduction mammoplasty for mastomegaly) recruited at Kaiser Permanente Medical Center in California. That study found an inverse association with both marine fatty acids (EPA and DHA) and the ratio of marine fatty acids to (n-6) and a positive association with (n-6). There was no association with levels of the short-chain (n-3) -linolenic acid.
Aggregated epidemiological evidence for marine fatty acids and breast cancer. Most epidemiological studies that have addressed the role of marine fatty acids and breast cancer risk have done so only indirectly through the examination of total fish consumption. The amounts of EPA and DHA relative to other fatty acids contained in fish vary between species, with relatively high amounts found in fatty fish, such as salmon, mackerel, sardines, and herring, species that are generally native to cold waters (9,36), and relatively little in lean fish, which typically are native to warmer waters. Thus, different types of fish may have different effects on processes related to cancer development. Assumptions regarding the type of fish consumed (and therefore EPA and DHA intake) can be made from the per capita intake of marine fatty acids (when such estimates are available). For example, total fish consumption in a Scandinavian population might reflect a greater intake of fatty fish than the same total fish consumption in a population in the United States, given the up to 5-fold greater per capita intake of (n-3) fatty acids in Scandinavia (32).
The results of seven prospective cohort studies (21,37–42) and 16 case-control studies (26,28,30,33,43–54) that have examined the association between total fish consumption and breast cancer risk are shown in Figures 1and 2 (relative risk estimates for the highest vs. lowest category of exposure and 95% CIs are shown in the log scale). These studies examined total fish consumption only, so that information on individuals’ intakes of specific marine fatty acids is lacking. Therefore, we considered the per capita intake of marine fatty acids in classifying the results of studies into two groups: those from countries with low per capita intakes of marine fatty acids (<0.25 g/d) (Fig. 1) and those from countries with high per capita intakes of marine fatty acids (0.25 g/d) (Fig. 2). Although most tend to show weak, statistically nonsignificant inverse associations for women with the highest fish consumption compared with those with the lowest, the studies as a whole do not support a clear association between fish consumption and risk of breast cancer. No clear difference exists between studies conducted in countries with high and with low per capita marine (n-3) intake. Three studies examined fatty and lean fish and found no clear association with either of these measures and breast cancer risk (23,55,56). Thirteen epidemiological studies examined levels of EPA and DHA (22,24,25,27,29,31,40,57–61) or both of these fatty acids combined (20,62) (Figs. 3and 4). In general, these studies showed inverse associations for women with the highest compared with those with the lowest marine (n-3) intakes, although most of the relative risk estimates were not statistically significant. No clear pattern emerged for the source of the (n-3) measures, including diet and adipose tissue, serum, plasma, and erythrocyte membrane concentrations. In general, adipose tissue may provide the best measure of long-term intake of dietary fatty acids, whereas blood lipid fractions and erythrocyte membranes may provide a better measure of short-term intake (63). Although adipose tissue measures can discriminate between those who consume fish long term and those who do not eat fish, the exact nature of the dose–response relationship between marine fatty acids intake and tissue marker levels remains unclear (63).
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Prostate cancer is the third most common cancer among men, although this disease is notably more common in developed than in developing countries (10,11) The estimated annual incidence is 543,000 cases worldwide, 189,000 in the United States, and 155,700 in Europe (11–13). Trends in prostate cancer incidence have varied over time, although in the United States, as well as worldwide, prostate cancer incidence rates have been rising briskly over the past few years (11–13). Prostate cancer is the most common cancer diagnosed among men in the United States, where it is the second leading cause of cancer deaths (4). The severalfold difference in cancer incidence between high- and low-incidence regions and the changes in incidence patterns observed in migrant studies suggest, as they do with breast cancer, the importance of environmental factors in prostate cancer etiology (66,67). Although still controversial, dietary factors such as total fat (66–68) and lycopene (69) have been relatively consistent in their association with prostate cancer risk in epidemiological studies. The epidemiological evidence regarding marine fatty acids is reviewed below.
Recent epidemiological studies of marine fatty acids intake and prostate cancer. Using data from a validated 276 food-item FFQ, Mannisto et al. (70) examined total fish consumption and prostate cancer risk in a prospective cohort study of 29,133 male smokers (246 cases) in Finland. No clear association was found between prostate cancer risk and serum EPA, serum DHA, or dietary intake of these fatty acids. Although this study population comprised only smokers, no clear evidence was found overall for effect modification of the association with marine fatty acids by amount smoked. Similarly, Kristal et al. (71) examined EPA and DHA intake and prostate cancer (605 cases) using data from a validated 99 food-item FFQ in a population-based case-control study in Washington. They found no clear association with intake of marine fatty acids for early stage or late-stage tumors. The authors also reported no association with fish oil supplements.
In Japan, a country with one of the highest per capita intakes of marine fatty acids (32), Sonoda et al. (72) examined total fish consumption and prostate cancer risk in a hospital-based case-control study (140 cases) using information from a validated 106-item FFQ. That study found that men in the highest consumption category (>130 g/d) had a 55% decreased risk compared with men with the lowest category (<47 g/d). The inverse trend for fish consumption was statistically significant.
Augustsson et al. (73) examined intake of fish and marine fatty acids in 47,882 men (2484 cases) participating in the Health Professionals’ Follow-up Study, a large prospective U.S. cohort study that used a validated FFQ to obtain information on a wide range of dietary and lifestyle variables and cancer. Statistically significant inverse associations observed for both total fish and marine fatty acids intake were strongest for metastatic cancers. However, no association was found with the intake of fish oil supplements. Adjustment for potentially confounding variables, including linoleic and -linolenic acids, did not alter the findings for fish or marine (n-3) intake. In an earlier study from the same cohort with considerably fewer cases, intake of marine fatty acids from fish was inversely associated only weakly (P = 0.30) with the risk of advanced prostate cancer (74). In a study that examined data from the Swedish Twin Registry, total fish consumption (presumed to contain a high proportion of fatty fish based on national dietary patterns) was inversely associated with prostate cancer incidence and mortality (75). Leitzmann et al. (76) recently studied the association between dietary intakes of EPA and DHA in the Health Professionals’ Follow-up Study, but the results were inconslusive. There was a suggestion of an increased risk among men with a high ratio of linoleic acid to marine fatty acids compared with men with a low ratio; however, confidence limits were wide.
The aggregated epidemiological evidence for marine fatty acids and prostate cancer. The results of 5 prospective cohort studies (73,75,77–79) and 7 case-control studies (45,72,80–84) that examined the association between total fish consumption and prostate cancer risk are shown in Figures 6and 7. In countries with relatively low per capita marine (n-3) intake (Fig. 6), the tendency for case-control studies to show weak or moderate inverse associations with risk is not seen in the prospective cohort studies and, overall, no clear association with prostate cancer risk is apparent. In contrast, 3 studies of total fish consumption (72,75,80) conducted in countries with relatively high per capita marine (n-3) intake (Fig. 7) showed moderate-to-strong inverse associations with risk. Ten epidemiological studies examined levels of EPA and DHA (48,85–90) or both of these fatty acids combined (71,73,74) (Figs. 8and 9). These studies, nearly all of which were conducted in countries with relatively low per capita marine (n-3) intake, tend to suggest null associations with prostate cancer risk; no clear pattern emerged in the findings according to the source of the (n-3) measures, including diet, adipose tissue, serum, plasma, or erythrocyte membranes.
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Ample evidence from in vitro and animal studies shows that EPA and DHA can inhibit the progression of tumors in various organs, particularly the breast and prostate (91–93). Studies of both international and intranational secular trends showed inverse associations between per capita consumption of marine fatty acids and incidence and mortality rates of prostate (94) and breast cancer (95–99). However, the evidence from analytical epidemiological studies is less clear. Important methodological factors, such as sample size, adjustment for potentially confounding variables, the detail and quality of the dietary assessment, unmeasured changes in diet over time, the stage of cancer at diagnosis, and estrogen receptor status of breast tumors likely have contributed to the discrepant findings. Furthermore, although the results of several human and animal studies suggest that reductions in epithelial cell proliferation rates, mammary tumorigenesis, and PGE2 biosynthesis can best be achieved with a relatively high ratio of (n-3) to (n-6) fatty acid intake (e.g., 0.5 and higher) (100–104), few epidemiological studies of breast and prostate cancers have examined this ratio or effect modification by these or other fatty acids in stratified analyses (20). Nevertheless, those that have examined the interrelated effects of marine (n-3) and (n-6) fatty acids have tended to show inverse associations with higher intakes of marine fatty acids (20,31,57,58,62,76).
Epidemiological investigations have increasingly addressed several important methodological issues plaguing earlier studies, for example, by using validated FFQs that discriminate among fish species and various cooking practices. As a result, an increasing number of epidemiological studies have examined specific fatty acids, including EPA and DHA and the ratio of these to (n-6) fatty acids. Although this was an important step, FFQs differ with respect to their ability to accurately assess the absolute intake of these fatty acids in a population, and estimates of per capita intake of marine fatty acids may still be useful when comparing the results of studies from different regions (32). When results are examined according to the per capita intake of marine fatty acids, there is some indication of stronger inverse associations among studies conducted in populations with high compared with low intakes; however, the differences are not pronounced, and, overall, the available data are equivocal with respect to the associations between marine fatty acids and the risk of breast and prostate cancers.
Several mechanisms were proposed by which the intake of marine fatty acids might lower the risk of cancer. Among the most salient of these is the inhibition of eicosanoid biosynthesis from AA, a (n-6) fatty acid metabolized in the body from linoleic acid. Eicosanoids are a class of compounds derived from polyunsaturated acids and include prostaglandins, hydroxyeicosatetraenoic acids (HETE), and leukotrienes. Prostaglandins are oxygenated, unsaturated cyclic fatty acids that perform various hormone-like actions. Prostaglandins converted from AA by the cyclooxygenase-2 enzyme, notably PGE2, have been linked to carcinogenesis in several types of studies: animal experiments of mammary tumor development; studies of the proliferation of breast and prostate cancer cell lines in vitro; and human studies of fish oil intake, epithelial cell proliferation rates, and PGE2 biosynthesis (9,105,106). Tumor cells typically produce large amounts of AA-derived PGE2, which may impede immune system function, possibly through their role in the generation of suppressor T cells (107–109). Marine fatty acids inhibit cyclooxygenase-2 and the oxidative metabolism of AA to PGE2 (9). EPA and DHA also inhibit lipoxygenases (5-, 12-, and 15-lipoxygenases), which metabolize AA to HETEs and leukotrienes. 12-HETE has been linked to the suppression of apoptosis, stimulation of angiogenesis, stimulation of tumor cell adhesion, and expression of the invasive phenotype (9). Lipoxygenase inhibitors were discussed as a potentially important class of chemopreventive agents (110).
Eicosanoids derived from AA may also be involved in other processes related to cancer progression as well as cancer initiation. These include alteration of tumor cell membranes (91), increased oncogene expression (9,111), formation of cytotoxic peroxidation products (9,112,113), inhibition of mitosis (114), promotion of insulin resistance (115), and modification of estrogen metabolism (116). Several recent studies focused specifically on DHA and its role in the development of breast and prostate cancers. For example, DHA may activate peroxisome proliferator-activated receptor-
(9), ligands of which have shown antiproliferative effects in vitro on prostate cancer cell lines (117). DHA also improves the response of breast tumors to cytotoxic agents (118).
In conclusion, it is too early to make recommendations regarding fish consumption in the prevention of hormone-mediated cancers. Recently, studies have begun to examine potential effect modification among specific fatty acids and to account for the possible variation in findings according to the stage of cancer at diagnosis and the hormone receptor status (of breast tumors). These practices, along with continuing attention to the accurate measurement of long-term diet, assessment of potential confounding variables, and enrollment of adequate sample sizes for stratified analyses, may help to reconcile the disparate findings.
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ACKNOWLEDGMENTS |
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FOOTNOTES |
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3 Abbreviations used: AA, arachidonic acid; DHA, docosahexaenoic acid; EPA, eicosapentaenoic acid; ER, estrogen receptor; HETE, hydroxyeicosatetraenoic acid; PGE2, prostaglandin E2.
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LITERATURE CITED |
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TOPABSTRACTLITERATURE CITED |
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0.25 g/d).
