Sociología del ocio

As shown in Table 1.4, sixteen case-control studies examining the effect of PUFA on breast cancer incidence have been conducted in populations across the globe, including Asian (n=3) [275-277], European (n=7) [99, 104, 269, 278-281], the U.S. (n=3) [285-287], Latin American (n=2) [283, 284], and Saudi Arabian (n=1) [282] populations.

two earlier case-control studies conducted among Asians [275, 276] reported results for only total PUFA intake without considering the different classes (e.g., ω-3 and ω-6). Shun-Zhang et al. reported increased breast cancer risks for women with higher intakes of total

polyunsaturated fatty acids, and the effect was stronger when polyunsaturated fatty acids were considered as a continuous variable (13 grams/day increase) versus tertiled [275]. Lee et al. reported increased breast cancer risk for total PUFA intake among postmenopausal women, but a risk reduction for premenopausal women [276]. However, both these earlier case-control studies included small sample sizes resulting in imprecise estimates of the PUFA and breast cancer association.

A third Asian case-control study, which was larger and conducted among a Korean population, examined the effects of total ω-3 fatty acid intake and LC ω-3 PUFAs [277]. The study reported risk reductions for all three exposures (e.g., total ω-3, DHA, and EPA), with stronger risk reductions seen among postmenopausal women consuming higher quantities of EPA and DHA. However, Kim et al. failed to estimate effects for ω-6 fatty acids and the relative intake of ω-3 and ω-6 PUFA intake in this Korean population. While Kim et al. had a larger sample size (N=718) than the earlier Asian studies, the effect estimates were still imprecise, even more so when stratified by menopausal status. Additionally, Kim et al. sampled controls from patients who attended the same hospital as the cases and received health check-ups and/or cancer screening [277]. This selection of hospital-based controls has the potential to bias the effect estimates if the distribution of ω-3 fatty acid intake differs between those attending the hospital versus the source population, and thus limiting the external validity of the study findings. Therefore, the conclusions from Asian case-control studies that examined the effects of PUFA intake and incidence of breast cancer are limited

due to a variety of reasons, including the lack of examination of all PUFAs, relative intake of ω-3 and ω-6 fatty acids, and issues with internal and external validity. However, among the few that have considered ω-3 alone, breast cancer risk reductions are apparent, but

information on ω-6 and the relative balance are not well studied.

Seven European case-control studies have been conducted regarding PUFA intake and breast cancer incidence [99, 104, 269, 278-281]. Results for total PUFA intake are inconsistent, with some reporting risk reductions [99, 104, 279] and two reporting an increased risk [278, 280]. One European study examined the effect of only LA intake, and reported increased risk for breast cancer for women consuming high intakes of LA (Quartile 4 versus 1 OR = 1.22; 95% CI = 0.89, 1.68) [280]. The estimate was stronger among premenopausal women (Quartile 4 versus 1 OR = 1.46; 95% CI = (0.86, 2.49). Another European study reported a 20% breast cancer risk reduction for total ω-3 fatty acid intake (Quintile 5 versus 1 OR = 0.8; 95% CI = 0.7, 1.0) [281]. However, both of these studies did not examine the effect of the relative intake of ω-3 and ω-6 PUFAs within their respective European populations. These differences in reported results could reflect differences in intake of different polyunsaturated fatty acids across different populations (e.g., ω-3 versus ω-6), differences in control sampling methods (e.g., hospital-based versus population-based controls), and differences in covariate adjustment sets.

One European case-control study comprehensively examined (including ω-3 subtypes, ω-6 subtypes, and the relative balance of ω-3 and ω-6 fatty acids) the effect of PUFA on breast cancer incidence [269]. Another comprehensive case-control study examined the effect of ω-6 (LA, AA, total ω-6 intake) and ω-3 (ALA, DPA, EPA, DHA, total ω-3) fatty acids on breast cancer incidence among a French-Canadian population in

Montreal [269]. However, the reported effect estimates were not consistent with the biologic plausibility of ω-3 and ω-6 fatty acids. Nkondjock et al. reported increased risks for ω-3 fatty acids and risk reductions for ω-6 fatty acids [269]. Also, a 26% increase in breast cancer risk was observed for the highest quantile of ω-3:ω-6 intake (Quartile 4 versus 1 OR = 1.26; 95% CI = 0.86, 1.86) [269]. In comparison, a 58% increase in breast cancer risk was observed for the third quartile of intake ω-3:ω-6. It is possible that in this population the consumption of ω-3 fatty acids is not enough, and that the dietary habits of this French- Canadian population resemble those of other North American populations where intake of ω- 6 fatty acid dominates. This may explain why the reported associations are not consistent with the animal and laboratory studies.

A few other case-control studies were conducted among Uruguayan [283], Saudi Arabian [282], and Mexican [284] populations. De Stefani et al. reported effects that are not consistent with the biology in their Urugauyan population, with increased risks for ALA, a long-chain ω-3 fatty acid and risk reduction for LA, a ω-6 fatty acid [283]. Aloithameen et al. reported only effects for total PUFA intake in a Saudi Arabian population [282]. The only comprehensive assessment of PUFA intake was conducted among a Mexican population and reported risk reduction for total ω-3 intake, increased risk for total ω-6 intake, and risk reduction for the favorable ratio of ω-3:ω-6 intake. The estimated increased risk and risk reductions reported were even stronger when examined among only premenopausal women [284].

In the U.S., only three studies examined the association between PUFAs assessed using dietary intake measures and breast cancer incidence [285-287]. However, two of these studies reported opposite effect estimates for LA intake, with one reporting increased risks

[287], and another reporting a risk reduction [285]. Another study conducted in Connecticut [286] reported risk reductions for LCω-3 fatty acids (EPA and DHA) among premenopausal women only. However, a nearly 20% risk reduction was observed when examining the effect of the ratio of ω-3:ω-6 fatty acids on breast cancer risk among all women, and this risk

reduction for the ratio was more pronounced among premenopausal women (Quartile 4 versus 1 OR = 0.59; 95% CI = 0.29, 1.19). However, the study lacked a comprehensive measure of PUFA intake (including ω-3 subtypes, ω-6 subtypes, and ratio of ω-3:ω-6 fatty acids). Inconsistent effect estimates are observed among case-control studies conducted in the U.S. for the estimate of LA on breast cancer risk. Also, the studies conducted in the U.S. could benefit from a comprehensive assessment of PUFA intake utilizing a large population- based study.

In sum, numerous case-control studies have been conducted examining the association between PUFA and breast cancer, though inconsistencies in the estimated association exist. Among the sixteen case-control studies, only one examined the PUFA exposure comprehensively by subtypes and relative balance [269]. However, the reported associations are not consistent with the biology of ω-3 and ω-6 fatty acids [269]. Only three studies were conducted in the U.S. [285-287], of which only one examined the relative balance of ω-3 and ω-6 fatty acid intake [286].