Dietary Fat and Breast Cancer in Postmenopausal Women According to Ethnicity and Hormone Receptor Status: The Multiethnic Cohort Study
Epidemiology Program, University of Hawaii Cancer Center, 1236 Lauhala Street, Honolulu, HI 96813, USA. Cancer Prevention Research
(Impact Factor: 4.44).
12/2011; 5(2):216-28. DOI: 10.1158/1940-6207.CAPR-11-0260
Dietary fat has been widely studied as a risk factor for breast cancer, with little consistency in results. The Multiethnic Cohort Study (MEC) provides an opportunity to assess this relationship for possible heterogeneity across different racial/ethnic groups, as well as by stratification on several other variables associated with risk. Therefore, we investigated the associations between dietary fat, overall and by type, and breast cancer risk among 85,089 postmenopausal women who entered the MEC by completing a comprehensive dietary questionnaire in 1993 to 1996. During a mean follow-up of 12 years, 3,885 incident invasive breast cancer cases were identified. The multivariate HR [95% confidence interval (CI)] for the highest versus lowest quintile of intake was 0.94 (95% CI, 0.85-1.05) for total fat and 0.93 (95% CI, 0.83-1.04) for saturated fat. Other specific types of dietary fat, including individual fatty acids, were not related to risk of postmenopausal breast cancer. We found no heterogeneity in these null findings across the five ethnic groups. Furthermore, we found no evidence that the association between dietary fat and postmenopausal breast cancer risk differed by estrogen/progesterone receptor status, tumor stage, body mass index, hormone replacement therapy use, follow-up period, family history of breast cancer, and smoking status at baseline. In conclusion, this comprehensive prospective analysis in the MEC does not support a role of adult intake of dietary fat in the etiology of postmenopausal breast cancer.
Available from: Tiago Franco de Oliveira
- "However, subsequent studies have generated conflicting data regarding the role of dietary fat in breast cancer, and different types of fats appear to have opposing effects on this disease  . For example, consumption of animal fat, consisting mainly of saturated fatty acids (SFA), is associated with increased risk of breast cancer in some studies   but not in others   . Furthermore, a reduction in dietary fat intake did not prevent the development of breast cancer in highrisk women . "
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ABSTRACT: The present study investigated whether early life exposure to high levels of animal fat increases breast cancer risk in adulthood in rats. Dams consumed a lard-based high-fat (HF) diet (60% fat-derived energy) or an AIN93G control diet (16% fat-derived energy) during gestation or gestation and lactation. Their 7-week-old female offspring were exposed to 7,12-dimethyl-benzo[a]anthracene to induce mammary tumors. Pregnant dams consuming a HF diet had higher circulating leptin levels than pregnant control dams. However, compared to the control offspring, significantly lower susceptibility to mammary cancer development was observed in the offspring of dams fed a HF diet during pregnancy (lower tumor incidence, multiplicity and weight), or pregnancy and lactation (lower tumor multiplicity only). Mammary epithelial elongation, cell proliferation (Ki67), and expression of NFκB p65 were significantly lower, and p21 expression and global H3K9me3 levels were higher in the mammary glands of rats exposed to a HF lard diet in utero. They also tended to have lower Rank/Rankl ratios (p=0.09) and serum progesterone levels (p=0.07) than control offspring. In the mammary glands of offspring of dams consuming a HF diet during both pregnancy and lactation, the number of terminal end buds, epithelial elongation and the BCL-2/BAX ratio were significantly lower, and serum leptin levels were higher than in the controls. Our data confirm that the breast cancer risk of offspring can be programmed by maternal dietary intake. However, contrary to our expectation, exposure to high levels of lard during early life decreased later susceptibility to breast cancer.
The Journal of nutritional biochemistry 06/2014; 25(6). DOI:10.1016/j.jnutbio.2014.02.002 · 3.79 Impact Factor
- "There are 5 studies concerning serum PL biomarker, where fatty acid compositions in serum PL was quantified by gas chromatography, and measurement unit was percentage of total fatty acids, except for 1 study (mg/L)
. One study provided data of pre- and post-menopausal women separately
, 1 study of pre-menopausal
, 4 studies of post-menopausal
[15,33,35,36], and 5 studies of combined women
[16,17,30,32,34]. Five studies were reported from Europe
[18,20,32,34,35], 4 studies from USA
[15,19,33,36], and 2 studies from Asia
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ABSTRACT: Increased ratio of n-3/n-6 polyunsaturated fatty acids (PUFAs) in diet or serum may have a protective effect on the risk of breast cancer (BC); however, the conclusions from prospective studies are still controversial. The purpose of this study is to ascertain the relationship between intake ratio of n-3/n-6 PUFAs and the risk of BC, and estimate the potential summarized dose-response trend.
Relevant English-language studies were identified through Cochrane Library, PubMed and EMBASE database till April 2013. Eligible prospective studies reporting the multivariate adjusted risk ratios (RRs) for association of n-3/n-6 PUFAs ratio in diet or serum with BC risk. Data extraction was conducted independently by 2 investigators; disagreements were reconciled by consensus. Study quality was assessed using the Newcastle-Ottawa scale. Study-specific RRs were combined via a random-effects model.
Six prospective nested case-control and 5 cohort studies, involving 8,331 BC events from 274,135 adult females across different countries, were included in present study. Subjects with higher dietary intake ratio of n-3/n-6 PUFAs have a significantly lower risk of BC among study populations (pooled RR = 0.90; 95% CI: 0.82, 0.99), and per 1/10 increment of ratio in diet was associated with a 6% reduction of BC risk (pooled RR = 0.94; 95% CI: 0.90, 0.99; P for linear trend = 0.012). USA subjects with higher ratio of n-3/n-6 in serum phospholipids (PL) have a significantly lower risk of BC (pooled RR = 0.62; 95% CI: 0.39, 0.97; I2 = 0.00%; P for metaregression = 0.103; P for a permutation test = 0.100), and per 1/10 increment of ratio in serum PL was associated with 27% reduction of BC risk (pooled RR = 0.73; 95% CI: 0.59, 0.91; P for linear trend = 0.004; P for metaregression = 0.082; P for a permutation test = 0.116).
Higher intake ratio of n-3/n-6 PUFAs is associated with lower risk of BC among females, which implies an important evidence for BC prevention and treatment is by increasing dietary intake ratio of n-3/n-6 PUFA. No firm conclusions from USA populations could be obtained, due to the limited numbers of USA studies.
BMC Cancer 02/2014; 14(1):105. DOI:10.1186/1471-2407-14-105 · 3.36 Impact Factor
Available from: Richard C Schwartz
- "Recent research has demonstrated no associations with breast cancer risk for adult intake of total fat, saturated fat, or other specific types of dietary fat. These findings did not vary by ethnicity, estrogen/progesterone receptor status, tumor stage, BMI, hormone replacement therapy use, follow-up period, family history of breast cancer, or smoking status at baseline . Lack of associations between dietary factors and breast cancer risk could be the result of numerous sources of bias, including misclassification of dietary intake. "
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ABSTRACT: Epidemiological studies linking dietary fat intake and obesity to breast cancer risk have produced inconsistent results. This may be due to the difficulty of dissociating fat intake from obesity, and/or the lack of defined periods of exposure in these studies. The pubertal mammary gland is highly sensitive to cancer-causing agents. We assessed how high fat diet (HFD) affects inflammation, proliferative, and developmental events in the pubertal gland, since dysregulation of these can promote mammary tumorigenesis. To test the effect of HFD initiated during puberty on tumorigenesis, we utilized BALB/c mice, for which HFD neither induces obesity nor metabolic syndrome, allowing dissociation of HFD effects from other conditions associated with HFD.
Pubertal BALB/c mice were fed a low fat diet (12% kcal fat) or a HFD (60% kcal fat), and subjected to carcinogen 7,12-dimethylbenz[a]anthracene (DMBA)-induced tumorigenesis.
HFD elevated mammary gland expression of inflammatory and growth factor genes at 3 and 4 weeks of diet. Receptor activator of nuclear factor kappa-B ligand (RANKL), robustly induced at 4 weeks, has direct mitogenic activity in mammary epithelial cells and, as a potent inducer of NF-kappaB activity, may induce inflammatory genes. Three weeks of HFD induced a transient influx of eosinophils into the mammary gland, consistent with elevated inflammatory factors. At 10 weeks, prior to the appearance of palpable tumors, there were increased numbers of abnormal mammary epithelial lesions, enhanced cellular proliferation, increased growth factors, chemokines associated with immune-suppressive regulatory T cells, increased vascularization, and elevated M2 macrophages. HFD dramatically reduced tumor latency. Early developing tumors were more proliferative and were associated with increased levels of tumor-related growth factors, including increased plasma levels of HGF in tumor-bearing animals. Early HFD tumors also had increased vascularization, and more intra-tumor and stromal M2 macrophages.
Taken together in this non-obesogenic context, HFD promotion of inflammatory processes, as well as local and systemically increased growth factor expression, are likely responsible for the enhanced tumorigenesis. It is noteworthy that although DMBA mutagenesis is virtually random in its targeting of genes in tumorigenesis, the short latency tumors arising in animals on HFD showed a unique gene expression profile, highlighting the potent overarching influence of HFD.
Breast cancer research: BCR 10/2013; 15(5):R100. DOI:10.1186/bcr3561 · 5.49 Impact Factor
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