Low-Fat Dietary Pattern and Risk of Invasive Breast Cancer

Prentice, Ross L.; Caan, Bette J.; Chlebowski, Rowan T.; Patterson, Ruth E.; Kuller, Lewis H.; Ockene, Judith K.; Margolis, Karen L.; Limacher, Marian C.; Manson, JoAnn E.; Parker, Lawrence N.; Paskett, Electra D.; Phillips, Lawrence S.; Robbins, John A.; Rossouw, Jacques E.; Sarto, Gloria E.; Shikany, James M.; Stefanick, Marcia L.; Thomson, Cynthia A.; Horn, Linda Van; Vitolins, Mara Z.; Wactawski‐Wende, Jean; Wallace, Robert B.; Wassertheil‐Smoller, Sylvia; Whitlock, Evelyn P; Yano, Katsuhiko; Adams‐Campbell, Lucile L.; Anderson, Garnet L.; Assaf, Annlouise R.; Beresford, Shirley A.A.; Black, Henry R.; Brunner, Robert L.; Brzyski, Robert G.; Ford, Lea Berrang; Gass, Margery; Hays, J. Ray; Heber, David; Heiss, Gerardo; Hendrix, Susan L.; Hsia, Judith; Hubbell, F. Allan; Jackson, Rebecca D.; Johnson, Karen C.; Kotchen, Jane Morley; LaCroix, Andrea Z.; Lane, Dorothy S.; Langer, Róbert; Lasser, Norman L.; Henderson, Maureen

doi:10.1001/jama.295.6.629

Cited by 693 publications

(181 citation statements)

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“…Total fat intake was 31.15 E% for the first tertile and 39.2 E% for the highest tertile, after adjustment for confounders). Similar conclusions were reached in other studies (Prentice et al, 2006;Chlebowski et al, 2006;Borugian et al, 2004;McEligot et al, 2006). Total fat intake has also been associated with higher risk of lung cancer.…”

Section: Cancersupporting

confidence: 91%

Scientific Opinion on Dietary Reference Values for fats, including saturated fatty acids, polyunsaturated fatty acids, monounsaturated fatty acids, trans fatty acids, and cholesterol

Publication¹

2010

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This Opinion of the EFSA Panel on Dietetic Products, Nutrition, and Allergies (NDA) deals with the setting of Dietary Reference Values (DRVs) for fats. A lower bound of the reference intake range for total fat of 20 energy % (E%) and an upper bound of 35 E% are proposed. Fat intake in infants can gradually be reduced from 40 E% in the 6-12 month period to 35-40 E% in the 2 nd and 3 rd year of life. For specific fatty acids the following is proposed: saturated fatty acid (SFA) and trans fatty acid intake should be as low as possible; not to set any DRV for cis-monounsaturated fatty acids; not to formulate a DRV for the intake of total cispolyunsaturated fatty acids (PUFA); not to set specific values for the n-3/n-6 ratio; to set an Adequate Intake (AI) of 4 E% for linoleic acid (LA); not to set any DRV for arachidonic acid; not to set an UL for total or any of the n-6 PUFA; to set an AI for alpha-linolenic acid (ALA) of 0.5 E%; not to set an UL for ALA; to set an AI of 250 mg for eicosapentaenoic acid (EPA) plus docosahexaenoic acid (DHA) for adults; to set an AI of 100 mg DHA for infants (>6 months) and young children <24 months; to increase by 100-200 mg preformed DHA in addition to the AI for adults as an adequate supply of n-3 long chain PUFA during pregnancy and lactation; not to set any DRV for conjugated linoleic acid. For cholesterol it was decided not to propose a reference value beside the limitation on the intake of SFA.

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Section: Cancersupporting

confidence: 91%

Scientific Opinion on Dietary Reference Values for fats, including saturated fatty acids, polyunsaturated fatty acids, monounsaturated fatty acids, trans fatty acids, and cholesterol

Publication¹

2010

EFS2

643

263

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“…While recent epidemiological evidence supports a role for dietary fibre intake in relation to lower endogenous hormone levels (Rock et al, 2004;Prentice et al, 2006), the question remains unsettled. In our study of endogenous oestrogen levels in postmenopausal women, oestradiol decreased monotonically from 10.6 to 6.2 pg ml À1 from the lowest to the highest quintile of dietary fibre intake (median intake of 9.9 -21.7 g per 1000 kcal), whereas soluble fibre, after adjustment for dietary fibre, was associated with an increase in oestradiol from 6.8 to 11.5 pg ml À1 from the lowest to the highest quintile of intake (median intake of 2.9 -7.1 g per 1000 kcal) (Monroe et al, 2007).…”

Section: Discussionmentioning

confidence: 99%

Prospective study of grapefruit intake and risk of breast cancer in postmenopausal women: the Multiethnic Cohort Study

et al. 2007

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In vitro and in vivo studies have shown that cytochrome P450 3A4 (CYP3A4) is involved in the metabolism of oestrogens. There is evidence that grapefruit, an inhibitor of CYP3A4, increases plasma oestrogen concentrations. Since it is well established that oestrogen is associated with breast cancer risk, it is plausible that regular intake of grapefruit would increase a woman's risk of breast cancer. We investigated the association of grapefruit intake with breast cancer risk in the Hawaii -Los Angeles Multiethnic Cohort Study, a prospective cohort that includes over 50 000 postmenopausal women from five racial/ethnic groups. A total of 1657 incident breast cancer cases were available for analysis. Grapefruit intake was significantly associated with an increased risk of breast cancer (relative risk ¼ 1.30, 95% confidence interval 1.06 -1.58) for subjects in the highest category of intake, that is, one-quarter grapefruit or more per day, compared to non-consumers (P trend ¼ 0.015). An increased risk of similar magnitude was seen in users of oestrogen therapy, users of oestrogen þ progestin therapy, and among never users of hormone therapy. Grapefruit intake may increase the risk of breast cancer among postmenopausal women. The inhibitory effect of grapefruit juice on the intestinal cytochrome P450 3A4 (CYP3A4) system was discovered accidentally in 1989 during a study designed to test the effect of ethanol on a calcium-channel blocker (Bailey et al, 1989(Bailey et al, , 1991. Grapefruit juice was given to subjects to mask the taste of ethanol. Subsequent investigations found that through the inhibition of the CYP3A4 enzyme system, primarily in the liver and small intestine (Guengerich, 1999;Veronese et al, 2003), grapefruit juice interacts with more than 60% of orally administered drugs leading to elevation of their serum concentrations (Maskalyk, 2002;Bailey and Dresser, 2004). Consumption of a single glass (six ounces) can produce the maximal acute pharmacokinetic effect (Edgar et al, 1992;Lundahl et al, 1995Lundahl et al, , 1997Dahan and Altman, 2004) with enhanced oral drug bioavailability occurring up to 24 h after juice consumption (Bailey and Dresser, 2004).Since 1989, the list of drug interactions with grapefruit juice has expanded to include oral 17b-oestradiol and progesterone (Guengerich, 1999;Maskalyk, 2002; Medical Letter, 2005). The US Food and Drug Administration (FDA) mandated labelling for hormone products for postmenopausal women now contains warnings that grapefruit juice may increase plasma concentrations of oestrogen (US Food and Drug Administration, 2006). Schubert et al (1994) found that grapefruit juice increased the area under the curve of oestradiol approximately 20% in ovariectomised women. Recently, we reported that endogenous oestrogen levels were about 30% higher in postmenopausal women in whom periods had stopped naturally and who were consuming the equivalent of 1 4 grapefruit or more per day (Monroe et al, 2007).It is well established that oestrogen is associated with breast cancer r...

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“…The initial design of the study was based on disease stage but not on tumor characteristics. There may be differential responses to a dietary intervention based on hormone receptor status (10). Indeed, the recent results from the Women's Health Initiative Dietary Modification Trial reported differential effects of the low-fat eating pattern by tumor hormone receptor status: the hazard ratio for progesterone receptor -negative breast cancers was 0.76 (95% confidence interval, 0.63-0.92; P < 0.004; ref.…”

mentioning

confidence: 99%

“…Indeed, the recent results from the Women's Health Initiative Dietary Modification Trial reported differential effects of the low-fat eating pattern by tumor hormone receptor status: the hazard ratio for progesterone receptor -negative breast cancers was 0.76 (95% confidence interval, 0.63-0.92; P < 0.004; ref. 10). Although the Women's Health Initiative tested breast cancer incidence and not recurrence, preliminary results from another dietary intervention trial in breast cancer survivors also reported differential effects of the intervention by hormone receptor status (11).…”

mentioning

confidence: 99%