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Adolescent drinking is associated with higher risks of proliferative benign breast disease (BBD) and invasive breast cancer (BC). Furthermore, adolescent nut and fiber consumptions are associated with lower risks of benign lesions and premenopausal BC. We hypothesize that diet (nuts, fiber) may mitigate the elevated BBD risk associated with alcohol. A prospective cohort of 9031 females, 9-15 years at baseline, completed questionnaires in 1996-2001, 2003, 2005, 2007, 2010, 2013, and 2014. Participants completed food frequency questionnaires in 1996-2001. In 2005, participants (>=18 years) began reporting biopsy-confirmed BBD (N = 173 cases). Multivariable logistic regression estimated associations between BBD and cross-classified intakes (14-17 years) of alcohol and peanut butter/nuts (separately, total dietary fiber). Only 19% of participants drank in high school; drinking was associated with elevated BBD risk (OR = 1.75, 95% CI: 1.20-2.56; p = 0.004) compared to nondrinkers. Participants consuming any nuts/butter had lower BBD risk (OR = 0.64, 95% CI: 0.45-0.90; p = 0.01) compared to those consuming none. Participants in top 75% fiber intake had lower risk (OR = 0.57, 95% CI: 0.40-0.81; p = 0.002) compared to bottom quartile. Testing our hypothesis that consuming nuts/butter mitigates the elevated alcohol risk, analyzing alcohol and nuts combined found that those who consumed both had lower risk (RR = 0.47, 95% CI: 0.24-0.89; p = 0.02) compared to drinkers eating no nuts. Our analysis of alcohol and fiber together did not demonstrate risk mitigation by fiber. For high school females who drink, their BBD risk may be attenuated by consuming nuts. Due to modest numbers, future studies need to replicate our findings in adolescent/adult females. However, high school students may be encouraged to eat nuts and fiber, and to avoid alcohol, to reduce risk of BBD and for general health benefits.

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Mammographic breast density is a strong risk factor for breast cancer. We comprehensively investigated the associations of body mass index (BMI) change from ages 10, 18, and 30 to age at mammogram with mammographic breast density in postmenopausal women. We used multivariable linear regression models, adjusted for confounders, to investigate the associations of BMI change with volumetric percent density, dense volume, and nondense volume, assessed using Volpara in 367 women. At the time of mammogram, the mean age was 57.9 years. Compared with women who had a BMI gain of 0.1-5 kg/m2 from age 10, women who had a BMI gain of 5.1-10 kg/m2 had a 24.4% decrease [95% confidence interval (CI), 6.0%-39.2%] in volumetric percent density; women who had a BMI gain of 10.1-15 kg/m2 had a 46.1% decrease (95% CI, 33.0%-56.7%) in volumetric percent density; and women who had a BMI gain of >15 kg/m2 had a 56.5% decrease (95% CI, 46.0%-65.0%) in volumetric percent density. Similar, but slightly attenuated associations were observed for BMI gain from ages 18 and 30 to age at mammogram and volumetric percent density. BMI gain over the life course was positively associated with nondense volume, but not dense volume. We observed strong associations between BMI change over the life course and mammographic breast density. The inverse associations between early-life adiposity change and volumetric percent density suggest that childhood adiposity may confer long-term protection against postmenopausal breast cancer via its effect of mammographic breast density.

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PURPOSE: Nutritional factors during different periods in life impact breast cancer risk. Because benign breast disease (BBD) is a well-established risk factor for breast cancer, we investigated childhood nutrition from birth through age 14 year and subsequent BBD. METHODS: A prospective cohort study of 9031 females, 9-15 year at baseline, completed questionnaires (including heights, weights) annually from 1996 to 2001, in 2003, 2005, 2007, 2010, 2013 and 2014. In 1996, mothers reported infant feeding practices during their daughters first year of life. Beginning in 1996, participants completed annual food frequency questionnaires. In 2005, participants (18 year +) began reporting whether they had ever been diagnosed with biopsy-confirmed BBD (N = 173 cases). Multivariable logistic regression models estimated associations between childhood nutrition and BBD, adjusted for maternal breast disease and childhood body size factors. RESULTS: Although no infant nutrition factors were associated with biopsy-confirmed BBD, certain adolescent dietary factors were. A multivariable model simultaneously included the most important diet and body size factors from different age periods: higher BBD risk was associated with greater age 10 year consumption of animal (non-dairy, energy-adjusted) fat (OR 2.27, p < .02, top vs. bottom quartiles) and with lower 14 year consumption of nuts/peanut butter (OR 0.60, p = .033, top vs. bottom quartiles). CONCLUSION: Greater intake of animal (non-dairy) fat at 10 year and lower intake of nuts/peanut butter at 14 year were independently associated with higher BBD risk. These dietary factors appeared to operate on BBD risk independent of childhood growth (gestational weight gain, childhood BMI and height, adolescent height growth velocity), young adult height and BMI, and family history.

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PURPOSE: To begin to explore the possible roles of childhood diet and growth in prostate cancer (PCa) development, we investigated these exposures in relation to two known/suspected PCa risk factors, earlier pubertal timing and greater attained height, in the Longitudinal Studies of Child Health and Development. METHODS: We used biannual/annual height, weight, and dietary history data to investigate childhood diet, body mass index (BMI), birth length, and childhood height in relation to PCa risk factors (age at peak height velocity (APHV), height at age 13, and adult height) for 64 Caucasian American boys. RESULTS: In adjusted models, childhood fat and animal protein intake was positively associated with height at age 13 and adult height (P < 0.05). A childhood diet high in fat and animal protein and low in vegetable protein was also associated with earlier APHV (P < 0.05), whereas no associations were observed for childhood energy intake or BMI. Birth length and childhood height were positively associated with height at age 13 and adult height, and childhood height was inversely associated with APHV (P < 0.05). CONCLUSION: Our findings suggest that both childhood diet and growth potential/growth contribute to earlier pubertal timing and taller attained height in males, supporting roles of these factors in PCa development.

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Although childhood adiposity is inversely associated with breast cancer risk, the association of childhood adiposity with mammographic density in premenopausal women has not been adequately studied. We analyzed data from 365 premenopausal women who came in for screening mammography at Washington University (St. Louis, MO) from 2015 to 2016. Body size at age 10 was self-reported using somatotype pictogram. Body mass index (BMI) at age 10 was imputed using data from Growing Up Today Study. Volpara software was used to evaluate volumetric percent density (VPD), dense volume (DV), and nondense volume (NDV). Adjusted multivariable linear regression models were used to evaluate the associations between adiposity at age 10 and mammographic density measures. Adiposity at age 10 was inversely associated with VPD and positively associated with NDV. A 1 kg/m2 increase in BMI at age 10 was associated with a 6.4% decrease in VPD, and a 6.9% increase in NDV (P < 0.001). Compared with women whose age 10 body size was 1 or 2, women with body size 3 or 4 had a 16.8% decrease in VPD and a 26.6% increase in NDV, women with body size 5 had a 32.2% decrease in VPD and a 58.5% increase in NDV, and women with body sizes ≥6 had a 47.8% decrease in VPD and a 80.9% increase in NDV (P < 0.05). The associations were attenuated, but still significant after adjusting for current BMI. Mechanistic studies to understand how childhood adiposity influences breast development, mammographic density, and breast cancer in premenopausal women are needed. Cancer Prev Res; 11(5); 287-94. ©2018 AACR.

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Obesity is a well-established cause of postmenopausal breast cancer. However, early life adiposity is inversely associated with breast cancer incidence. To understand these conflicting relations, we use validated measures to assess adiposity in childhood and late adolescence, as well as weight change, in relation to total invasive breast cancer incidence and receptor subtypes. We conducted a prospective observational study among 74,177 women from the Nurses' Health Study from 1980-2012, with updated risk factors every 2 years during which 4,965 incident invasive breast cancers occurred. Overall, weight at age 18 was inversely associated with both premenopausal (HR per 30 kg = 0.52, 95% CI = 0.39-0.71) and postmenopausal (HR per 30 kg = 0.81, 95% CI = 0.72-0.92) breast cancer which was largely explained by adiposity at age 10. Long-term weight gain from age 18 both during premenopause and postmenopause were positively associated with postmenopausal breast cancer risk. However, premenopausal weight gain was not related to premenopausal breast cancer risk. Furthermore, weight gain since age 18 was positively associated with ER+/PR+ postmenopausal breast cancer (HR per 30 kg = 1.50, 95% CI = 1.36-1.65) but not ER+/PR- (HR per 30 kg = 0.96, 95% CI = 0.78-1.19) or ER-/PR- (HR per 30 kg = 1.16, 95% CI = 0.95-1.42) postmenopausal breast cancer. Overall, 17% of ER+/PR+ postmenopausal breast cancer and 14% of total postmenopausal breast cancer are attributable to weight gain of > 5 kg since age 18.

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PURPOSE: Body size, from birth throughout adulthood, is associated with breast cancer risk, but few studies have investigated early-life body size and benign breast disease (BBD), a well-established breast cancer risk factor. We consider whether prenatal factors and size at birth, 10, 18 year, and intervening growth, are related to BBD risk. METHODS: The Growing Up Today Study includes 9032 females who completed questionnaires annually from 1996 to 2001, then 2003, 2005, 2007, 2010, and 2013. In 1996, their mothers provided pregnancy-related data. From 2005 to 2013, participants (18 year+) reported whether they had ever been diagnosed with biopsy-confirmed BBD (N = 142 cases). RESULTS: Girls had greater adiposity (BMI; kg/m2) at 10 year if they were larger at birth, if mother's pre-pregnancy BMI was higher, or if gestational weight gain was greater (all p < .01). Maternal height was (positively) associated (p < .05) with adolescent peak height growth velocity (PHV; in./year). Greater 10 year adiposity was associated with lower PHV and less height growth 10-18 year (both p < .01). Adiposity at 10 year was inversely associated with BBD (OR 0.83/(kg/m2), p < .01) as was increasing adiposity 10-18 year (OR 0.85/(kg/m2), p = .01). In a separate model, 10 year height (OR 1.13/in., p = .02) and height growth 10-18 year (OR 1.19/in.; p < .01) were positively associated. PHV was similarly positively associated (OR 2.58, p = .01, fastest versus slowest growth quartiles). In a multivariable model of BBD risk, gestational weight gain (daughters at highest risk if <20 lb gained), PHV (slowest growing girls at lowest risk), age 10 year height (positive), and BMI (inverse) were the most critical childhood risk factors (each p < .05). CONCLUSIONS: Body size factors from pregnancy through adolescence were independently associated with BBD risk in young women.

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Benign breast disease (BBD) is a well-established risk factor for breast cancer, but little work has considered a girl's early life and her risk for BBD in adulthood. We investigated factors, from pre-conception through infant feeding practices, in relation to subsequent BBD risk in young women. The Growing Up Today Study (GUTS) includes 9032 females, born 1980-1987, who completed questionnaires annually from 1996 through 2001, then 2003, 2005, 2007, 2010, and 2013. In 1996, their mothers provided each participant's birth weight and length, gestational age, biological father's height, and infant feeding factors (e.g., breast-fed, type of formula). In 1999, their mothers reported maternal pre-pregnancy weight and weight gain during index pregnancy. Beginning in 2005, daughters (18 years+) reported whether they had ever been diagnosed with biopsy-confirmed BBD (n = 142 cases, through 2013). Logistic regression estimated associations between early life factors and biopsy-confirmed BBD. Girls whose mother's BMI prior to pregnancy was 20-25 kg/m(2) were at lower risk of BBD as young women (OR = 0.66, p = 0.04, vs. maternal pre-pregnancy BMI < 20). Girls whose mothers gained 20 + pounds (vs. <20 pounds) during pregnancy were at lower risk (among full-term singleton births: OR = 0.48, p = 0.007, if mother gained 20-35 pounds). However, neither birth weight nor BMI at birth were associated with subsequent BBD risk. We found no evidence that infant feeding practices were linked to BBD. A healthy maternal BMI before pregnancy and sufficient weight gain during pregnancy may produce daughters at lower risk for BBD as young women. Further examination of these findings is needed.

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PURPOSE: Vitamin D may reduce cell proliferation and tumor growth in breast tissue, and exposure may be most important during adolescence when breast tissue is developing. In the Nurses' Health Study II, higher recalled adolescent vitamin D intake was associated with a lower risk of benign breast disease (BBD). Our study aimed to assess adolescent vitamin D exposure in relation to BBD in young women. METHODS: Vitamin D was assessed in 6,593 adolescent girls (9-15 years of age at baseline) in the prospective Growing Up Today Study cohort using the mean energy-adjusted intakes from food frequency questionnaires in 1996, 1997, and 1998. In 1999, 5,286 girls reported skin color, sunscreen use, tanning bed use, and number of sunburns in the past year, and we used state of residence to assess low versus high ultraviolet index. Biopsy-confirmed BBD was reported on questionnaires in 2005, 2007, and 2010 (n = 122). RESULTS: Dietary vitamin D, tanning behaviors, and other sun exposure variables were not significantly associated with BBD in logistic regression models adjusted for age, family history of breast cancer or BBD, age at menarche, nulliparity, alcohol intake, body mass index, and physical activity. The relative risk for the top (>467 IU/day) versus bottom (<243 IU/day) quartile of vitamin D intake was 0.76 (95 % CI 0.47, 1.23). CONCLUSIONS: Sun exposure was not significantly associated with BBD in this prospective cohort. However, a suggestive inverse association between dietary vitamin D and BBD was observed that merits further study.

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In previous investigations of adolescent activity recalled in adulthood, modest reductions in risk of benign breast disease (BBD) and premenopausal breast cancer were seen with moderate-strenuous activity during high school. We therefore investigated physical activity, walking, and recreational inactivity (watching TV-videos, playing computer-videogames) reported by adolescent girls in relation to their subsequent risk for BBD as young women. The Growing Up Today Study includes 9,039 females, 9-15 years at study initiation (1996), who completed questionnaires annually through 2001, then in 2003, 2005, 2007, 2010 and 2013. Annual surveys (1996-2001) obtained data on physical and sedentary activities during the past year. Beginning in 2005, women (≥18 years) reported whether they had ever been diagnosed with BBD confirmed by breast biopsy (n = 133 cases, to 11/01/2013). Logistic regression (adjusted for baseline adiposity and age; additional factors in multivariable-adjusted models) estimated associations between adolescent activities (moderate-vigorous, walking, METS, inactivity) and biopsy-confirmed BBD in young women. Girls who walked the most had significantly lower risk of BBD (multivariable-adjusted OR = 0.61, ≥30 vs ≤15 min/day; p = .049). We observed no evidence that inactivity (≥3 vs <2 h/day OR = 1.02, p = .92) or METS (top vs bottom tertile OR = 1.19, p = .42) were associated with BBD. Accounting for factors including family history, childhood adiposity, and other activities and inactivities, adolescent girls who walked the most were at lower risk for BBD. We found no evidence that high moderate-vigorous activity might reduce risk, nor did we observe any association with inactivity. Continued follow-up will re-evaluate these findings as more BBD cases, and ultimately breast cancer, are diagnosed.

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Nearly one in four breast cancers is diagnosed before the age of 50, and many early-stage premalignant lesions are present but not yet diagnosed. Therefore, we review evidence to support the strategy that breast cancer prevention efforts must begin early in life. This study follows the literature review methods and format. Exposures during childhood and adolescence affect a woman's long-term risk of breast cancer, but have received far less research attention than exposures that occur later in life. Breast tissue undergoes rapid cellular proliferation between menarche and first full-term pregnancy, and risk accumulates rapidly until the terminal differentiation that accompanies first pregnancy. Evidence on childhood diet and growth in height, and adolescent alcohol intake, among other adolescent factors is related to breast cancer risk and risk of premalignant proliferative benign lesions. Breast cancer prevention efforts will have the greatest effect when initiated at an early age and continued over a lifetime. Gaps in knowledge are identified and deserve increase attention to inform prevention.

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BACKGROUND: Carotenoids may reduce risk of benign breast disease (BBD), an independent risk factor for breast cancer, through antioxidative or antiproliferative mechanisms. Exposure to carotenoids may be most important during adolescence when breast tissue is still developing. We examined adolescent carotenoid intake in relation to BBD in young women. METHODS: In 6593 adolescent girls in the prospective Growing Up Today Study cohort, intakes of α-carotene, ß-carotene, ß-cryptoxanthin, lutein/zeaxanthin, and lycopene were assessed by using the means from food-frequency questionnaires in 1996, 1997, and 1998. Girls reported biopsy-confirmed BBD on questionnaires in 2005, 2007, and 2010 (n = 122). We conducted logistic regression of energy-adjusted carotenoid intakes in relation to BBD, adjusted for age, family history of breast cancer or BBD, age at menarche, nulliparity, alcohol intake, BMI, and physical activity. RESULTS: Mean (SD) age at baseline was 12.0 (1.6) years. ß-Carotene intake was inversely associated with BBD; comparing the highest to lowest quartile, the multivariate-adjusted odds ratio was 0.58 (95% confidence interval: 0.34-1.00; P-trend = .03). α-Carotene and lutein/zeaxanthin were also inversely associated with BBD, but the associations were not statistically significant. CONCLUSIONS: Adolescent carotenoid intake may be associated with lower BBD risk; these findings warrant further study.

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Previous investigations, of adolescent diet recalled in adulthood, found lower risk for benign breast disease (BBD) with higher intakes of vegetable fat and nuts during high school. We investigate whether vegetable protein and fat, derived from diets reported during pre-adolescence and adolescence, are associated with subsequent risk for BBD in young women. The Growing Up Today Study includes 9,039 females, 9-15 years in 1996, who completed questionnaires annually through 2001, and then in 2003, 2005, 2007, and 2010. Food frequency questionnaires (1996-2001) obtained intake data on a variety of foods. Beginning in 2005, women (18-30 years) reported whether they had ever been diagnosed with BBD that was confirmed by breast biopsy (n = 112 cases). Logistic regression estimated associations between intakes of vegetable protein and fat and biopsy-confirmed BBD. Those individual foods that were the largest contributors of protein and fat in this cohort were also investigated. In analyses of intakes from 1996 through 1998, when our cohort was youngest, vegetable fat (OR = 0.72/(10 gm/day), 95 % CI 0.53-0.98; p = 0.04) was inversely associated with BBD risk. The greatest sources of vegetable fat and protein in these girls were peanut butter, peanuts, nuts, beans (beans, lentils, and soybeans), and corn. A daily serving of any one of these was associated with lower risk (OR = 0.32/(serv/day), 95 % CI 0.13-0.79; p = 0.01). Peanut butter (and nuts) at age 11 years was inversely associated with risk (p = 0.01). In analyses of intakes at age 14 years, vegetable protein was associated with lower BBD risk (OR = 0.64/(10 gm/day), 95 % CI 0.43-0.95; p = 0.03). A daily serving at 14 years of any one of the foods was associated with lower risk (OR = 0.34, 95 % CI 0.16-0.75; p = 0.01), as was peanut butter (and nuts) (p = 0.02). Girls with a family history of breast cancer had significantly lower risk if they consumed these foods or vegetable fat. In conclusion, consumption of vegetable protein, fat, peanut butter, or nuts by older girls may help reduce their risk of BBD as young women.

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BACKGROUND: Adult alcohol consumption during the previous year is related to breast cancer risk. Breast tissue is particularly susceptible to carcinogens between menarche and first full-term pregnancy. No study has characterized the contribution of alcohol consumption during this interval to risks of proliferative benign breast disease (BBD) and breast cancer. METHODS: We used data from 91,005 parous women in the Nurses' Health Study II who had no cancer history, completed questions on early alcohol consumption in 1989, and were followed through June 30, 2009, to analyze breast cancer risk. A subset of 60,093 women who had no history of BBD or cancer in 1991 and were followed through June 30, 2001, were included in the analysis of proliferative BBD. Relative risks (RRs) were estimated using Cox proportional hazard regression. RESULTS: We identified 1609 breast cancer cases and 970 proliferative BBD cases confirmed by central histology review. Alcohol consumption between menarche and first pregnancy, adjusted for drinking after first pregnancy, was associated with risks of breast cancer (RR = 1.11 per 10 g/day intake; 95% confidence interval [CI] = 1.00 to 1.23) and proliferative BBD (RR = 1.16 per 10 g/day intake; 95% CI = 1.02 to 1.32). Drinking after first pregnancy had a similar risk for breast cancer (RR = 1.09 per 10 g/day intake; 95% CI = 0.96 to 1.23) but not for BBD. The association between drinking before first pregnancy and breast neoplasia appeared to be stronger with longer menarche to first pregnancy intervals. CONCLUSIONS: Alcohol consumption before first pregnancy was consistently associated with increased risks of proliferative BBD and breast cancer.

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Previous investigations found high dairy intakes in girls associated with rapid height growth and excess weight gain, which had opposite relationships with benign breast disease (BBD) in young women. We use data from the longitudinal Growing Up Today Study (GUTS) to investigate whether dairy intakes, in older children/adolescents, are associated with BBD risk in young women. GUTS includes 9,039 females, ages 9-15 years in 1996, who completed questionnaires annually through 2001, then in 2003, 2005, 2007, and 2010. Dietary food frequencies (1996-2001) obtained milk, yogurt, and cheese intakes. On 2005-2010 surveys, 7,011 females (18-29 years) reported whether a health care provider ever diagnosed them with BBD (n = 250) and if confirmed by breast biopsy (n = 105). Logistic regression models estimated associations between prevalent biopsy-confirmed BBD and dairy intakes, adjusted for age and energy. Multivariable-adjusted models additionally included menarche age, childhood adiposity, adolescent alcohol consumption, and pregnancy. Further analyses stratified by family history. Age-energy-adjusted models of dairy (milk, yogurt, cheese, total dairy servings, dairy protein, dairy fat) intakes at 14 yr found no significant associations with BBD risk [milk: OR, 0.90/(serving/d); 95% confidence interval (CI), 0.76-1.05; dairy protein: OR, 0.98/(10 g/d); 95% CI, 0.82-1.17). Separate analyses of dairy intakes at 10 yr, intakes before the growth spurt, during the growth spurt, before menses-onset, and after menses-onset provided no significant associations with BBD. Multivariable adjustment, and family history stratification, did not alter the above findings. We conclude that dairy intakes by older girls have no strong relation with BBD risk in young women. Because of small number of cases, it is important to continue follow-up and re-examine later.

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Vitamin D and calcium have been shown to have protective effects against breast cancer development in animal studies. Vitamin D and calcium play important anticarcinogenic roles in animal studies. Exposures between menarche and first birth may be important in breast development and future breast cancer risk. However, the relations between adolescent vitamin D and calcium intake and the risk of proliferative benign breast disease (BBD), a marker of increased breast cancer risk, have not yet been evaluated. We examined these associations in the Nurses' Health Study II. Among the 29,480 women who completed an adolescent diet questionnaire in 1998, 682 proliferative BBD cases were identified and confirmed by centralized pathology review between 1991 and 2001. Hazard ratios (HRs) and 95 % confidence intervals (CIs) were estimated by Cox proportional hazards regression and adjusted for potential confounders. A suggestive inverse association was observed between adolescent total vitamin D intake and proliferative BBD. Women in the highest quintile of vitamin D intake during adolescence had a 21 % lower risk (multivariate HR (95 % CI): 0.79 (0.61, 1.01), p-trend = 0.07) of proliferative BBD than women in the lowest quintile. Results were essentially the same when the analysis was restricted to prospective cases (n = 142) diagnosed after return of the adolescent diet questionnaire and independent of adult vitamin D intake. Adolescent total milk intake was positively associated with proliferative BBD (≥3 servings/day vs. <1 serving/day HR (95 % CI): 1.41 (0.91, 2.17), p-trend = 0.03), after additional adjustment for total vitamin D. Calcium intake during adolescence was not associated with proliferative BBD (p-trend = 0.91). Vitamin D intake during adolescence may be important in the earlier stage of breast carcinogenesis. These findings, if corroborated, may suggest new pathways and strategies for breast cancer prevention.

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OBJECTIVES: To examine the combined effect of alcohol and folate intake during adolescence on the risk of proliferative benign breast disease (BBD). METHODS: We used data from 29 117 women in the Nurses' Health Study II who completed both adolescent alcohol consumption questions in 1989 and an adolescent diet questionnaire in 1998. A total of 659 women with proliferative BBD diagnosed between 1991 and 2001 were confirmed by central pathology review. Cox proportional hazards models were used to estimate hazard ratios and 95% confidence intervals (CIs), adjusted for established risk factors of breast cancer. RESULTS: Adolescent alcohol consumption was dose-dependently associated with an increased risk of proliferative BBD (hazard ratio = 1.15 per 10 g/day consumption; 95% CI, 1.03-1.28). There was no significant association between adolescent folate intake and the risk of proliferative BBD. Stratified analyses showed that each 10-g/day alcohol intake during adolescence was associated with a 21% (95% CI, 1.01-1.45) increase in the risk of proliferative BBD among women with low folate intake during adolescence, which was not significantly different from the alcohol-associated risk among women with moderate and high folate intake during adolescence (P for interaction = 0.18). CONCLUSIONS: Adolescent alcohol consumption is associated with increased risk of proliferative BBD, which may not be reduced by increased folate intake during adolescence.

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BACKGROUND: Breast cancer (BC) patients wonder how their daughters might reduce their risk. The authors investigated childhood/adolescent risk factors for benign breast disease (BBD), a well-documented risk factor for BC, among girls with a family history. METHODS: GUTS (the Growing Up Today Study) includes females, aged 9 to 15 years in 1996, who completed annual questionnaires during 1996 to 2001, then in 2003, 2005, and 2007. Participants provided information regarding alcohol, menarche, height, and body mass index (BMI; kg/m(2)). Peak height growth velocity (PHV; in./y) was estimated from longitudinal heights. On 2005-2007 surveys, 6888 women (18-27 years old) reported whether they were diagnosed with biopsy-confirmed BBD (n = 67 cases); 6741 women (noncases) reported no BBD. Participants' mothers reported their own biopsy-confirmed BBD and BC, and BC in their sisters and mothers. Stratified by family history, logistic models investigated BBD risk factors. RESULTS: Young women whose mothers or aunts had BC were more likely to be diagnosed with BBD (odds ratio [OR], 2.34; P = .01), as were those with maternal BBD (OR, 1.59; P = .095). Adolescents with BC family history (mother, aunt, grandmother) who consumed alcohol (7 drinks/wk) doubled their BBD risk (OR, 2.28; P = .01), similar to those with maternal BBD (OR, 1.96; P = .02). Girls whose mother or aunt had BC saw their BBD risk elevated with higher PHV (OR, 1.82 [inch/yr]; P = .05). Among girls with no family history, BBD risk appeared to be related to other factors: childhood BMI, adolescent waist circumference, and adult height. CONCLUSIONS: Adolescents with family history may reduce their risk by avoiding alcohol. Separate risk factors were observed among girls with family history versus girls with no family history, possibly reflecting different causes of BC.

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BACKGROUND: In adult women with retrospective data, childhood adiposity, pubertal growth and development were associated with benign breast disease (BBD) and/or breast cancer. The authors prospectively evaluated these childhood/adolescent characteristics and BBD risk. METHODS: The Growing Up Today Study (GUTS) included females, aged 9-15 years in 1996, who completed annual questionnaires through 2001, then 2003, 2005, and 2007. Participants annually/biennially provided information on menarche, height, and weight, from which the authors derived body mass index (BMI in kg/m(2) ). Peak height growth velocity (PHV in cm/year) was estimated from longitudinal data. On 2005-2007 surveys, 6899 females (18-27 years of age) reported whether a healthcare provider ever diagnosed BBD (n = 147), and whether it was confirmed by biopsy (n = 67). Logistic models investigated risk factors adjusted for age, alcohol, pregnancy, and maternal history. RESULTS: More childhood adiposity (odds ratio [OR], 0.91/[kg/m(2) ]; P = .04) and shorter adult height (OR, 0.93/inch shorter; P = .07) were associated with lower risk of biopsy-confirmed BBD. Girls with most rapid height growth were at increased risk (OR, 2.12; P = .09) relative to those with the slowest growth. Age at menarche was not associated (OR, 1.11/year; P = .32) nor was adult BMI (adjusted for childhood BMI: OR, 1.01/[kg/m(2) ]; P = .98); larger BMI increases (childhood to adulthood) were not protective (OR + 1.04/[kg/m(2) ]; P = .37). Among girls with maternal breast cancer, those with more rapid growth had higher risk (OR, 1.47/[cm/year]; P = .02). All estimates were age-adjusted. CONCLUSIONS: Increased BBD risk (likely evolving to elevated breast cancer risk) was observed in thinner girls, girls with the most rapid growth, and taller women. Contrary to expectations, later menarche age was not protective against BBD, consistent with studies that found BBD patients are not protected against breast cancer by later menarche.

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OBJECTIVE: To investigate prospectively, using alcoholic beverage consumption data collected in real time, the association between adolescent drinking and risk of biopsy-confirmed benign breast disease (BBD) in young women. PARTICIPANTS AND METHODS: The Growing Up Today Study is a prospective cohort study of US girls, aged 9 to 15 years at baseline, with annual questionnaires from 1996 through 2001, followed by questionnaires in 2003, 2005, and 2007. On the 2003 survey, the participants (then aged 16-23 years) provided information about their alcoholic beverage consumption in the previous year. On the 2005 and 2007 surveys, a total of 6899 women (aged 18-27 years) reported whether a health care provider had ever diagnosed them with BBD (n = 147 cases) and whether it was confirmed by biopsy (n = 67 cases); 6752 women reported never being diagnosed with BBD. RESULTS: Adjusted for age and BMI, quantity of alcohol consumed was associated with increased risk of biopsy-confirmed BBD (odds ratio: 1.50 per drink per day [95% confidence interval: 1.19-1.90]). Girls who typically drank 6 or 7 days/week were at higher risk (odds ratio: 5.50 [95% confidence interval: 1.23-24.53]) compared with those who never drank or who drank less than once per week. CONCLUSIONS: Higher amounts consumed, and more frequent consumption, of alcoholic beverages in adolescence may increase the occurrence of BBD in young women. Advising teenagers to avoid alcoholic beverages, along with smoking and sun exposure, may reduce cancer incidence in adulthood.

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