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Amy Trentham-Dietz

Publications and source records attributed to Amy Trentham-Dietz.

At least 19 recordsLinked to original sources
PubMed2007

Genetic variation in tumor necrosis factor and lymphotoxin-alpha (TNF-LTA) and breast cancer risk.

Tumor necrosis factor (TNF) is critical to regulation of inflammation. Genetic variation in the promoter region of TNF has been associated with expression differences, and a range of auto-immune, infectious, and oncologic diseases. We analyzed eight common single nucleotide polymorphisms (SNPs) (rs746868, rs909253, rs1799964, rs1800630, rs1800750, rs1800629, rs361525, and rs1800610) to capture most of the genetic variation in TNF in addition to SNPs in lymphotoxin-alpha (LTA), a pro-inflammatory cytokine in linkage disequilibrium with the TNF promoter region. SNPs were genotyped in a USA population-based case-control study (3,318 cases, 2,841 controls). Promising results were followed-up in an independent population-based case-control study in Poland (2,228 cases, 2,378 controls). In both studies, women carrying the variant allele of rs361525 were at elevated breast cancer risk compared to the GG genotype (per allele OR = 1.18, 95% CI 1.04-1.35; P for trend = 0.008). Other SNPs were not significantly associated with breast cancer risk. Haplotype analyses did not reveal any additional associations between TNF and breast cancer risk. Data from 5,269 cases and 4,982 controls suggested that the rs361525 A allele, located in the TNF promoter region, was associated with a modest increase in breast cancer risk. Additional studies are required to replicate these findings and to determine whether rs361525 is a causative SNP or is a marker of a causative SNP.

Adult↗
PubMed2006

Breast cancer risk factors and second primary malignancies among women with breast cancer.

PURPOSE: To examine the association between breast cancer risk factors and second primary cancers (independent diagnoses occurring at least 12 months after the initial breast cancer diagnosis) among breast cancer survivors. METHODS: In this population-based study, cancer outcomes among breast cancer survivors first diagnosed during 1987-2000 were investigated. Invasive breast cancer cases were identified from the statewide tumor registry and interviewed regarding their pre-diagnosis risk factors, including reproductive and lifestyle characteristics, approximately 1 year after diagnosis. Data on second primary cancers (not recurrences) and deaths were obtained by linkage with tumor registry reports and death certificates through December 31, 2002. Hazard ratios (HR) were estimated using proportional hazards regression stratified by age and adjusted for stage and other factors. RESULTS: Among the 10,953 breast cancer cases, 10.8% experienced a second cancer diagnosis within an average of 7 years (including 488 breast, 132 colorectal, 113 endometrial, and 36 ovarian cancers). Risk of a second primary breast cancer increased according to low parity (P = 0.002), older age at menopause (P = 0.08), greater body mass index (P = 0.003) and adult weight gain (P = 0.02), and a family history of breast cancer-particularly among women with 2 or more first-degree affected relatives (HR = 1.8, 95% CI: 1.1-2.9). Reduced risk of colorectal cancer after breast cancer was observed in relation to older ages at menarche (P = 0.05), younger age at menopause (P = 0.04), postmenopausal hormone use (HR = 0.4, 95% CI: 0.3-0.7), normal body mass index (P = 0.07), and infrequent alcohol consumption (P = 0.01). Second endometrial cancer risk was associated with increasing body mass index (P < 0.01) and adult weight gain (P = 0.03). Risk of second ovarian cancer appeared related to recent alcohol intake and family history of breast cancer. Women who reported consuming any alcohol appeared to have a 55% reduction in ovarian cancer risk (95% CI: 0.2-1.0) compared to non-drinkers, while having 2 or more first-degree relatives with breast cancer was associated with an increased risk of ovarian cancer (HR = 4.3, 95% CI: 1.3-14.6). CONCLUSION: This study suggests that family history of breast cancer as well as potentially modifiable characteristics including body weight, alcohol intake, and postmenopausal hormone use may be associated with risk of a second cancer diagnosis among breast cancer cases.

Adolescent↗
PubMed2006

Alcohol consumption and ovarian cancer risk in a population-based case-control study.

Alcohol consumption has been investigated as a possible risk factor for ovarian cancer in several epidemiological studies, with inconsistent findings. Recent studies have suggested that the association between alcohol consumption and ovarian cancer may vary according to histologic subtype of ovarian cancer and type of alcohol consumed (e.g., wine, beer, or liquor). We examined these associations in a population-based case-control study comprised of 762 incident cases of epithelial ovarian cancer and 6,271 population controls from Massachusetts and Wisconsin aged 40-79 years. Women reported their usual alcohol consumption as young adults (20-30 years of age) and in the recent past. Odds ratios (ORs) and 95% confidence intervals (CIs) were calculated. There was no significant association of ovarian cancer with increasing alcohol consumption either during ages 20-30 years (p trend 0.42) or in the recent past (p trend 0.83). Regular drinking of beer (1 drink/day or more) during ages 20-30 (OR 1.55, 95% CI 1.07-2.26), though not liquor (OR 1.35, 95% CI 0.86-2.11) or wine (OR 0.99, 95% CI 0.49-2.00), was associated with a statistically significant increase in risk of invasive tumors, whereas no significant relationships were observed for recent drinking, regardless of alcohol type. The elevated risk for early adult regular drinking was confined to serous invasive tumors (OR 1.52, 95% CI 1.01-2.30), though results for other subtypes were based on sparse data and results were imprecise. In this study, neither total alcohol consumption as a young adult nor recently was associated with an increase in the risk of ovarian cancer.

Adenocarcinoma, Mucinous↗
PubMed2006

From menarche to menopause: trends among US Women born from 1912 to 1969.

The authors investigated secular trends in age at menarche, age at menopause, and reproductive life span within a population-based cohort of US women. Study subjects were 22,774 women selected randomly as controls for a case-control study. Eligible controls were residents of Wisconsin, Massachusetts, or New Hampshire born between 1910 and 1969. Subjects completed telephone interviews in 1988-2001 and answered questions regarding reproductive and lifestyle factors. Birth cohorts were created using 5- and 10-year periods, and statistical comparisons were performed with analysis of variance. The mean age at menarche decreased by approximately 6 months for those born between 1910 and 1949 (13.1 vs. 12.7 years; p < 0.001), with a subsequent increase to 13.0 years among women born between 1960 and 1969 (p < 0.001). Among naturally menopausal women aged 60 or more years who reported never use of postmenopausal hormone therapy, the authors observed a 17-month increase in the mean age at menopause for those born between 1915 and 1939 (49.1 vs. 50.5 years; p = 0.001) after adjustment for potential confounders. They also observed an increase in the average number of reproductive years (subtracting age at menarche from age at natural menopause), from 36.1 years among women born between 1915 and 1919 to 37.7 years among the 1935-1939 cohort (p = 0.0001). These findings have implications for women's lifetime exposure to circulating endogenous hormones.

Age Factors↗
PubMed2006

Familial relative risk estimates for use in epidemiologic analyses.

Commonly used crude measures of disease risk or relative risk in a family, such as the presence/absence of disease or the number of affected relatives, do not take into account family structures and ages at disease occurrence. The Family History Score incorporates these factors and has been used widely in epidemiology. However, the Family History Score is not an estimate of familial relative risk; rather, it corresponds to a measure of statistical significance against a null hypothesis that the family's disease risk is equal to that expected from reference rates. In this paper, the authors consider an estimate of familial relative risk using the empirical Bayes framework. The approach uses a two-level hierarchical model in which the first level models familial relative risk and the second considers a Poisson count of the number of affected relatives given the familial relative risk from the first level. The authors illustrate the utility of this methodology in a large, population-based case-control study of breast cancer, showing that, compared with commonly used summaries of family history including the Family History Score, the new estimates are more strongly associated with case-control status and more clearly detect effect modification of an environmental risk factor by familial relative risk.

Aged↗
PubMed2006

Risk of breast cancer for women living in rural areas from adult exposure to atrazine from well water in Wisconsin.

Research has suggested possible human health effects from low-level widespread exposure to environmental contaminants. We employed a novel exposure estimation technique using a publicly available data set to examine atrazine exposure, a suspected endocrine disruptor, in relation to breast cancer risk for women living in rural areas of Wisconsin. Incident breast cancer cases who were 20-79 years of age from 1987 to 2000 (n=3,275) and living in rural areas of Wisconsin at the time of interview were identified from Wisconsin's statewide cancer registry. Female controls of similar age and living in rural areas of Wisconsin were randomly selected from population lists (n=3,669). The addresses at diagnosis or reference year of study participants were assigned latitude/longitude coordinates (geocoded). The results from three statewide random studies of atrazine levels in well water in 1994, 1996, and 2001 were obtained from the Wisconsin Department of Agriculture, Trade, and Consumer Protection. Natural neighbor interpolation was used to estimate atrazine exposure levels separately for each of the 3 years. The mean atrazine exposure level was assigned to each participant based on her geocode. After adjustment for established breast cancer risk factors, compared to women in the lowest category of atrazine exposure (<0.15 ppb), the odds ratio of breast cancer for women exposed to atrazine concentrations of 1.0-2.9 ppb was 1.1 (95% CI 0.9-1.4). Results from this large population-based study do not suggest an increased risk of breast cancer from adult exposure to atrazine in drinking water. The possible risk for women exposed to levels of atrazine at or above statutory action levels of >or=3 ppb (OR 1.3, 95% CI 0.3-6.5) could not be ruled out due to small numbers in this category.

Adult↗
PubMed2006

Cadmium exposure and breast cancer risk.

Cadmium, a highly persistent heavy metal, has been categorized as a probable human carcinogen by the U.S. Environmental Protection Agency. Primary exposure sources include food and tobacco smoke. We carried out a population-based case-control study of 246 women, aged 20-69 years, with breast cancer and 254 age-matched control subjects. We measured cadmium levels in urine samples by inductively coupled plasma mass spectrometry and conducted interviews by telephone to obtain information on known breast cancer risk factors. Odds ratios (ORs) and 95% confidence intervals (CIs) for breast cancer by creatinine-adjusted cadmium levels were calculated by multivariable analysis. Statistical tests were two-sided. Women in the highest quartile of creatinine-adjusted cadmium level (> or = 0.58 microg/g) had twice the breast cancer risk of those in the lowest quartile (<0.26 microg/g; OR = 2.29, 95% CI = 1.3 to 4.2) after adjustment for established risk factors, and there was a statistically significant increase in risk with increasing cadmium level (P(trend) = .01). Based on this study, the absolute risk difference is 45 (95% CI = 0 to 77) per 100,000 given an overall breast cancer rate of 124 per 100,000. Whether increased cadmium is a causal factor for breast cancer or reflects the effects of treatment or disease remains to be determined.

Adult↗
PubMed2006

Retrospective cost-effectiveness analysis of screening mammography.

BACKGROUND: Many guidelines recommend screening mammography every 1-2 years for women older than 40 years; more than 70% of women now participate in routine screening. No studies have examined the societal impact of screening practices over the past decade in the United States on costs and quality-adjusted life-years (QALYs). We performed a retrospective cost-effectiveness analysis comparing actual and alternative screening mammography scenarios. METHODS: We used a discrete-event simulation model of breast cancer epidemiology to estimate the costs and the number of QALYs that were associated with observed screening mammography patterns in the United States from 1990 to 2000 for women aged 40 years or older. We also estimated costs and QALYS for no screening and for 64 alternative screening scenarios. Incremental cost-effectiveness ratios were computed. Sensitivity analyses were performed on key parameters. RESULTS: Actual U.S. screening patterns from 1990 to 2000 accrued 947.5 million QALYs and cost $166 billion over the lifetimes of the screened women, resulting in a gain of 1.7 million QALYs for an additional cost of $62.5 billion compared with no screening. Among those polices that were not dominated--i.e., for which no alternative existed that produced more QALYs for lower costs--screening all women aged 40-80 years annually per some U.S. guidelines was the most expensive option, costing $58,000 per additional QALY gained compared with the next most costly alternative, screening all women aged 45-80 years annually. Many alternative screening scenarios generated more QALYs for less cost (with savings up to $6 billion) than actual screening patterns over the study period. Sensitivity analysis showed that conclusions about the cost-effectiveness of screening mammography policies were highly sensitive to small, short-term detrimental effects on quality of life from the screening test itself. CONCLUSIONS: Choosing among the efficient policies to guide current screening recommendations requires consideration of costs to promote participation in screening and measurement of acute quality-of-life effects of mammography.

Adult↗
PubMed2006

Body mass index and the risk of death following the diagnosis of colorectal cancer in postmenopausal women (United States).

OBJECTIVES: Although overweight body mass is an established risk factor for colorectal cancer incidence, few studies have examined the association between body mass index (BMI) and mortality after colorectal cancer diagnosis. We examined survival in a group of postmenopausal women according to BMI. METHODS: Using the Wisconsin Cancer Reporting System we identified and enrolled 633 postmenopausal women aged 38-74 years who were diagnosed with colorectal cancer in 1988-1991. These women were interviewed by telephone; vital status was ascertained via Wisconsin death certificates. Cox proportional hazards regression was used to estimate multivariate risks of colorectal cancer-specific and all-cause mortality. RESULTS: Both underweight (BMI <20.0 kg/m2) (Hazard Ratio (HR) 2.3, 95% Confidence Interval (CI) 1.0-5.4) and obese (BMI > or = 30.0 kg/m2) women (HR 2.1, 95% CI 1.1-3.8) were at increased risk of colon cancer death, as compared to normal weight women (BMI 20.0-24.9 kg/m2). No association was observed for those with rectal cancer. Approximately 50% increases in all-cause mortality were observed among underweight and obese women with colorectal cancer. Postmenopausal hormone use did not appear to modify these associations. CONCLUSIONS: Underweight and obese postmenopausal women with colon cancer were at increased risk of death, though comorbidities may partially account for this risk.

Adult↗
PubMed2006

Relation of anthropometric measurements to ovarian cancer risk in a population-based case-control study (United States).

OBJECTIVE: To examine the relationship between anthropometric measures and ovarian cancer by menopausal status. METHODS: We analyzed data from a population-based case-control study comprised of 700 incident cases of epithelial ovarian cancer and 5,943 population controls from Massachusetts and Wisconsin enrolled between 1993 and 2001. In a telephone interview, information was gathered on established ovarian cancer risk factors, as well as adult height and age-specific body weight. Logistic regression was used to estimate multivariate-adjusted odds ratios (ORs) and 95% confidence intervals (CIs) for body mass index (BMI) throughout life. RESULTS: Recent BMI had no significant association with ovarian cancer risk (P-trend 0.14 for continuous BMI), after adjustment for age and other ovarian cancer risk factors. However, a non-significant positive association (overall P-trend 0.08) was observed for BMI at age 20; the risk estimate comparing a body mass of >25 kg/m2 to the lowest quintile (<or=18.88 kg/m2) was moderately but non-significantly elevated (OR 1.46; 95% CI 0.92, 2.31). CONCLUSION: Results of this study suggest that maintenance of a lean body mass, particularly in early adult life, may decrease ovarian cancer risk.

Adult↗
PubMed2006

The Wisconsin Breast Cancer Epidemiology Simulation Model.

The Wisconsin Breast Cancer Epidemiology Simulation Model is a discrete-event, stochastic simulation model using a systems-science modeling approach to replicate breast cancer incidence and mortality in the U.S. population from 1975 to 2000. Four interacting processes are modeled over time: (1) natural history of breast cancer, (2) breast cancer detection, (3) breast cancer treatment, and (4) competing cause mortality. These components form a complex interacting system simulating the lives of 2.95 million women (approximately 1/50 the U.S. population) from 1950 to 2000 in 6-month cycles. After a "burn in" of 25 years to stabilize prevalent occult cancers, the model outputs age-specific incidence rates by stage and age-specific mortality rates from 1975 to 2000. The model simulates occult as well as detected disease at the individual level and can be used to address "What if?" questions about effectiveness of screening and treatment protocols, as well as to estimate benefits to women of specific ages and screening histories.

Adult↗
PubMed2006

Duration of sleep and breast cancer risk in a large population-based case-control study.

One important function of sleep may be its contribution to the maintenance of the immune system and regulation of the circadian rhythms by melatonin. Researchers have speculated that disruption of immune functions involving cortisol levels and natural killer cell activity may increase breast cancer risk whereas increased melatonin exposure may protect against breast cancer. We conducted a multistate population-based case-control study of 4,033 women with invasive breast cancer and 5,314 community women without breast cancer in which we inquired about women's sleep habits in the recent past and during adult lifetime. Relative to women who slept 7.0-7.9 h/night, the multivariate odds ratio for developing breast cancer among women who slept an average of 9 h or more per night approximately 2 years prior to interview was 1.13 (95% CI 0.93-1.37). The multivariate-adjusted odds ratio for the continuous term was 1.06 (95% CI 1.01-1.11), suggesting a 6% increase in risk for every additional hour of sleep. Similar patterns were observed for average lifetime adult sleep duration. We found little evidence that sleeping few hours per night was associated with breast cancer risk. The results of this study suggest that increasing sleep duration is modestly associated with an increased breast cancer risk. In contrast, short duration of sleep (<7 h/night) is not substantially associated with increased risk. Further research in this area is warranted.

Adult↗
PubMed2006

Trends in childhood cancer incidence in Wisconsin, 1980-1999.

OBJECTIVES: Characterizing the burden of childhood cancer in Wisconsin is the first step to assessing the impact of prevention efforts, identifying especially vulnerable subgroups, and directing etiologic research. To support these goals, population-level data were used to examine trends in childhood cancer incidence among children aged 0-14 years in Wisconsin from 1980 to 1999. METHODS: Data for Wisconsin was provided by the Wisconsin Cancer Reporting System and compared to national data. Annual age-adjusted childhood cancer incidence rates for the entire population and subgroups by age, sex, race, time period, diagnostic code, and geographic region were described. Correlational analysis was conducted to assess the relation between community socioeconomic status and childhood cancer incidence using census data. RESULTS: Overall, Wisconsin's annual incidence rate for childhood cancers was 14.4 cases per 100,000 children aged 0-14 years during 1980-1999. This rate increased 10.9% (95% confidence interval 1-22%) between 1980 and 1999. Children in the 0-4 age group (20.9 per 100,000 per year) had the highest incidence rates as compared to 5-9 year olds (10.4 per 100,000 per year) and 10-14 year olds (12.0 per 100,000 per year). In males, the age-adjusted incidence of childhood cancers between 1980 and 1999 was 15.5 cases per 100,000 per year, whereas females had an incidence rate of 13.1 per 100,000 per year. Rates for whites were similar to the rates for all other racial groups combined. Leukemia had the highest age-adjusted incidence rate among childhood cancer diagnostic subtypes (4.3 cases per 100,000 per year); leukemia incidence increased by 32% between 1980 and 1999. Among the 13 hospital referral regions in Wisconsin with reported cancer cases, the Dubuque region had the highest annual age-adjusted incidence rate of 24.6 cases per 100,000, followed by Madison with 15.6 per 100,000, and Milwaukee with 15.5 per 100,000. In general, higher socioeconomic status as reflected by census indicators was positively correlated with higher rates of childhood cancer. SUMMARY: Wisconsin experienced childhood cancer incidence rates and trends similar to those throughout the United States between 1980 and 1999. Analysis of Wisconsin data, which is subject to small numbers in absolute terms (3,138 cases during 1980-1999), suggests that not all children have similar risk--infants and younger children (<5 years of age) as well as children living in areas with higher socioeconomic status may be especially vulnerable.

Adolescent↗
PubMed2005

A case-control study of the HER2 Ile655Val polymorphism in relation to risk of invasive breast cancer.

BACKGROUND: Overexpression of the HER2 proto-oncogene in human cancer cells has been associated with a poor prognosis, and survival improves with therapy targeting the HER2 gene. Animal studies and protein modeling suggest that the Ile655Val polymorphism located in the transmembrane domain of the HER2 protein might influence breast cancer development by altering the efficiency of homodimerization. METHODS: To investigate this genetic polymorphism, incident cases of invasive breast cancer (N = 1,094) and population controls of a similar age (N = 976) were interviewed during 2001 to 2003 regarding their risk factors for breast cancer. By using DNA collected from buccal samples mailed by the participants, the HER2 Ile655Val polymorphism was evaluated with the Applied Biosystems allelic discrimination assay. Odds ratios (ORs) and 95% confidence intervals (95% CIs) were estimated by logistic regression adjusted for numerous breast cancer risk factors. Analysis was restricted to women with self-reported European descent. RESULTS: Prevalence of the Val/Val genotype was 5.6% in cases and 7.1% in controls. In comparison with the Ile/Ile genotype, the Ile/Val genotype was not significantly associated with breast cancer risk (OR 0.97, 95% CI 0.79 to 1.18), whereas the Val/Val genotype was associated with a reduced risk (OR 0.63, 95% CI 0.42 to 0.92). This inverse association seemed strongest in older women (OR 0.51, 95% CI 0.29 to 0.89 for women aged more than 55 years), women without a family history of breast cancer (OR 0.54, 95% CI 0.35 to 0.84), postmenopausal women with greater body mass index (OR 0.43, 95% CI 0.20 to 0.91 for a body mass index of 25.3 kg/m2 or more), and cases diagnosed with non-localized breast cancer (OR 0.49, 95% CI 0.26 to 0.90). CONCLUSION: Although results from our population-based case-control study show an inverse association between the HER2 Ile655Val polymorphism and risk of invasive breast cancer, most other studies of this single-nucleotide polymorphism suggest an overall null association. Any further study of this polymorphism should involve sample populations with complete risk factor information and sufficient power to evaluate gene-environment interactions between the HER2 polymorphism and factors such as age and family history of breast cancer.

Adult↗
PubMed2005

Oral contraceptive use, reproductive factors, and colorectal cancer risk: findings from Wisconsin.

We investigated the association of oral contraceptive (OC) use and reproductive factors with colorectal cancer risk in a large population-based case-control study. Cases were women ages 20 to 74 years, living in Wisconsin, with a new diagnosis of colon (n = 1,122) or rectal (n = 366) cancer. Control participants were randomly selected from population lists of similarly aged female Wisconsin residents (n = 4,297). Risk factor information was collected through structured telephone interviews. Compared with never users, OC users had an odds ratio (OR) of 0.89 [95% confidence interval (95% CI), 0.75-1.06] for colorectal cancer. OC use associations did not differ significantly between colon and rectal cancer sites; however, when compared with never users, recent OC users (<14 years) seemed at reduced risk of rectal cancer (OR, 0.53; 95% CI, 0.28-1.00). Women with age at first birth older than the median (23 years) had 0.83 times the risk of colon cancer compared with women with age at first birth below the median (95% CI, 0.70-0.98). We observed an inverse trend between increasing parity and rectal cancer risk (P = 0.05). Compared with nulliparous women, women with five or more births had 0.66 times the risk of rectal cancer (95% CI, 0.43-1.02). Compared with postmenopausal women, premenopausal women were at reduced risk (OR, 0.67; 95% CI, 0.47-0.97) of colorectal cancer. No significant associations were observed between colorectal cancer risk and age at menarche or age at menopause. These findings suggest differential roles of reproductive factors in colon and rectal cancer etiology.

Adult↗
PubMed2005

Differences in breast cancer risk factors by tumor marker subtypes among premenopausal Vietnamese and Chinese women.

We evaluated associations between reproductive and lifestyle risk factors with breast cancer tumor marker status in a case-control study. Cases were premenopausal women living in Vietnam and China who were eligible for a clinical trial of oophorectomy and tamoxifen as treatment for breast cancer (n = 682). Controls were nonrelative hospital visitors, matched on age to the cases (n = 649). Immunohistochemical analysis was used to identify the presence of estrogen receptor (ER) and progesterone receptor and the overexpression of HER-2/neu oncogene. Odds ratios (OR) and 95% confidence intervals (95% CI) were estimated using unconditional logistic regression, adjusted for known confounders. Overall, 280 (61%) tumor samples were ER positive and 176 (38%) were ER negative. HER-2/neu overexpression was detected in 161 (35%) samples, whereas 286 (26%) samples were HER-2/neu negative. We observed an inverse trend between increasing parity and decreasing breast cancer risk (P = 0.002). Women ages > or =25 years at first birth had increased breast cancer risk compared with women ages <25 years at first birth (OR, 1.53; 95% CI, 1.20-1.95). Women who consumed alcohol had increased risk of breast cancer compared with women who did not (OR,1.85; 95% CI, 1.32-2.61). Compared with controls, OR estimates for breast cancer by parity and age at first birth were significantly associated with ER and/or HER-2/neu tumor status by Wald test (P < 0.05). Family history, age at menarche, cumulative lactation, body mass index, and education were not significantly related to breast cancer risk. Our findings support the hypothesis that some breast cancer risk factors differ by ER and HER-2/neu tumor marker subtypes.

Adult↗
PubMed2005

Correlates of age at menarche among sixth grade students in Wisconsin.

We conducted a cross-sectional, school-based survey of sixth-grade girls living in the Reedsburg, Wis area school district to explore factors associated with age at menarche. Data collection included parent and student questionnaires for demographic, menstrual, physical activity, and nutritional information. School nurses conducted physical examinations to provide anthropometric measurements. Salivary samples were obtained for laboratory analysis of estradiol, estrone, estriol, and progesterone levels. Students (n=59) were an average of 11.9 years of age (range: 10-13). Nineteen students (32%) reported menarche, with an average of 11.4 years of age (range: 8-12). Cycle length of the menstruating students averaged 32.0 days (range: 25-46 days). Students' age at menarche was positively correlated with their mothers' age at menarche (r=0.53, P=0.02). Total caloric intake, macronutrients, hormone levels, birthweight, and family size were not associated with menstrual status. We observed an inverse association between increasing weight and earlier age at menarche (P=0.03). Students past menarche watched more television (P=0.03) and participated in fewer hours of sporting activity (P=0.08) than students who had not yet reached menarche. These preliminary data suggest that further investigation of the determinants of menarche is both feasible and warranted.

Adolescent↗