Adulthood Density Research Articles

Peduli Lingkungan melalui Persediaan Tempat Sampah Pilah di Desa Setren, Kecamatan Rejoso, Kabupaten Nganjuk

Economic growth and increasing population density in adulthood require awareness regarding environmental concern. Caring for the environment is an important thing that must be done to prevent natural damage and maintain ecosystem balance. Nganjuk Regency, with a population density of around 1,103,902 people in 2020, of course produces quite a lot of household waste. There is a need to increase awareness and change attitudes regarding waste sorting and processing to create a clean and healthy environment, which is the aim of holding waste bin procurement activities. Seeing that Setren Village SDGs number 12, namely Environmentally Conscious Village Consumption and Production, still has not met the target score that must be achieved, knowledge regarding waste sorting needs to be emphasized more. The method used was direct observation in the Setren Village environment, then a Focus Group Discussion was held regarding handling waste problems to create a healthy environment. The results of the community service carried out are the provision of waste sorting bins and socialization of waste sorting. Apart from that, there has been an increase in knowledge regarding types of waste for the people of Setren Village.

Interrelationship between muscle fitness in childhood and bone mineral density in adulthood: mediation analysis of muscle fitness in adulthood

BackgroundThis study was aimed to examine the relationship between muscular fitness indicators in childhood and areal bone mineral density (aBMD) in adulthood and to verify whether the relationship is mediated by performance on muscular fitness indicators in adulthood.MethodsA sample of 138 healthy adults (69 males; 22.3 years) were followed after a previous assessment at the age of 7–10 years. Stature, body mass and muscular fitness indicators (handgrip strength, standing long jump and sit-ups tests) were assessed in childhood and adulthood. Additionally, total body, upper limbs, lower limbs, right femoral neck and lumbar spine aBMD was assessed in adulthood using dual X-ray absorptiometry. Analysis included descriptive statistics; t-test or Mann-Whitney U-test for comparison between males and females, multiple linear regression for the prediction aBMD from muscular fitness indicators in childhood, mediation analysis of the respective muscular fitness indicators in adulthood and the relationship between muscular fitness indicators in childhood and aBMD.ResultsMales were stronger compared to females regarding muscular fitness indicators in childhood and adulthood, and presented higher mean values for aBMD in adulthood, except for lumbar spine (p < 0.05). Regression analysis revealed that some muscular fitness indicators in childhood showed significant positive relationship with bone health indicators in adulthood, such as: handgrip strength and total body aBMD (β = 0.005; R2 = 0.35; p = 0.040) and upper limbs aBMD (β = 0.005; R2 = 0.55; p = 0.019); and sit-ups test was a significant predictors of lumbar spine BMD (β = 0.003; R2 = 0.06; p = 0.039). Mediation analysis pointed out the following: adulthood handgrip strength mediated relationships between childhood handgrip strength and total aBMD (indirect effect (IE) = 0.0025; 95%CI = 0.0005–0.0048), and upper limbs aBMD (IE = 0.0040; 95%CI = 0.0017–0.0069).ConclusionsMuscular fitness indicators in childhood showed significant relationship with bone health indicators in adulthood and the sit-ups test in childhood had direct effect on lumbar spine aBMD in adulthood. Adulthood handgrip strength mediated the relationship between childhood handgrip strength and total body and upper limb aBMD, pointing out that muscular fitness in childhood may be a aBMD determinant in adulthood, especially when higher muscle fitness performance is maintained in adulthood.

Is repeated childhood fracture related to areal bone density or body composition in middle age?

SummaryChildhood fracture is common, but whether it predicts adult fracture is not clear. Repeat childhood fracture was associated with adult (≤ 45 years) fracture, and in women, lower areal bone density was associated with repeat childhood fracture. Identifying fracture-prone children can modify adult fracture risk management.IntroductionA quarter of boys and 15% of girls will suffer multiple fractures, but it is not clear whether multiple fractures during growth predict fracture risk and areal bone density in adulthood. This study evaluated whether children who repeatedly fracture were at increased risk of low areal bone density, abnormal body composition, and fractures by age 45.MethodsA subsample of a large birth cohort study with childhood fracture cases had areal bone density assessed at age 45 years. Participants were questioned regularly across their lifetime about fractures during childhood (ages 0–18 years of age) and adulthood (any fracture between 18 and 45 years). The number of fractures was collapsed into three categories: no fractures; 1 fracture; and > 1 fracture, separately for child and adult groups.ResultsAt age 45 years, areal bone mineral density (g/cm2) and body composition were measured with dual X-ray absorptiometry in n = 555 participants. Compared to no fractures, twice as many girls (14% vs 7%, P = 0.156) and boys (31.4% vs 14.1%, P = 0.004) who repeatedly fractured in childhood sustained multiple fractures as adults. Both girls and boys who were fracture-free tended to remain fracture-free as adults (79.8% compared with 62.8%, P = 0.045, and 64.8% compared with 51.4%, P = 0.025, in males and females, respectively). Participants were more than twice as likely to fracture repeatedly as adults if they had sustained multiple fractures as a child (OR 2.5 95% CI: 1.4, 4.6). Women who repeatedly fractured during childhood had lower areal bone density, whereas repeated fracturing during childhood was not associated with areal bone density or body composition in men, even after adjustment for other factors known to influence fracture history.ConclusionChildhood fracture history is associated with persistent skeletal fragility in adulthood (≤ 45 years), even after adjustment for behavioral and demographic factors known to influence fracture history.

Developmental oxidative stress leads to T-type Ca2+ channel hypofunction in thalamic reticular nucleus of mouse models pertinent to schizophrenia

Impairment of parvalbumin interneurons induced by oxidative stress (OxS) is a “hub” on which converge several genetic and environmental risk factors associated with schizophrenia. In patients, this could be a mechanism leading to anomalies of the thalamic reticular nucleus (TRN) whose major neuronal population expresses parvalbumin. The TRN shapes the information flow within thalamo-cortical circuits. The low-threshold voltage-gated T-type Ca2+ (T-Ca2+) channels (CaV3.2, CaV3.3) contribute to the excitability and rhythmic bursting of TRN neurons which mediates cortical sleep spindles, known to be affected in schizophrenia. Here, we investigated the impact of OxS during postnatal development and adulthood on firing properties and T-Ca2+ channels of TRN neurons. In Gclm knock-out (KO) mice, which display GSH deficit and OxS in TRN, we found a reduction of T-Ca2+ current density in adulthood, but not at peripuberty. In KO adults, the decreased T-Ca2+ currents were accompanied with a decrease of CaV3.3 expression, and a shift towards more hyperpolarized membrane potentials for burst firing leading to less prominent bursting profile. In young KO mice, an early-life oxidative challenge precipitated the hypofunction of T-Ca2+ channels. This was prevented by a treatment with N-acetylcysteine. The concomitant presence of OxS and hypofunction of T-Ca2+ channels were also observed in TRN of a neurodevelopmental model relevant to psychosis (MAM mice). Collectively, these data indicate that OxS-mediated T-Ca2+ hypofunction in TRN begins early in life. This also points to T-Ca2+ channels as one target of antioxidant-based treatments aiming to mitigate abnormal thalamo-cortical communication and pathogenesis of schizophrenia.

Bone structure assessed with pQCT in prepubertal males with delayed puberty or congenital hypogonadotropic hypogonadism

Congenital hypogonadotropic hypogonadism (CHH) is associated with impaired bone mineral density in adulthood, whereas the estimates on bone structure in adolescents with CHH has not been previously evaluated. This study describes bone structure in CHH patients and compares it to that in boys with constitutional delay of growth and puberty (CDGP). A cross-sectional study. Peripheral quantitative computed tomography (pQCT) of non-dominant arm and left leg were performed. Volumetric bone mineral density (BMD), bone mineral content, and area in trabecular and cortical bone compartments were evaluated, and bone age-adjusted Z-scores for the bone parameters were determined. The participants with CHH had more advanced bone age and were older, taller and heavier than the CDGP boys, yet they had lower trabecular BMD in distal radius (147.7mg/mm3 [95% CI, 128-168mg/mm3 ] vs. 181.2mg/mm3 [172-192mg/mm3 ], p=.002) and distal tibia (167.6mg/mm3 [145-190mg/mm3 ] vs. 207.2mg/mm3 [187-227mg/mm3 ], p=.012), respectively. CHH males had lower cortical thickness at diaphyseal tibia than the participants with CDGP (p=.001). These between-group differences remained significant in corresponding Z-scores adjusted for bone age and height (p=.001). In CDGP group, serum testosterone correlated positively with trabecular BMD (r=0.51, p=.013) at distal radius, and estradiol levels correlated positively with trabecular BMD at the distal site of tibia (r=0.58, p=.004). Five treatment-naïve male patients with CHH exhibited poorer trabecular BMD than untreated males with CDGP. We speculate that timely low-dose sex steroid replacement in CHH males may benefit skeletal health in adulthood.

Variation in early life maternal care predicts later long range frontal cortex synapse development in mice

Empirical and theoretical work suggests that early postnatal experience may inform later developing synaptic connectivity to adapt the brain to its environment. We hypothesized that early maternal experience may program the development of synaptic density on long range frontal cortex projections. To test this idea, we used maternal separation (MS) to generate environmental variability and examined how MS affected 1) maternal care and 2) synapse density on virally-labeled long range axons of offspring reared in MS or control conditions. We found that MS and variation in maternal care predicted bouton density on dorsal frontal cortex axons that terminated in the basolateral amygdala (BLA) and dorsomedial striatum (DMS) with more, fragmented care associated with higher density. The effects of maternal care on these distinct axonal projections of the frontal cortex were manifest at different ages. Maternal care measures were correlated with frontal cortex → BLA bouton density at mid-adolescence postnatal (P) day 35 and frontal cortex → DMS bouton density in adulthood (P85). Meanwhile, we found no evidence that MS or maternal care affected bouton density on ascending orbitofrontal cortex (OFC) or BLA axons that terminated in the dorsal frontal cortices. Our data show that variation in early experience can alter development in a circuit-specific and age-dependent manner that may be relevant to understanding the effects of early life adversity.

Early-Life Adversity, but Not Suicide, Is Associated With Less Prefrontal Cortex Gray Matter in Adulthood.

BackgroundSuicide and major depression are prevalent in individuals reporting early-life adversity. Prefrontal cortex volume is reduced by stress acutely and progressively, and changes in neuron and glia density are reported in depressed suicide decedents. We previously found reduced neurotrophic factor brain-derived neurotrophic factor in suicide decedents and with early-life adversity, and we sought to determine whether cortex thickness or neuron or glia density in the dorsolateral prefrontal and anterior cingulate cortex are associated with early-life adversity or suicide.MethodsA total of 52 brains, constituting 13 quadruplets of nonpsychiatric controls and major depressive disorder suicide decedents with and without early-life adversity, were matched for age, sex, race, and postmortem interval. Brains were collected at autopsy and frozen, and dorsolateral prefrontal cortex and anterior cingulate cortex were later dissected, postfixed, and sectioned. Sections were immunostained for neuron-specific nuclear protein (NeuN) to label neurons and counterstained with thionin to stain glial cell nuclei. Cortex thickness, neuron and glial density, and neuron volume were measured by stereology.ResultsCortical thickness was 6% less with early-life adversity in dorsolateral prefrontal cortex and 12% less in anterior cingulate cortex (P < .05), but not in depressed suicide decedents in either region. Neuron density was not different in early-life adversity or with suicide, but glial density was 17% greater with early-life adversity in dorsolateral prefrontal cortex and 15% greater in anterior cingulate cortex, but not in suicides. Neuron volume was not different with early-life adversity or suicide.ConclusionsReported early-life adversity, but not the stress associated with suicide, is associated with thinner prefrontal cortex and greater glia density in adulthood. Early-life adversity may alter normal neurodevelopment and contribute to suicide risk.

Childhood Exposure to Passive Smoking and Bone Health in Adulthood: The Cardiovascular Risk in Young Finns Study.

Passive smoke exposure has been linked to the risk of osteoporosis in adults. We examined the independent effects of childhood passive smoke exposure on adult bone health. Longitudinal, the Cardiovascular Risk in Young Finns Study. The study cohort included 1422 individuals followed for 28 years since baseline in 1980 (age 3 to 18 years). Exposure to passive smoking was determined in childhood. In adulthood, peripheral bone traits were assessed with peripheral quantitative CT (pQCT) at the tibia and radius, and calcaneal mineral density was estimated with quantitative ultrasound. Fracture data were gathered by questionnaires. Parental smoking in childhood was associated with lower pQCT-derived bone sum index in adulthood (β± SE, -0.064 ± 0.023 per smoking parent; P = 0.004) in multivariate models adjusted for age, sex, active smoking, body mass index, serum 25-OH vitamin D concentration, physical activity, and parental socioeconomic position. Similarly, parental smoking was associated with lower heel ultrasound estimated bone mineral density in adulthood (β± SE, -0.097 ± 0.041 per smoking parent; P = 0.02). Parental smoking was also associated with the incidence of low-energy fractures (OR, 1.28; 95% CI, 1.01 to 1.62). Individuals with elevated cotinine levels (3 to 20 ng/mL) in childhood had lower bone sum index with pQCT (β± SE, -0.206 ± 0.057; P = 0.0003). Children whose parents smoked and had high cotinine levels (3 to 20 ng/mL) had significantly lower pQCT-derived bone sum index compared with those with smoking parents but had low cotinine levels (<3 ng/mL) (β± SE, -0.192 ± 0.072; P = 0.008). Children of parents who smoke have evidence of impaired bone health in adulthood.

Abstract P4-01-01: Adiposity at age 10 and mammographic density among premenopausal women

Abstract Background: Higher mammographic breast density is a strong risk factor for breast cancer. Early-life factors may influence breast development and subsequent breast density in adulthood. Although childhood adiposity is inversely associated with breast cancer risk, the association of childhood adiposity with mammographic breast density in premenopausal women has not been adequately studied. This knowledge could provide insight into pathways linking mammographic density and breast cancer risk. We investigated the associations between adiposity at age 10 and mammographic density. Methods: We collected data from 370 premenopausal women during their routine screening mammograms at Washington University in St. Louis, MO from December 2015 to October 2016. Body size at age 10 was self-reported using the Stunkard 9-figure Somatotype pictogram. For these analyses, the Stunkard pictogram was collapsed into 4 groups: (i) body size 1 or 2, (ii) body size 3 or 4, (iii) body size 5, (iv) body size 6 or higher. Body mass index (BMI) at age 10 was imputed using BMI and Stunkard data from the Growing Up Today Study. Trained personnel collected womens' height and weight, which were used to calculate current BMI. We used the Volpara software to evaluate the following volumetric mammographic density measures: volumetric percent density (VPD), dense volume (DV) and non-dense volume (NDV). Age-adjusted Pearson correlations and multivariable linear regression models (adjusted for age, age at each given birth, family history, race, education, oral contraceptive use, and breast feeding history) were used to evaluate the associations between adiposity at age 10 and volumetric mammographic density measures. Results: The mean age at the time of screening mammogram was 47.1 years. The majority of the women (43.8%) reported having body size 1 or 2, followed by body size 3 or 4 (34.9%), body size 5 (13.8%) and body size 6 (7.6%) at age 10. We observed a negative correlation between BMI at age 10 (r= -0.28, p-value&amp;lt;0.001) and VPD, and a positive correlation between BMI at age 10 (r= 0.27, p-value&amp;lt;0.001) and NDV. In multivariable regression models, adiposity at age 10 was significantly inversely associated with VPD, and positively associated with NDV. A 1kg/m2 increase in BMI at age 10 was associated with a 6.3% decrease in VPD (p-value &amp;lt;0.001), and a 6.7% increase in NDV (p-value &amp;lt;0.001). Compared to women whose body sizes were 1 and 2 at age 10, women with body size 3 or 4 had a 17.6% decrease in VPD, and a 28.5% increase in NDV; women with body size 5 had a 32.3% decrease in VPD, and a 58.1% increase in NDV, and women with body sizes ≥6 had a 46.6% decrease in VPD, and a 75.1% increase in NDV (all p-values &amp;lt;0.05). The associations of body size at age 10 and VPD were attenuated, but still statistically significant when we adjusted for current BMI. No statistically significant associations were found between adiposity at age 10 and DV. Conclusions: Our findings of an inverse association between adiposity at age 10 and percent density suggest that adiposity at age 10 could impact breast cancer development via its effect on mammographic density. Mechanistic studies to understand how childhood adiposity reduces mammographic density and breast cancer development in premenopausal women are needed. Citation Format: Alimujiang A, Imm KR, Appleton CM, Colditz GA, Berkey CS, Toriola AT. Adiposity at age 10 and mammographic density among premenopausal women [abstract]. In: Proceedings of the 2017 San Antonio Breast Cancer Symposium; 2017 Dec 5-9; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2018;78(4 Suppl):Abstract nr P4-01-01.

Early life socioeconomic environment and mammographic breast density

BackgroundEarly life social environment may influence breast cancer through shaping risk factors operating in early life, adolescence and adulthood, or may be associated with breast cancer risk independent of known risk factors. We investigated the associations between early life socioeconomic status (SES) and mammographic density, a strong risk factor for breast cancer, and the extent to which these associations were independent of risk factors across the lifecourse.MethodsWe used data from an adult follow-up study of two U.S. birth cohorts of women (average age = 43 years) with prospectively collected data starting during the pregnancy of the mother and continuing through early childhood of the offspring. We collected data on factors in later life periods through computer-assisted interviews with the offspring as adults, and obtained routine clinical mammograms for measurement of percent density and dense and nondense breast areas using a computer assisted method. We used generalized estimating equation models for multivariable analysis to account for correlated data for sibling sets within the study sample (n = 700 composed of 441 individuals and 127 sibling sets).ResultsHighest vs. lowest family income level around the time of birth was associated with smaller dense breast area after adjustment for early life factors (e.g., birthweight, maternal smoking during pregnancy) and risk factors in later life periods, including adult body mass index (BMI) and adult SES (β = −8.2 cm2, 95% confidence interval [CI]: −13.3, −3.2). Highest vs. lowest parental educational attainment was associated with higher percent density in models that adjusted for age at mammogram and adult BMI (e.g., β = 4.8, 95% CI = 0.6, 9.1 for maternal education of college or higher degree vs. less than high school), but the association was attenuated and no longer statistically significant after further adjustment for early life factors. There were no associations between early life SES indicators and non-dense area after adjustment for adult BMI. Neither adult education nor adult income was statistically significantly associated with any measure of mammographic density after adjusting for age and adult BMI.ConclusionsWe did not observe consistent associations between different measures of early life SES and mammographic density in adulthood.

Physical Activity Benefits the Skeleton of Children Genetically Predisposed to Lower Bone Density in Adulthood.

Both genetics and physical activity (PA) contribute to bone mineral density (BMD), but it is unknown if the benefits of physical activity on childhood bone accretion depend on genetic risk. We, therefore, aimed to determine if PA influenced the effect of bone fragility genetic variants on BMD in childhood. Our sample comprised US children of European ancestry enrolled in the Bone Mineral Density in Childhood Study (N = 918, aged 5 to 19 years, and 52.4% female). We used a questionnaire to estimate hours per day spent in total, high-, and low-impact PA. We calculated a BMD genetic score (% BMD lowering alleles) using adult genome-wide association study (GWAS)-implicated BMD variants. We used dual-energy X-ray absorptiometry to estimate femoral neck, total hip, and spine areal-BMD and total body less head (TBLH) bone mineral content (BMC) Z-scores. The BMD genetic score was negatively associated with each bone Z-score (eg, TBLH-BMC: estimate = -0.03, p = 1.3 × 10(-6) ). Total PA was positively associated with bone Z-scores; these associations were driven by time spent in high-impact PA (eg, TBLH-BMC: estimate = 0.05, p = 4.0 × 10(-10) ) and were observed even for children with lower than average bone Z-scores. We found no evidence of PA-adult genetic score interactions (p interaction > 0.05) at any skeletal site, and there was no evidence of PA-genetic score-Tanner stage interactions at any skeletal site (p interaction > 0.05). However, exploratory analyses at the individual variant level revealed that PA statistically interacted with rs2887571 (ERC1/WNT5B) to influence TBLH-BMC in males (p interaction = 7.1 × 10(-5) ), where PA was associated with higher TBLH-BMC Z-score among the BMD-lowering allele carriers (rs2887571 AA homozygotes: estimate = 0.08 [95% CI 0.06, 0.11], p = 2.7 × 10(-9) ). In conclusion, the beneficial effect of PA on bone, especially high-impact PA, applies to the average child and those genetically predisposed to lower adult BMD (based on GWAS-implicated BMD variants). Independent replication of our exploratory individual variant findings is warranted. © 2016 American Society for Bone and Mineral Research.

A rare cause of increased bone mineral density in adulthood: autosomal dominant osteopetrosis

Searchable abstracts of presentations at key conferences in endocrinology ISSN 1470-3947 (print) | ISSN 1479-6848 (online)

Postoperative changes in bone metabolism and bone mineral density in Japanese patients with acromegaly: a 3-year prospective study.

Growth hormone and insulin-like growth factor-I play important roles in regulating bone metabolism and bone mineral density in adulthood. However, the effect of excess growth hormone on bone metabolism and bone mineral density is not fully understood. Here, we investigated the long-term changes in bone metabolism and bone mineral density after a rapid decline in growth hormone levels due to transsphenoidal surgery in acromegalic patients. Eighteen acromegalic patients (10 males and 8 females) who underwent transsphenoidal surgery were enrolled in this prospective study. Bone formation marker (serum bone alkaline phosphatase), bone resorption marker (urinary type I collagen cross-linked N-telopeptide), and bone mineral density were measured before surgery and at 3 months, 1 year, and 3 years after transsphenoidal surgery. While both serum bone alkaline phosphatase and urinary type I collagen cross-linked N-telopeptide levels decreased significantly after surgery, serum bone alkaline phosphatase/urinary type I collagen cross-linked N-telopeptide ratio was significantly increased at 3 months and 3 years after surgery. Bone mineral density did not change markedly after surgery. In conclusion, the rapid decline in growth hormone levels following transsphenoidal surgery had no marked effect on bone mineral density for up to 3 years, despite significant changes in levels of bone turnover makers post-surgery.

Early life factors and adult mammographic density

Early life factors have shown to be related to breast cancer risk. The pathophysiological link could be mammographic density, a strong risk factor for breast cancer. Mammary gland development already starts in utero and early life factors might affect the number of mammary cells at risk. In this study, we investigated the association between early life factors and mammographic density in adulthood. The study was conducted within 2,588, mainly postmenopausal women of the Prospect-European Prospective Investigation into Cancer and Nutrition cohort. This ongoing study recruited breast cancer screening participants who filled out extensive questionnaires. Information on the early life factors birth weight, gestational age, maternal and paternal age, multiple births, birth rank, exposure to parental smoking, and leg length as a proxy for growth at childhood was obtained using questionnaires. Generalized linear models and linear regression models were used to study the relation between early life factors and mammographic density. Analyses were adjusted for potential confounders. Women who had an older mother (p = 0.06) or father (p = 0.002) at birth tended to have a higher mammographic density. Furthermore, greater leg length seemed to be related to higher mammographic density, although not statistically significantly (p = 0.16). After adjustment for confounders, none of the early life factors showed any statistically significant relationship with mammographic density in adulthood. Although we cannot exclude small effects that go undetected due to measurement error in recall of early life factors, the results suggest that mammographic density is not a major pathway in any observed relationship between these early life events and breast cancer risk.

Nectin-3 links CRHR1 signaling to stress-induced memory deficits and spine loss

Stress impairs cognition via corticotropin-releasing hormone receptor 1 (CRHR1), but the molecular link between abnormal CRHR1 signaling and stress-induced cognitive impairments remains unclear. We investigated whether the cell adhesion molecule nectin-3 is required for the effects of CRHR1 on cognition and structural remodeling after early-life stress exposure. Postnatally stressed adult mice had decreased hippocampal nectin-3 levels, which could be attenuated by CRHR1 inactivation and mimicked by corticotropin-releasing hormone (CRH) overexpression in forebrain neurons. Acute stress dynamically reduced hippocampal nectin-3 levels, which involved CRH-CRHR1, but not glucocorticoid receptor, signaling. Suppression of hippocampal nectin-3 caused spatial memory deficits and dendritic spine loss, whereas enhancing hippocampal nectin-3 expression rescued the detrimental effects of early-life stress on memory and spine density in adulthood. Our findings suggest that hippocampal nectin-3 is necessary for the effects of stress on memory and structural plasticity and indicate that the CRH-CRHR1 system interacts with the nectin-afadin complex to mediate such effects.

Diet across the Lifespan and the Association with Breast Density in Adulthood

Studies have shown inconsistent results regarding the association between dietary factors across the lifespan and breast density and breast cancer in women. Breast density is a strong risk factor for breast cancer, and the mechanism through which it influences cancer risk remains unclear. Breast density has been shown to be modifiable, potentially through dietary modifications. The goal of this paper is to summarize the current studies on diet and diet-related factors across all ages, determine which dietary factors show the strongest association with breast density, the most critical age of exposure, and identify future directions. We identified 28 studies, many of which are cross-sectional, and found that the strongest associations are among vitamin D, calcium, dietary fat, and alcohol in premenopausal women. Longitudinal studies with repeated dietary measures as well as the examination of overall diet over time are needed to confirm these findings.

Lifecourse predictors of mammographic density: the Newcastle Thousand Families cohort Study

Dense mammographic patterns are a strong predictor of breast cancer risk. Factors at differing stages of life have been linked to breast cancer risk, although rarely studied simultaneously. We aimed to investigate whether birth weight and factors later in life were associated with mammographic density in the Newcastle Thousand Families Study. The Study originally consisted of all 1142 babies born in May and June 1947 to mothers resident in Newcastle upon Tyne in Northern England. Detailed information was collected prospectively during childhood, including birth weight and socio-economic circumstances. At age 49-51 years, 574 study members completed a 'Health and Lifestyle' questionnaire. Of the 307 surviving women who returned these questionnaires, 199 returned a further questionnaire asking for details of routine mammographic screening, their reproductive and contraceptive history. Mammographic patterns were coded into Wolfe categories. This was analysed, by ordinal logistic regression, in relation to a range of variables at different stages of life. Increased standardised birth weight (odds ratio, OR 1.32 (95% CI 1.02-1.71) P = 0.03) was a significant independent predictor of higher density. Increasing body mass index (BMI) was predictive of lower density (OR 0.86 per Kg/m(2) (95% CI 0.81-0.92) P < 0.001), as was having reached menopause (OR, compared to pre- and peri-menopausal, 0.41 (95% CI 0.23-0.73) P = 0.002). Interactions were seen between menopausal status and both BMI and age at menarche (P = 0.06) on density, although for neither did the direction of association change. After adjustment for factors acting throughout life, we identified a significant association between standardised birth weight and density in adulthood, consistent with previous research suggesting that heavier babies have an increased risk of breast cancer in later life. We also confirmed associations between both BMI and menopausal status.

042 Lifecourse predictors of adult parenchymal breast tissue density: results from the Newcastle Thousand Families Study

ObjectiveTo investigate the relative influences of factors acting throughout life on breast tissue density at age 49-58 years.DesignFollow-up of the Newcastle Thousand Families birth cohort study.SettingIn 1947, all 1142 babies...

Bone Loading During Young Adulthood Predicts Bone Mineral Density in Physically Active, Middle-Aged Men

Background: Physical activity during growth induces skeletal adaptations that increase bone strength; however, it remains unclear whether these benefits persist into middle age. Objective: We sought to determine if bone loading during adolescence (ages 13–18 years) or young adulthood (ages 19–29 years) in men is associated with greater bone mineral density (BMD) and reduced risk of low bone density in adulthood. We also sought to determine if participation in high-impact activities (ie, those that produce a ground reaction force [GRF] > 4 times the individual's body weight] during adolescence and/or young adulthood has a lasting positive effect on adult BMD. Methods: Eighty-six, apparently healthy, physically active men (aged 30–60 years) participated in this cross-sectional study. Bone loading during adolescence, young adulthood, and adulthood were calculated based on GRFs of the reported physical activities. Whole body, lumbar spine, total hip, and femoral neck BMD were assessed using dual-energy x-ray absorptiometry (DXA). Multiple linear regression was used to examine relationships between BMD and bone loading, including body weight and/or age as covariates; logistic regression was used to predict low bone density for age. Participants were grouped based on participation in high-impact activity (never [n = 42], adolescence only [n = 19], or both adolescence and young adulthood [n=23]), and BMDs were compared. Results: Bone loading during young adulthood, but not adolescence, was a significant positive predictor of adult BMD, with the full models explaining 33.4%, 31.7%, 44.6%, and 50.6% of the variance in whole body, lumbar spine, total hip, and femoral neck BMD, respectively. Ten participants (11.6%) had low bone density for age based on z scores of the hip or spine. Body weight and lean body mass, but not bone loading, were associated with reduced risk of low bone density for age. Individuals who participated in high-impact activity during both adolescence and young adulthood had greater BMD at all measured sites compared with those participated only during adolescence. Conclusion: The results of the study support a lifelong exercise prescription for bone health to preserve the skeletal benefits of activity derived from activity during adolescence and young adulthood.

Prenatal cocaine exposure increases anxiety, impairs cognitive function and increases dendritic spine density in adult rats: influence of sex

Cocaine exposure during pregnancy can impact brain development and have long-term behavioral consequences. The present study examined the lasting consequences of prenatal cocaine (PN-COC) exposure on the performance of cognitive tasks and dendritic spine density in adult male and female rats. From gestational day 8 to 20, dams were treated daily with 30 mg/kg (ip) of cocaine HCl or saline. At 62 days of age, offspring were tested consecutively for anxiety, locomotion, visual memory and spatial memory. PN-COC exposure significantly increased anxiety in both sexes. Object recognition (OR) and placement (OP) tasks were used to assess cognitive function. Behavioral tests consisted of an exploration trial (T1) and a recognition trial (T2) that were separated by an inter-trial delay of varying lengths. Male PN-COC subjects displayed significantly less time investigating new objects or object locations during T2 in both OR and OP tasks. By contrast, female PN-COC subjects exhibited impairments only in OR and only at the longest inter-trial delay interval. In addition, gestational cocaine increased dendritic spine density in the prefrontal cortex and nucleus accumbens in both genders, but only females had increased spine density in the CA1 region of the hippocampus. These data reveal that in-utero exposure to cocaine results in enduring alterations in anxiety, cognitive function and spine density in adulthood. Moreover, cognitive deficits were more profound in males than in females.