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A novel quantitative approach to women's reproductive strategies.

ABSTRACT: The patterned way in which individuals allocate finite resources to various components of reproduction (e.g. mating effort, reproductive timing and parental investment) is described as a reproductive strategy. As energy is limited, trade-offs between and within aspects of reproductive strategies are expected. The first aim of this study was to derive aspects of reproductive strategies using complete reproductive histories from 718 parous Western Australian women. Factor analysis using a subset of these participants resulted in six factors that represented 'short-term mating strategy', 'early onset of sexual activity', 'reproductive output', 'timing of childbearing', 'breastfeeding', and 'child spacing'. This factor structure was internally validated by replication using a second independent subset of the data. The second aim of this study examined trade-offs between aspects of reproductive strategies derived from aim one. Factor scores calculated for each woman were incorporated in generalised linear models and interaction terms were employed to examine the effect of mating behaviour on the relationships between reproductive timing, parental investment and overall reproductive success. Early sexual activity correlates with early reproductive onset for women displaying more long-term mating strategies. Women with more short-term mating strategies exhibit a trade-off between child quantity and child quality not observed in women with a long-term mating strategy. However, women with a short-term mating strategy who delay reproductive timing exhibit levels of parental investment (measured as breastfeeding duration per child) similar to that of women with long-term mating strategies. Reproductive delay has fitness costs (fewer births) for women displaying more short-term mating strategies. We provide empirical evidence that reproductive histories of contemporary women reflect aspects of reproductive strategies, and associations between these strategic elements, as predicted from life history theory.

SUBMITTER: Milne FH

PROVIDER: S-EPMC3462799 | biostudies-literature | 2012

REPOSITORIES: biostudies-literature

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A novel quantitative approach to women's reproductive strategies.

Milne Fritha H FH Judge Debra S DS

PloS one 20121002 10

The patterned way in which individuals allocate finite resources to various components of reproduction (e.g. mating effort, reproductive timing and parental investment) is described as a reproductive strategy. As energy is limited, trade-offs between and within aspects of reproductive strategies are expected. The first aim of this study was to derive aspects of reproductive strategies using complete reproductive histories from 718 parous Western Australian women. Factor analysis using a subset o ...[more]

PMID: 23056440

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Project description:BackgroundWomen's reproductive factors include their age at menarche and menopause, the age at which they start and stop having children and the number of children they have. Studies that have linked these factors with disease risk have largely investigated individual reproductive factors and have not considered the genetic correlation and total interplay that may occur between them. This study aimed to investigate the nature of the relationships between eight female reproductive factors.MethodsWe used data from the UK Biobank and genetic consortia with data available for the following reproductive factors: age at menarche, age at menopause, age at first birth, age at last birth, number of births, being parous, age first had sexual intercourse and lifetime number of sexual partners. Linkage disequilibrium score regression (LDSC) was performed to investigate the genetic correlation between reproductive factors. We then applied Mendelian randomisation (MR) methods to estimate the causal relationships between these factors. Sensitivity analyses were used to investigate directionality of the effects, test for evidence of pleiotropy and account for sample overlap.ResultsLDSC indicated that most reproductive factors are genetically correlated (rg range: |0.06-0.94|), though there was little evidence for genetic correlations between lifetime number of sexual partners and age at last birth, number of births and ever being parous (rg < 0.01). MR revealed potential causal relationships between many reproductive factors, including later age at menarche (1 SD increase) leading to a later age at first sexual intercourse (beta (B) = 0.09 SD, 95% confidence intervals (CI) = 0.06,0.11), age at first birth (B = 0.07 SD, CI = 0.04,0.10), age at last birth (B = 0.06 SD, CI = 0.04,0.09) and age at menopause (B = 0.06 SD, CI = 0.03,0.10). Later age at first birth was found to lead to a later age at menopause (B = 0.21 SD, CI = 0.13,0.29), age at last birth (B = 0.72 SD, CI = 0.67, 0.77) and a lower number of births (B = -0.38 SD, CI = -0.44, -0.32).ConclusionThis study presents evidence that women's reproductive factors are genetically correlated and causally related. Future studies examining the health sequelae of reproductive factors should consider a woman's entire reproductive history, including the causal interplay between reproductive factors.

Project description:BackgroundThe COVID-19 pandemic has profoundly affected the lives of the global population. It is known that periods of stress and psychological distress can affect women's menstrual cycles. We therefore performed an observational study of women's reproductive health over the course of the pandemic thus far.Materials and methodsAn anonymous digital survey was shared by the authors via social media in September 2020. All women of reproductive age were invited to complete the survey.Results1031 women completed the survey. Mean age was 36.7 ± 6.6 years (range, 15-54). 693/70% reported recording their cycles using an app or diary. 233/23% were using hormonal contraception. 441/46% reported a change in their menstrual cycle since the beginning of the pandemic. 483/53% reported worsening premenstrual symptoms, 100/18% reported new menorrhagia (p = 0.003) and 173/30% new dysmenorrhea (p < 0.0001) compared to before the pandemic. 72/9% reported missed periods who not previously missed periods (p = 0.003) and the median number of missed periods was 2 (1-3). 17/21% of those who "occasionally" missed periods pre-pandemic missed periods "often" during pandemic. 467/45% reported a reduced libido. There was no change in the median cycle length (28 days) or days of bleeding (5) but there was a wider variability of cycle length (p = 0.01) and a 1 day median decrease in the minimum (p < 0.0001) and maximum (p = 0.009) cycle length. Women reported a median 2 kg increase in self-reported weight and a 30-min increase in median weekly exercise. 517/50% of women stated that their diet was worse and 232/23% that it was better than before the pandemic. 407/40% reported working more and 169/16% were working less. Women related a significant increase in low mood (p < 0.0001), poor appetite (p < 0.0001), binge eating (p < 0.0001), poor concentration (p < 0.0001), anxiety (p < 0.0001), poor sleep (p < 0.0001), loneliness (p < 0.0001) and excess alcohol use (p < 0.0001). Specific stressors reported included work stress (499/48%), difficulty accessing healthcare (254/25%), change in financial (201/19%) situation, difficulties with home schooling (191/19%) or childcare (99/10%), family or partner conflict (170/16%), family illness or bereavement (156/15%).ConclusionsThe COVID-19 pandemic has significantly impacted the reproductive health of women. The long term health implications of this are yet to be determined and future studies should address this.

Project description:Melanoma is one of the most lethal forms of skin cancer and its incidence is continuing to rise in the United States. Therefore, novel mechanism and target-based strategies are needed for the management of this disease. SIRT1, a NAD(+)-dependent class III histone deacetylase, has been implicated in a variety of physiological processes and pathological conditions. We recently demonstrated that SIRT1 is upregulated in melanoma and its inhibition by a small-molecule, tenovin-1, inhibits cell proliferation and clonogenic survival of melanoma cells, possibly via activating p53. Here, we employed a gel free quantitative proteomics approach to identify the downstream effectors and targets of SIRT1 in melanoma. The human malignant melanoma, G361 cells were treated with tenovin-1 followed by protein extraction, in liquid trypsin digestion, and peptide analyses using nanoLC-MS/MS. A total of 1091 proteins were identified, of which 20 proteins showed significant differential expression with 95% confidence interval. These proteins were subjected to gene ontology and Ingenuity Pathway Analysis (IPA) to obtain the information regarding their biological and molecular functions. Real-Time qRT-PCR validation showed that five of these (PSAP, MYO1B, MOCOS, HIS1H4A and BUB3) were differentially expressed at mRNA levels. Based on their important role in cell cycle regulation, we selected to focus on BUB family proteins (BUB3, as well as BUB1 and BUBR1) for subsequent validation. The qRT-PCR and immunoblot analyses showed that tenovin-1 inhibition of SIRT1 resulted in a downregulation of BUB3, BUB1 and BUBR1 in multiple melanoma cell lines. Since tenovin-1 is an inhibitor of both SIRT1 and SIRT2, we employed lentivirus mediated silencing of SIRT1 and SIRT2 in G361 cells to determine if the observed effects on BUB family proteins are due to SIRT1- or SIRT2- inhibition. We found that only SIRT1 inhibition resulted in a decrease in BUB3, BUB1 and BUBR1. Our study identified the mitotic checkpoint regulator BUB family proteins as novel downstream targets of SIRT1. However, further validation is needed in appropriate models to confirm our findings and expand on our observations.

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A novel quantitative approach to women's reproductive strategies.

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A novel quantitative approach to women's reproductive strategies.

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