14 resultados para maternal effect

em Deakin Research Online - Australia


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1. Hormone-mediated maternal effects and developmental plasticity are important sources of phenotypic variation, with potential consequences for trait evolution. Yet our understanding of the importance of maternal hormones for offspring fitness in natural populations is very limited, particularly in non-avian species.

2. We experimentally elevated yolk testosterone by injection of a physiological dose into eggs of the lizard Ctenophorus fordi Storr, to investigate its roles in offspring development, growth and survival.

3. Yolk testosterone did not influence incubation period, basic hatchling morphology or survival under natural conditions. However, there was evidence for increased growth in hatchlings from testosterone-treated eggs, suggesting that maternal hormones have potential fitness consequences in natural populations.

4. The positive effect of prenatal testosterone exposure on postnatal growth could represent a taxonomically widespread developmental mechanism that has evolved into an adaptive maternal effect in some taxa, but remains deleterious or selectively neutral in others.

5. A broader taxonomic perspective should increase our understanding of the role of physiological constraints in the evolution of endocrine maternal effects.

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Background/Objectives: We tested the hypothesis that the relationship between maternal 25-hydroxyvitamin D (25-(OH)D) and offspring birth size differs according to offspring vitamin D receptor (VDR) genotype (Apa1, Bsm1, Fok1 or Taq1).

Subjects/Methods: Mothers of 354 singleton babies had serum 25-(OH)D concentration measured at 28–30 weeks of gestation and consented to measurement of their babies soon after birth. DNA was extracted from the babies’ Guthrie cards.

Results: There was evidence of effect modification by infant FokI genotype. Babies of deficient mothers had lower birth weight with FF or Ff, but not ff genotype (P-value for interaction after adjustment for potential confounding factors=0.02), but thicker subscapular and suprailiac skinfolds with ff, but not FF or Ff genotype (P=0.008 and 0.02, respectively). Sample size was insufficient to investigate effect modification by the other VDR polymorphisms.

Conclusions:
These preliminary findings suggest that studies of maternal vitamin D status and birth size may need to take VDR genotype into account.

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Background: Maternal education is consistently found to be inversely related to children’s television viewing and is associated with aspects of the family television environment. This study investigates whether family television environment mediates the relationship between maternal education and children’s television viewing.

Methods: Parents of 1484 children reported maternal education, time their child spends watching television, and 21 aspects of the family television environment (potential mediators) during 2002 and 2003. Separate regression analyses were conducted in 2006 for each potential mediator that met two initial conditions for mediation (associated with both maternal education and children’s television viewing (p<0.10)), to assess whether inclusion reduced the association between maternal education and children’s television viewing. Multivariable regression assessed the combined impact of all mediators.

Results: Twelve of 21 potential mediators met the initial conditions for mediation. Inclusion of each resulted in decreased β values (3.2% to 15.2%) for the association between maternal education and television viewing. Number and placement of televisions in the home appeared to have the greatest mediating effect, followed by frequency of eating dinner in front of the television with the child and rules about television viewing during mealtimes. Together, the 12 mediators accounted for more than one-third of the association between maternal education and children’s television viewing time.

Conclusions: This study suggests the strong inverse relationship between maternal education and children’s television viewing is partly mediated by aspects of the family television environment.


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Fish consumption during gestation can provide the fetus with long-chain polyunsaturated fatty acids (LCPUFA) and other nutrients essential for growth and development of the brain. However, fish consumption also exposes the fetus to the neurotoxicant, methyl mercury (MeHg). We studied the association between these fetal exposures and early child development in the Seychelles Child Development Nutrition Study (SCDNS). Specifically, we examined a priori models of Ω-3 and Ω-6 LCPUFA measures in maternal serum to test the hypothesis that these LCPUFA families before or after adjusting for prenatal MeHg exposure would reveal associations with child development assessed by the BSID-II at ages 9 and 30 months. There were 229 children with complete outcome and covariate data available for analysis. At 9 months, the PDI was positively associated with total Ω-3 LCPUFA and negatively associated with the ratio of Ω-6/Ω-3 LCPUFA. These associations were stronger in models adjusted for prenatal MeHg exposure. Secondary models suggested that the MeHg effect at 9 months varied by the ratio of Ω-6/Ω-3 LCPUFA. There were no significant associations between LCPUFA measures and the PDI at 30 months. There were significant adverse associations, however, between prenatal MeHg and the 30-month PDI when the LCPUFA measures were included in the regression analysis. The BSID-II mental developmental index (MDI) was not associated with any exposure variable. These data support the potential importance to child development of prenatal availability of Ω-3 LCPUFA present in fish and of LCPUFA in the overall diet. Furthermore, they indicate that the beneficial effects of LCPUFA can obscure the determination of adverse effects of prenatal MeHg exposure in longitudinal observational studies.

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The aim of this project was to investigate the effects of oral contraceptives on the nutrient composition of breast milk. The design of the study also allowed the effects of stage of lactation and maternal diet on milk composition to be observed. A prospective study was designed to measure maternal dietary intake and vitamin and trace element concentration in milk and plasma. Vitamin A, ascorbic acid and iron, copper, zinc, manganese, selenium, cobalt, chromium, rubidium and caesium were measured. Two groups of women participated, oral contraceptive users and controls. Fasting milk and blood samples and 24-hour food records were collected from the women once a week for 20 weeks commencing 3-8 weeks post-partum, and 1-2 weeks before they began to take oral contraceptives. Fifteen women participated in the study; 5 took progestogen-only oral contraceptives, 1 took an oestrogen-progestogen oral contraceptive and 9 acted as controls. Progestogen-only oral contraceptives did not affect the milk or plasma concentration of the vitamins and trace elements measured. As only 1 subject took an oestrogen-progestogen preparation no conclusion could be drawn as to its effect. The mean milk and plasma concentration of all nutrients studied did not change significantly with the progression of lactation, with the exception of iron and zinc. The mean milk iron concentration was significantly higher at 16 weeks post-partum than at 8 and 23 weeks post-partum. The mean milk zinc concentration was significantly lower at 23 weeks post-partum than at 8 and 16 weeks post-partum. The infants1 mean estimated daily intakes of ascorbic acid and vitamin A from breast milk were above the U.S. and British Recommended Dietary Allowance for those vitamins. However, their mean estimated intakes of iron, zinc, copper, manganese and selenium were well below the U.S. recommendations. Effects of the maternal dietary intake on milk and plasma composition were variable. Implications of these findings have been discussed.

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Female birds have been shown to have a remarkable degree of control over the sex ratio of the offspring they produce. However, it remains poorly understood how these skews are achieved. Female condition, and consequent variation in circulating hormones, provides a plausible mechanistic link between offspring sex biases and the environmental and social stresses commonly invoked to explain adaptive sex allocation, such as diet, territory quality, and body condition. However, although experimental studies have shown that female perception of male phenotype alone can lead to sex ratio biases, it is unknown how partner quality influences female physiological state. Using a controlled within-female experimental design where female Gouldian finches (Erythrura gouldiae) bred with both high- and low-quality males, we found that partner quality directly affects female hormonal status and subsequent fitness. When constrained to breeding with low-quality males, females had highly elevated stress responses (corticosterone levels) and produced adaptive male-biased sex ratios, whereas when they bred with high-quality males, females had low corticosterone levels and produced an equal offspring sex ratio. There was no effect of other maternal hormones (e.g., testosterone) or body condition on offspring sex ratios. Female physiological condition during egg production, and variation in circulating hormones in particular, may provide a general mechanistic route for strategic sex allocation in birds.

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Skipping meals is particularly common during adolescence and can have a detrimental effect on multiple aspects of adolescent health. Understanding the correlates of meal-skipping behaviours is important for the design of nutrition interventions. The present study examined maternal and best friends’ influences on adolescent meal-skipping behaviours. Frequency of skipping breakfast, lunch and dinner was assessed using a Web-based survey completed by 3001 adolescent boys and girls from years 7 and 9 of secondary schools in Victoria, Australia. Perceived best friend and maternal meal skipping, modelling of healthy eating (eating healthy food, limiting junk food, eating fruit and vegetables) and weight watching were assessed. Best friend and maternal factors were differentially associated with meal-skipping behaviours. For example, boys and girls who perceived that their best friend often skipped meals were more likely to skip lunch (OR ¼ 2·01, 95% CI 1·33, 3·04 and OR ¼ 1·93, 95% CI 1·41, 2·65; P,0·001). Boys and girls who perceived that their mother often skipped meals were more likely to skip breakfast (OR ¼ 1·48, 95% CI 1·01, 2·15; P,0·05 and OR ¼ 1·93, 95% CI 1·42, 2·59; P,0·001) and lunch (OR ¼ 2·05, 95% CI 1·35, 3·12 and OR ¼ 2·02, 95% CI 1·43, 2·86; P,0·001). Educating adolescents on how to assess and interpret unhealthy eating behaviours that they observe from significant others may be one nutrition promotion strategy to reduce meal-skipping behaviour. The involvement of mothers may be particularly important in such efforts. Encouraging a peer subculture that promotes regular consumption of meals and educates adolescents on the detrimental impact of meal-skipping behaviour on health may also offer a promising nutrition promotion strategy.

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There is a strong inverse relationship between a females own birth weight and her subsequent risk for gestational diabetes with increased risk of developing diabetes later in life. We have shown that growth restricted females develop loss of glucose tolerance during late pregnancy with normal pancreatic function. 


The aim of this study was to determine whether growth restricted females develop long-term impairment of metabolic control after an adverse pregnancy adaptation. Uteroplacental insufficiency was induced by bilateral uterine vessel ligation (Restricted) or sham surgery (Control) in late pregnancy (E18) in F0 female rats. F1 Control and Restricted female offspring were mated with normal males and allowed to deliver (termed Ex-Pregnant). Age-matched Control and Restricted Virgins were also studied and glucose tolerance and insulin secretion were determined. Pancreatic morphology and hepatic glycogen and triacylglycerol content were quantified respectively.

Restricted females were born lighter than Control and remained lighter at all time points studied (p<0.05). Glucose tolerance, first phase insulin secretion and liver glycogen and triacylglycerol content were not different across groups, with no changes in β-cell mass. Second phase insulin secretion was reduced in Restricted Virgins (-34%, p<0.05) compared to Control Virgins, suggestive of enhanced peripheral insulin sensitivity but this was lost after pregnancy. Growth restriction was associated with enhanced basal hepatic insulin sensitivity, which may provide compensatory benefits to prevent adverse metabolic outcomes often associated with being born small. A prior pregnancy was associated with reduced hepatic insulin sensitivity with effects more pronounced in Controls than Restricted.

Our data suggests that pregnancy ameliorates the enhanced peripheral insulin sensitivity in growth restricted females and has deleterious effects for hepatic insulin sensitivity, regardless of maternal birth weight.

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We have previously reported that maternal creatine supplementation protects the neonate from hypoxic injury. Here, we investigated whether maternal creatine supplementation altered expression of the creatine synthesis enzymes (arginine:glycine amidinotransferase [AGAT], guanidinoaceteate methyltransferase [GAMT]) and the creatine transporter (solute carrier family 6 [neurotransmitter transporter, creatine] member 8: SLC6A8) in the term offspring. Pregnant spiny mice were fed a 5% creatine monohydrate diet from midgestation (day 20) to term (39 days). Placentas and neonatal kidney, liver, heart, and brain collected at 24 hours of age underwent quantitative polymerase chain reaction and Western blot analysis. Maternal creatine had no effect on the expression of AGAT and GAMT in neonatal kidney and liver, but mRNA expression of AGAT in brain tissues was significantly decreased in both male and female neonates born to mothers who were fed the creatine diet. SLC6A8 expression was not affected by maternal dietary creatine loading in any tissues. Maternal dietary creatine supplementation from midgestation in the spiny mouse did not alter the capacity for creatine synthesis or transport.

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Objectives

In this study, we assess the importance of area-based partnerships in an initiative to improve access to Maternal and Child Health (MCH) services (known as Best Start) in socially disadvantaged communities in Victoria, Australia.

Methods:
The study assessed changes in MCH attendance rates, parental attitudes and local partnership formation before and after the introduction of Best Start projects. Partners involved in Best Start projects were surveyed regarding the extent of local partnership formation (before 54; after 84). Data was collected for MCH attendance using routine records for Best Start with MCH projects (before 1,739; after 1437) and the rest of the State (before 45,497; after 45,953). Two cross-sectional surveys of parents of 3-year old children were used to assess changes in parent’s knowledge about, and confidence in using relevant services as well as parental confidence more generally (before 1666; after 1838).

Results:
Best Start was significantly associated with improving:
- levels of partnership formation (5 of 7 relevant factors)
- attendance at the 3.5 year MCH visit in Best Start Sites with MCH projects between 2001/02-2004/05.
- parent’s access to information (partnership effect);
- confidence about attending the 3.5 year MCH visits (partnership effect); and
- overall parental confidence (project effect only).

Conclusion:
Best Start improves participation in the MCH attendance. This is related most directly to improving parent’s access to information and overall parental confidence either through local partnership or direct project effects.

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Background
To investigate the effect of an early childhood obesity prevention intervention, incorporating a parent modelling component, on fathers’ obesity risk-related behaviours.

Methods

Cluster randomized-controlled trial in the setting of pre-existing first-time parents groups organised by Maternal and Child Health Nurses in Victoria, Australia. Participants were 460 first-time fathers mean age = 34.2 (s.d.4.90) years. Dietary pattern scores of fathers were derived using principal component analysis, total physical activity and total television viewing time were assessed at baseline (infant aged three to four months) and after 15 months.

Results
No significant beneficial intervention effect was observed on fathers’ dietary pattern scores, total physical activity or total television viewing time.

Conclusion

Despite a strong focus on parent modelling (targeting parents own diet, physical activity and television viewing behaviours), and beneficial impact on mothers’ obesity risk behaviours, this intervention, with mothers as the point of contact, had no effect on fathers’ obesity risk-related behaviours. Based on the established links between children’s obesity risk-related behaviors and that of their fathers, a need exists for research testing the effectiveness of interventions with a stronger engagement of fathers.

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High intrauterine cortisol exposure can inhibit fetal growth and have programming effects for the child's subsequent stress reactivity. Placental 11beta-hydroxysteroid dehydrogenase (11β-HSD2) limits the amount of maternal cortisol transferred to the fetus. However, the relationship between maternal psychopathology and 11β-HSD2 remains poorly defined. This study examined the effect of maternal depressive disorder, antidepressant use and symptoms of depression and anxiety in pregnancy on placental 11β-HSD2 gene (HSD11B2) expression. Drawing on data from the Mercy Pregnancy and Emotional Wellbeing Study, placental HSD11B2 expression was compared among 33 pregnant women, who were selected based on membership of three groups; depressed (untreated), taking antidepressants and controls. Furthermore, associations between placental HSD11B2 and scores on the State-Trait Anxiety Inventory (STAI) and Edinburgh Postnatal Depression Scale (EPDS) during 12-18 and 28-34 weeks gestation were examined. Findings revealed negative correlations between HSD11B2 and both the EPDS and STAI (r = -0.11 to -0.28), with associations being particularly prominent during late gestation. Depressed and antidepressant exposed groups also displayed markedly lower placental HSD11B2 expression levels than controls. These findings suggest that maternal depression and anxiety may impact on fetal programming by down-regulating HSD11B2, and antidepressant treatment alone is unlikely to protect against this effect.

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BACKGROUND: It is well established that maternal age at childbirth has implications for women's mental health in the short term, however there has been little research regarding longer term implications and whether this association has changed over time. We investigated longer term mental health consequences for young mothers in Australia and contrasted the effects between three birth cohorts. METHODS: Using thirteen waves of data from 4262 women aged 40 years or above participating in the Household, Income and Labour Dynamics in Australia Survey, we compared the mental health of women who had their first child aged 15-19 years, 20-24 years, and 25 years and older. Mental health was measured using the mental health component summary score of the SF-36. We used random-effects linear regression models to generate estimates of the association between age at first birth and mental health, adjusted for early life socioeconomic characteristics (country of birth, parents' employment status and occupation) and later life socioeconomic characteristics (education, employment, income, housing tenure, relationship status and social support). We examined whether the association changed over time, testing for effect modification across three successive birth cohorts. RESULTS: In models adjusted for early life and later life socioeconomic characteristics, there was strong evidence of an association between teenage births and poor mental health, with mental health scores on average 2.76 to 3.96 points lower for mothers aged younger than 20 years than for mothers aged 25 years and older (Late Baby Boom (born 1936-1945): -3.96, 95% CI -5.38, -2.54; Early Baby Boom (born 1946-1955): -3.01, 95% CI -4.32, -1.69; Lucky Few (born 1956-1965): -2.76, 95% CI -4.34, -1.18), and evidence of an association for mothers aged 20-24 years compared to mothers aged 25 years and older in the most recent birth cohort only (-1.09, 95% CI -2.01, -0.17). There was some indication (though weak) that the association increased in more recent cohorts. CONCLUSION: This study highlights that young mothers, and particularly teenage mothers, are a vulnerable group at high risk of poor mental health outcomes compared to mothers aged 25 years and above, and there was some suggestion (though weak) that the health disparities increased over time.

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Maternal mental health during pregnancy has been linked to health outcomes in progeny. Mounting evidence implicates fetal “programming” in this process, possibly via epigenetic disruption. Maternal mental health has been associated with glucocorticoid receptor methylation (nuclear receptor subfamily 3, group C, member 1 [NR3C1]) in the neonate; however, most studies have been small (n < 100) and have failed to control for multiple testing in the statistical analysis. The Barwon Infant Study is a population-derived birth cohort with antenatal recruitment. Maternal depression and anxiety were assessed using the Edinburgh Postnatal Depression Scale and psychological distress using the Perceived Stress Scale. NR3C1 cord blood methylation levels were determined using Sequenom MassArray for 481 participants. Maternal psychological distress and anxiety were associated with a small increase in neonate NR3C1 methylation at specific CpG sites, thus replicating some previous findings. However, associations were only nominally significant and did not remain after correction for the number of CpG sites and exposures investigated. As the largest study to explore the relationship between maternal well-being and offspring NR3C1 cord blood methylation, our results highlight the need for caution when interpreting previous findings in this area. Future studies must ensure they are adequately powered to detect the likely small effect sizes while controlling for multiple testing.