Cancer risk in individuals with autism spectrum disorder.

BACKGROUND: Whether individuals with autism spectrum disorders (ASDs) have a higher-than-expected risk of cancer remains unknown. PATIENTS AND METHODS: We carried out a population-based cohort study including 2.3 million individuals live-born to mothers from Nordic countries during 1987-2013 in Sweden with follow-up through 2016 (up to age 30 years). Individuals with ASD were ascertained through the Swedish National Patient Register. We estimated the relative risk of cancer in relation to ASD by odds ratios (ORs) and associated 95% confidence intervals (CIs) derived from logistic regression, after detailed adjustment for potential confounders. We also carried out a sibling comparison to address familial confounding and a genetic correlation analysis using the genome-wide association study summary statistics to address confounding due to potential polygenetic pleiotropy between ASD and cancer. RESULTS: We observed an overall increased risk of any cancer among individuals with ASD (OR 1.3, 95% CI 1.2-1.5), compared with individuals without ASD. The association for any cancer was primarily noted for narrowly defined autistic disorder (OR 1.7, 95% CI 1.3-2.1) and ASD with comorbid birth defects (OR 2.1, 95% CI 1.5-2.9) or both birth defects and intellectual disability (ID; OR 4.8, 95% CI 3.4-6.6). An association was also suggested for ASD with comorbid ID (OR 1.4; 95% CI 0.9-2.1), but was not statistically significant. ASD alone (i.e. without comorbid ID or birth defects) was not associated with an increased risk of any cancer (OR 1.0, 95% CI 0.8-1.2). Sibling comparison and genetic correlation analysis showed little evidence for familial confounding or confounding due to polygenetic pleiotropy between ASD and cancer. CONCLUSIONS: ASD per se is not associated with an increased risk for cancer in early life. The increased cancer risk among individuals with ASD is likely mainly attributable to co-occurring ID and/or birth defects in ASD.

A proof-of-concept study of growth hormone in children with Phelan-McDermid syndrome.

BACKGROUND: Phelan-McDermid syndrome (PMS) is caused by 22q13 deletions including SHANK3 or pathogenic sequence variants in SHANK3 and is among the more common rare genetic findings in autism spectrum disorder (ASD). SHANK3 is critical for synaptic function, and preclinical and clinical studies suggest that insulin-like growth factor-1 (IGF-1) can reverse a range of deficits in PMS. IGF-1 release is stimulated by growth hormone secretion from the anterior pituitary gland, and this study sought to assess the feasibility of increasing IGF-1 levels through recombinant human growth hormone (rhGH) treatment, in addition to establishing safety and exploring efficacy of rhGH in children with PMS. METHODS: rhGH was administered once daily for 12 weeks to six children with PMS using an open-label design. IGF-1 levels, safety, and efficacy assessments were measured every 4 weeks throughout the study. RESULTS: rhGH administration increased levels of IGF-1 by at least 2 standard deviations and was well tolerated without serious adverse events. rhGH treatment was also associated with clinical improvement in social withdrawal, hyperactivity, and sensory symptoms. LIMITATIONS: Results should be interpreted with caution given the small sample size and lack of a placebo control. CONCLUSIONS: Overall, findings are promising and indicate the need for larger studies with rhGH in PMS. Trial registration NCT04003207. Registered July 1, 2019, https://clinicaltrials.gov/ct2/show/NCT04003207 .

A randomized controlled trial of intranasal oxytocin in Phelan-McDermid syndrome.

BACKGROUND: Phelan-McDermid syndrome (PMS) is a rare neurodevelopmental disorder caused by haploinsufficiency of the SHANK3 gene and characterized by global developmental delays, deficits in speech and motor function, and autism spectrum disorder (ASD). Monogenic causes of ASD such as PMS are well suited to investigations with novel therapeutics, as interventions can be targeted based on established genetic etiology. While preclinical studies have demonstrated that the neuropeptide oxytocin can reverse electrophysiological, attentional, and social recognition memory deficits in Shank3-deficient rats, there have been no trials in individuals with PMS. The purpose of this study is to assess the efficacy and safety of intranasal oxytocin as a treatment for the core symptoms of ASD in a cohort of children with PMS. METHODS: Eighteen children aged 5-17 with PMS were enrolled. Participants were randomized to receive intranasal oxytocin or placebo (intranasal saline) and underwent treatment during a 12-week double-blind, parallel group phase, followed by a 12-week open-label extension phase during which all participants received oxytocin. Efficacy was assessed using the primary outcome of the Aberrant Behavior Checklist-Social Withdrawal (ABC-SW) subscale as well as a number of secondary outcome measures related to the core symptoms of ASD. Safety was monitored throughout the study period. RESULTS: There was no statistically significant improvement with oxytocin as compared to placebo on the ABC-SW (Mann-Whitney U = 50, p = 0.055), or on any secondary outcome measures, during either the double-blind or open-label phases. Oxytocin was generally well tolerated, and there were no serious adverse events. LIMITATIONS: The small sample size, potential challenges with drug administration, and expectancy bias due to relying on parent reported outcome measures may all contribute to limitations in interpreting results. CONCLUSION: Our results suggest that intranasal oxytocin is not efficacious in improving the core symptoms of ASD in children with PMS. Trial registration NCT02710084.

Associations between sun exposure and other lifestyle variables in Swedish women.

PURPOSE: Sun exposure is associated with risk of several chronic diseases including cancer. The study aim is to investigate whether sun behaviors are related to other lifestyle risk factors of cancer. METHODS: We analyzed data collected in 2003-2004 by self-completed questionnaire from 34,402 Swedish women aged 40-61 years, who comprised 70% of a cohort of originally recruited from a population registry in 1991-1992 (n = 49,259). Participants were asked about annual number of sunburns and annual number of weeks of swimming and sunbathing during 1991-2002, solarium use during 1991-1998 and current sunscreen use. RESULTS: Compared to non-drinkers, the prevalence ratio (95% CI) in women who drank >10 g of alcohol per day was 1.64 (1.49, 1.81) for having >1 sunburn per year, 1.39 (1.29, 1.51) for swimming and sunbathing >2.5 weeks per year and 1.55 (1.41, 1.70) for using a solarium >1 time per 2 months, adjusting for demographic and lifestyle variables. Tobacco smokers were less likely to report sunburn and to use sunscreen, and more likely to sunbath and use solaria, compared with non-smokers. Physical activity was associated positively with swimming and sunbathing, and with the separate use of solaria and sunscreens, but not with number of sunburns. The lifestyle variables that explained most of the variation in sun behavior were alcohol and smoking. CONCLUSIONS: Our results suggest that alcohol consumption and tobacco smoking are potential lifestyle confounders which should be adjusted in studies investigating the association that sun and/or solarium exposure may have with risk of several cancer sites.

Autism risk following antidepressant medication during pregnancy.

BACKGROUND: Previous studies have examined if maternal antidepressant medication during pregnancy increase the risk of autism spectrum disorder (ASD) in the offspring, but the results have been conflicting. METHODS: In a population-based cohort of 179 007 children born in 2006 and 2007 and followed through 2014 when aged 7 and 8, we estimated relative risks (RRs) of ASD and 95% confidence intervals (CIs) from Cox regression in children exposed to any antidepressant medication during pregnancy, and nine specific antidepressant drugs. Analyses were adjusted for potential confounders and were conducted in the full population sample, and in a clinically relevant sub-sample of mothers with at least one diagnosis of depression or anxiety during life. RESULTS: The adjusted RR of ASD in children of mothers who used antidepressant medication during pregnancy was estimated at 1.23 (95% CI 0.96-1.57), and at 1.07 (95% CI 0.80-1.43) in women with a history of depression or anxiety. Analyses of specific antidepressants initially revealed increased RRs of offspring ASD confined to citalopram and escitalopram (RR: 1.47; 95% CI 0.92-2.35) and clomipramine (RR: 2.86; 95% CI 1.04-7.82). CONCLUSION: Medication with antidepressants during pregnancy does not appear to be causally associated with an increased risk of ASD in the offspring. Instead, the results suggest that the association is explained by factors related to the underlying susceptibility to psychiatric disorders. Based on these findings, the risk of ASD in the offspring should not be a consideration to withhold treatment with commonly used antidepressant drugs from pregnant women.

Short-term effects of atmospheric pressure, temperature, and rainfall on notification rate of community-acquired Legionnaires' disease in four European countries.

Legionnaires' disease (LD) is caused by the inhalation of aerosols containing Legionella, a Gram-negative bacteria. Previous national- or regional-level studies have suggested an impact of climate on LD incidence. The objective of this study was to investigate the effect of temperature, rainfall, and atmospheric pressure on short-term variations in LD notification rate. EU/EEA Member States report their LD surveillance data to the European Centre for Disease Prevention and Control. Community-acquired LD cases reported by Denmark, Germany, Italy, and The Netherlands with onset date in 2007-2012 were aggregated by onset week and region of residence. Weather variables were extracted from the European Climate Assessment & Dataset project. We fitted Poisson regression models to estimate the association between meteorological variables and the weekly number of community-acquired LD cases. Temperature, rainfall and atmospheric pressure were all associated with LD risk with higher risk associated with simultaneous increase in temperature and rainfall. Temperatures >20 °C were not associated with a higher risk for LD. LD cases occurring during wintertime may be associated with sources less influenced by meteorological conditions.

Lytic to temperate switching of viral communities.

Microbial viruses can control host abundances via density-dependent lytic predator-prey dynamics. Less clear is how temperate viruses, which coexist and replicate with their host, influence microbial communities. Here we show that virus-like particles are relatively less abundant at high host densities. This suggests suppressed lysis where established models predict lytic dynamics are favoured. Meta-analysis of published viral and microbial densities showed that this trend was widespread in diverse ecosystems ranging from soil to freshwater to human lungs. Experimental manipulations showed viral densities more consistent with temperate than lytic life cycles at increasing microbial abundance. An analysis of 24 coral reef viromes showed a relative increase in the abundance of hallmark genes encoded by temperate viruses with increased microbial abundance. Based on these four lines of evidence, we propose the Piggyback-the-Winner model wherein temperate dynamics become increasingly important in ecosystems with high microbial densities; thus 'more microbes, fewer viruses'.

ViPAR: a software platform for the Virtual Pooling and Analysis of Research Data.

BACKGROUND: Research studies exploring the determinants of disease require sufficient statistical power to detect meaningful effects. Sample size is often increased through centralized pooling of disparately located datasets, though ethical, privacy and data ownership issues can often hamper this process. Methods that facilitate the sharing of research data that are sympathetic with these issues and which allow flexible and detailed statistical analyses are therefore in critical need. We have created a software platform for the Virtual Pooling and Analysis of Research data (ViPAR), which employs free and open source methods to provide researchers with a web-based platform to analyse datasets housed in disparate locations. METHODS: Database federation permits controlled access to remotely located datasets from a central location. The Secure Shell protocol allows data to be securely exchanged between devices over an insecure network. ViPAR combines these free technologies into a solution that facilitates 'virtual pooling' where data can be temporarily pooled into computer memory and made available for analysis without the need for permanent central storage. RESULTS: Within the ViPAR infrastructure, remote sites manage their own harmonized research dataset in a database hosted at their site, while a central server hosts the data federation component and a secure analysis portal. When an analysis is initiated, requested data are retrieved from each remote site and virtually pooled at the central site. The data are then analysed by statistical software and, on completion, results of the analysis are returned to the user and the virtually pooled data are removed from memory. CONCLUSIONS: ViPAR is a secure, flexible and powerful analysis platform built on open source technology that is currently in use by large international consortia, and is made publicly available at [http://bioinformatics.childhealthresearch.org.au/software/vipar/].

Autism risk associated with parental age and with increasing difference in age between the parents.

Advancing paternal and maternal age have both been associated with risk for autism spectrum disorders (ASD). However, the shape of the association remains unclear, and results on the joint associations is lacking. This study tests if advancing paternal and maternal ages are independently associated with ASD risk and estimates the functional form of the associations. In a population-based cohort study from five countries (Denmark, Israel, Norway, Sweden and Western Australia) comprising 5 766 794 children born 1985-2004 and followed up to the end of 2004-2009, the relative risk (RR) of ASD was estimated by using logistic regression and splines. Our analyses included 30 902 cases of ASD. Advancing paternal and maternal age were each associated with increased RR of ASD after adjusting for confounding and the other parent's age (mothers 40-49 years vs 20-29 years, RR=1.15 (95% confidence interval (CI): 1.06-1.24), P-value<0.001; fathers⩾50 years vs 20-29 years, RR=1.66 (95% CI: 1.49-1.85), P-value<0.001). Younger maternal age was also associated with increased risk for ASD (mothers <20 years vs 20-29 years, RR=1.18 (95% CI: 1.08-1.29), P-value<0.001). There was a joint effect of maternal and paternal age with increasing risk of ASD for couples with increasing differences in parental ages. We did not find any support for a modifying effect by the sex of the offspring. In conclusion, as shown in multiple geographic regions, increases in ASD was not only limited to advancing paternal or maternal age alone but also to differences parental age including younger or older similarly aged parents as well as disparately aged parents.

No association between adherence to the healthy Nordic food index and cardiovascular disease amongst Swedish women: a cohort study.

BACKGROUND: In several intervention trials, a healthy Nordic diet showed beneficial effects on markers of cardiovascular disease. We investigated the association between a healthy Nordic diet and clinical diagnosis of cardiovascular disease. OBJECTIVE: Our aim was first to examine the association between a healthy Nordic food index (wholegrain bread, oatmeal, apples/pears, root vegetables, cabbages and fish) and the incidence of overall cardiovascular disease (ischaemic heart disease, stroke, arrhythmia, thrombosis and hypertensive disease), and secondly to test for possible effect modification by smoking, body mass index (BMI), alcohol consumption and age. METHODS: We conducted an analysis of data from the prospective Swedish Women's Lifestyle and Health cohort, including 43 310 women who completed a food frequency questionnaire in 1991-1992, and followed up until 31 December 2012 through Swedish registries. Hazard ratios (HRs) and 95% confidence intervals (CIs) were calculated using Cox proportional hazards models. RESULTS: During follow-up, 8383 women developed cardiovascular disease. We found no association between the healthy Nordic food index and overall cardiovascular disease risk or any of the subgroups investigated. There was a statistically significant interaction with smoking status (P = 0.02), with a beneficial effect only amongst former smokers (HR 0.96, 95% CI 0.94-0.99 per 1-point increment). CONCLUSION: The present results do not support an association between a healthy Nordic food index and risk of cardiovascular disease in Swedish women. There was also no effect modification by alcohol intake, BMI or age. Our finding of an interaction with smoking status requires reproduction.

Global assessment of the status of coral reef herbivorous fishes: evidence for fishing effects.

On coral reefs, herbivorous fishes consume benthic primary producers and regulate competition between fleshy algae and reef-building corals. Many of these species are also important fishery targets, yet little is known about their global status. Using a large-scale synthesis of peer-reviewed and unpublished data, we examine variability in abundance and biomass of herbivorous reef fishes and explore evidence for fishing impacts globally and within regions. We show that biomass is more than twice as high in locations not accessible to fisheries relative to fisheries-accessible locations. Although there are large biogeographic differences in total biomass, the effects of fishing are consistent in nearly all regions. We also show that exposure to fishing alters the structure of the herbivore community by disproportionately reducing biomass of large-bodied functional groups (scraper/excavators, browsers, grazer/detritivores), while increasing biomass and abundance of territorial algal-farming damselfishes (Pomacentridae). The browser functional group that consumes macroalgae and can help to prevent coral-macroalgal phase shifts appears to be most susceptible to fishing. This fishing down the herbivore guild probably alters the effectiveness of these fishes in regulating algal abundance on reefs. Finally, data from remote and unfished locations provide important baselines for setting management and conservation targets for this important group of fishes.

Offspring death and subsequent psychiatric morbidity in bereaved parents: addressing mechanisms in a total population cohort.

BACKGROUND: It is unclear if psychiatric morbidity among parents bereaved of a child is related to major loss in general or if the cause of death matters. Whether such a link is consistent with a causal explanation also remains uncertain. METHOD: We identified 3,114,564 parents through linkage of Swedish nationwide registers. Risk of psychiatric hospitalization was assessed with log-linear Poisson regression and family-based analyses were used to explore familial confounding. RESULTS: A total of 3284 suicides and 14,095 any-cause deaths were identified in offspring between 12 and 25 years of age. Parents exposed to offspring suicide had considerably higher risk of subsequent psychiatric hospitalization than unexposed parents [relative risk (RR) 1.90, 95% confidence interval (CI) 1.72-2.09], higher than parents exposed to offspring non-suicide death relative to controls (RR 1.18, 95% CI 1.11-1.26). We found no risk increase among stepfathers differentially exposed to biologically unrelated stepchildren's death or suicide, and the relative risk was notably lower among full siblings differentially exposed to offspring death or suicide. CONCLUSIONS: Parental psychiatric hospitalization following offspring death was primarily found in offspring suicide. Familial (e.g. shared genetic) effects seemed important, judging from both lack of psychiatric hospitalization in bereaved stepfathers and attenuated risk when bereaved parents were contrasted to their non-bereaved siblings. We conclude that offspring suicide does not 'cause' psychiatric hospitalization in bereaved parents.

Janzen-Connell effects in a broadcast-spawning Caribbean coral: distance-dependent survival of larvae and settlers.

The Janzen-Connell hypothesis states that host-specific biotic enemies (pathogens and predators) promote the coexistence of tree species in tropical forests by causing distance- or density-dependent mortality of seeds and seedlings. Although coral reefs are the aquatic analogues of tropical forests, the Janzen-Connell model has never been proposed as an explanation for high diversity in these ecosystems. We tested the central predictions of the Janzen-Connell model in a coral reef, using swimming larvae and settled polyps of the common Caribbean coral Montastraea faveolata. In a field experiment to test for distance- or density-dependent mortality, coral settler mortality was higher and more strongly density dependent in locations down-current from adult corals. Survival did not increase monotoilically with distance, however, revealing the influence of fluid dynamics around adult corals in structuring spatial patterns of mortality. Complementary microbial profiles around adult coral heads revealed that one potential cause of settler mortality, marine microbial communities, are structured at the same spatial scale. In a field experiment to test whether factors causing juvenile mortality are host specific, settler mortality was 2.3-3.0 times higher near conspecific adults vs. near adult corals of other genera or in open reef areas. In four laboratory experiments to test for distance-dependent, host-specific mortality, swimming coral larvae were exposed to water collected near conspecific adult corals, near other coral genera, and in open areas of the reef. Microbial abundance in these water samples was manipulated with filters and antibiotics to test whether the cause of mortality was biotic (i.e., microbial). Juvenile survivorship was lowest in unfiltered water collected near conspecifics, and survivorship increased when this water was filter sterilized, collected farther away, or collected near other adult coral genera. Together these results demonstrate for the first time that the diversity-promoting mechanisms embodied in the Janzen-Connell model can operate in a marine ecosystem and in an animal. The distribution of adult corals across a reef will thus influence the spatial pattern of juvenile survival. When rare coral species have a survival advantage, coral species diversity per se becomes increasingly important for the persistence and recovery of coral cover on tropical reefs.

Parental schizophrenia and increased offspring suicide risk: exploring the causal hypothesis using cousin comparisons.

BACKGROUND: Little is known about suicide risk among offspring of parents hospitalized for schizophrenia and the mechanisms behind this association. METHOD: We applied a nested case-control design based on linkage of Swedish population-based registers. Among 12- to 30-year-old offspring, we identified 68 318 offspring with suicidal behavior (attempted and completed suicide) and their parents. Five healthy control-parent pairs were matched to each suicidal case-parent pair and conditional logistic regression used to obtain odds ratios (ORs). Further, to disentangle familial confounding from causal environmental mechanisms, we compared the population-based suicide risk with the risk found within full-cousins and half-cousins differentially exposed to parental schizophrenia. RESULTS: Offspring of parents with schizophrenia had significantly increased suicide risk after accounting for socio-economic status, parental suicidal behavior and offspring mental illness [OR 1.68, 95% confidence interval (CI) 1.53-1.85]. Suicide risks in offspring of schizophrenic mothers and fathers were similar in magnitude; so were risks across different developmental periods. Importantly, offspring suicide risk remained essentially unchanged across genetically different relationships; offspring of siblings discordant for schizophrenia had equivalent risk increases within full-cousins (OR 1.96, 95% CI 1.66-2.31) and half-cousins (OR 1.69, 95% CI 1.17-2.44). CONCLUSIONS: Parental schizophrenia was associated with increased risk of offspring suicidal behavior, independent of gender of the schizophrenic parent, and persisting into adulthood. The suicide risk in offspring remained at a similar level when comparing genetically different relationships, which suggests that at least part of the association is due to environmental mechanisms. These findings should inspire increased attention to suicidal ideation and prevention efforts in offspring of parents with schizophrenia.

Fishing top predators indirectly affects condition and reproduction in a reef-fish community.

To examine the indirect effects of fishing on energy allocation in non-target prey species, condition and reproductive potential were measured for five representative species (two-spot red snapper Lutjanus bohar, arc-eye hawkfish Paracirrhites arcatus, blackbar devil Plectroglyphidodon dickii, bicolour chromis Chromis margaritifer and whitecheek surgeonfish Acanthurus nigricans) from three reef-fish communities with different levels of fishing and predator abundance in the northern Line Islands, central Pacific Ocean. Predator abundance differed by five to seven-fold among islands, and despite no clear differences in prey abundance, differences in prey condition and reproductive potential among islands were found. Body condition (mean body mass adjusted for length) was consistently lower at sites with higher predator abundance for three of the four prey species. Mean liver mass (adjusted for total body mass), an indicator of energy reserves, was also lower at sites with higher predator abundance for three of the prey species and the predator. Trends in reproductive potential were less clear. Mean gonad mass (adjusted for total body mass) was high where predator abundance was high for only one of the three species in which it was measured. Evidence of consistently low prey body condition and energy reserves in a diverse suite of species at reefs with high predator abundance suggests that fishing may indirectly affect non-target prey-fish populations through changes in predation and predation risk.

Advancing paternal age and risk of autism: new evidence from a population-based study and a meta-analysis of epidemiological studies.

Advanced paternal age has been suggested as a risk factor for autism, but empirical evidence is mixed. This study examines whether the association between paternal age and autism in the offspring (1) persists controlling for documented autism risk factors, including family psychiatric history, perinatal conditions, infant characteristics and demographic variables; (2) may be explained by familial traits associated with the autism phenotype, or confounding by parity; and (3) is consistent across epidemiological studies. Multiple study methods were adopted. First, a Swedish 10-year birth cohort (N=1 075 588) was established. Linkage to the National Patient Register ascertained all autism cases (N=883). Second, 660 families identified within the birth cohort had siblings discordant for autism. Finally, meta-analysis included population-based epidemiological studies. In the birth cohort, autism risk increased monotonically with increasing paternal age. Offspring of men aged ≥50 years were 2.2 times (95% confidence interval: 1.26-3.88: P=0.006) more likely to have autism than offspring of men aged ≤29 years, after controlling for maternal age and documented risk factors for autism. Within-family analysis of discordant siblings showed that affected siblings had older paternal age, adjusting for maternal age and parity (P<0.0001). Meta-analysis demonstrated advancing paternal age association with increased risk of autism across studies. These findings provide the strongest evidence to date that advanced paternal age is a risk factor for autism in the offspring. Possible biological mechanisms include de novo aberration and mutations or epigenetic alterations associated with aging.

Dietary fat intake and gestational weight gain in relation to estradiol and progesterone plasma levels during pregnancy: a longitudinal study in Swedish women.

BACKGROUND: Elevated pregnancy hormone levels, such as oestrogen and progesterone, may increase the risk of developing breast cancer both in mothers and offspring. However, the reasons for large inter-individual variations in estrogen and progesterone levels during pregnancy remain unknown. The objectives of this study were to investigate whether a) intakes of total dietary fat, types of fat (monounsaturated: MUFA, polyunsaturated: n-3 and n-6 PUFA, and saturated) and b) gestational weight gain are associated with estradiol and progesterone levels in plasma during pregnancy. METHODS: We measured body weight as well as estradiol and progesterone in plasma among 226 healthy pregnant Swedish women on gestation weeks 12, 25 and 33. At the same time points, dietary intake of total fat and types of fat (MUFA, PUFA, SFA, n-3 and n-6 PUFA) were estimated using 3-day food diaries. RESULTS: A large variation in estradiol and progesterone levels was evident.Nulliparous women had 37%, 12% and 30% higher mean estradiol levels on gestation weeks 12, 25 and 33 compared to parous women (P = 0.008). No associations were found between dietary intake of total fat or fat subtypes (including n-3 PUFA and n-6 PUFA) and plasma estradiol or progesterone levels. Gestational weight gain was associated with progesterone levels (P = 0.03) but the effect was very small (20% increase in progesterone levels between gestational weeks 12 and 33 per kg body weight/week). CONCLUSION: No associations among gestational weight gain, maternal dietary fat intake (total or subtypes including n-3 PUFA and n-6 PUFA) and plasma estradiol levels were found. However, pregnancy progesterone levels correlated with weight gain during pregnancy. Identification of other possible determinants of pregnancy estradiol and progesterone levels, important for the development of breast cancer in both mothers and offspring, are needed.

Survival and settlement success of coral planulae: independent and synergistic effects of macroalgae and microbes.

Restoration of degraded coral reef communities is dependent on successful recruitment and survival of new coral planulae. Degraded reefs are often characterized by high cover of fleshy algae and high microbial densities, complemented by low abundance of coral and coral recruits. Here, we investigated how the presence and abundance of macroalgae and microbes affected recruitment success of a common Hawaiian coral. We found that the presence of algae reduced survivorship and settlement success of planulae. With the addition of the broad-spectrum antibiotic, ampicillin, these negative effects were reversed, suggesting that algae indirectly cause planular mortality by enhancing microbial concentrations or by weakening the coral's resistance to microbial infections. Algae further reduced recruitment success of corals as planulae preferentially settled on algal surfaces, but later suffered 100% mortality. In contrast to survival, settlement was unsuccessful in treatments containing antibiotics, suggesting that benthic microbes may be necessary to induce settlement. These experiments highlight potential complex interactions that govern the relationships between microbes, algae and corals and emphasize the importance of microbial dynamics in coral reef ecology and restoration.