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Purpose: To promote greater muscular strength across the life course and, in turn, help improve long-term health outcomes, strategies aimed at increasing muscular strength are required. To inform these strategies, this study identified childhood factors associated with muscular strength trajectories. Methods: Prospective longitudinal study of 1280 Childhood Determinants of Adult Health participants who had a range of potentially modifiable factors (e.g., anthropometric measures, physical activity) and health and risk motivation items (e.g., attitudes, beliefs, and intentions on health-related actions) measured in childhood and had their muscular strength assessed up to three times between childhood and midlife. Associations between childhood factors and three predetermined life course muscular strength trajectories (identified previously using group-base trajectory modeling as follows: above average and increasing, average, and below average and decreasing) were examined using log multinomial regression. Results: Greater physical fitness, physical activity, fat-free mass, enjoyment of physical activity, physical education, and school sports, and positive attitudes regarding the importance of exercising, staying fit, and body image were associated with a lower likelihood of being in the below average and decreasing muscular strength trajectory (relative risk range, 0.45–0.98). Greater physical fitness, physical activity, and fat-free mass, and attending an independent school were associated with a higher likelihood of being in the above average and increasing muscular strength trajectory (relative risk range, 1.03–1.93). Conclusions: In addition to providing health benefits in the short term, physical activity, physical fitness, positive health attitudes, and healthy weight in childhood may lead to better muscular strength in the long term.

Unifying models have shown that the amount of space used by animals (e.g., activity space, home range) scales allometrically with body mass for terrestrial taxa; however, such relationships are far less clear for marine species. We compiled movement data from 1,596 individuals across 79 taxa collected using a continental passive acoustic telemetry network of acoustic receivers to assess allometric scaling of activity space. We found that ectothermic marine taxa do exhibit allometric scaling for activity space, with an overall scaling exponent of 0.64. However, body mass alone explained only 35% of the variation, with the remaining variation best explained by trophic position for teleosts and latitude for sharks, rays, and marine reptiles. Taxon-specific allometric relationships highlighted weaker scaling exponents among teleost fish species (0.07) than sharks (0.96), rays (0.55), and marine reptiles (0.57). The allometric scaling relationship and scaling exponents for the marine taxonomic groups examined were lower than those reported from studies that had collated both marine and terrestrial species data derived using various tracking methods. We propose that these disparities arise because previous work integrated summarized data across many studies that used differing methods for collecting and quantifying activity space, introducing considerable uncertainty into slope estimates. Our findings highlight the benefit of using large-scale, coordinated animal biotelemetry networks to address cross-taxa evolutionary and ecological questions.

Low muscular strength associates with the metabolic syndrome (MetS). However, how muscular strength measured at different life stages contribute to the development of MetS is unknown. This study compared the contribution of muscular strength measured in youth, young- and mid-adulthood with MetS in midlife.Prospective longitudinal study of 267 Childhood Determinants of Adult Health Study participants who between 1985 and 2019 had measures of muscular strength (dominant grip strength) at three life stages (youth = 9-15 years, young adulthood = 26-36 years, mid-adulthood = 36-49 years) and had their MetS status assessed in mid-adulthood. Bayesian relevant life-course exposure models quantified associations between muscular strength at each life stage with MetS and estimated the maximum accumulated effect of lifelong muscular strength. The contribution of muscular strength at each life stage with MetS was equal (youth = 38%, young adulthood = 28%, mid-adulthood = 34%). A one standard deviation increase in cumulative muscular strength was associated with 46% reduced odds of MetS. Of all MetS components, muscular strength was most strongly negatively associated with high waist circumference.A life-course approach demonstrated reduced odds of MetS in midlife was associated with cumulatively high muscular strength since youth. This supports efforts to promote physical fitness throughout life.

Aims Most international guidelines recommend that repeat blood pressure (BP) readings are required for BP classification. Two international guidelines diverge from this by recommending that no further BP measurements are required if the first clinic BP is below a hypertension threshold. The extent to which within-visit BP variability patterns change over time, and whether this could impact BP classification is unknown. We sought to examine this. Methods and results Data were from the Cardiovascular Risk in Young Finns Study, a prospective cohort study. Up to 2799 participants were followed from childhood (9–15 years) to adulthood (18–49 years) over up to six visits. Patterns of within-visit systolic BP (SBP) variability were defined as no-change, decrease, increase between consecutive readings (with 5 mmHg change thresholds). Classification of SBP (normal, high-normal, hypertension) using the first reading was compared with repeat readings. On average, SBP decreased with subsequent measures, but with major individual variability (no-change: 56.9–62.7%; decrease: 24.1–31.6%; increase: 11.5–16.8%). Patterns of SBP variability were broadly similar from childhood to adulthood, with the highest prevalence of an increase among participants categorized with normal SBP (12.6–20.3%). The highest prevalence of SBP reclassification occurred among participants with hypertension (28.9–45.3% reclassified as normal or high-normal). The prevalence of reclassification increased with the magnitude of change between readings. Conclusion There is a major individual variation of within-visit SBP change in childhood and adulthood and can influence BP classification. This highlights the importance of consistency among guidelines recommending that repeat BP measurements are needed for BP classification.

Much of what we know about sexual offenders and risk management is derived from empirical studies on sex offender populations in North America. In comparison to Canada and the United States, the evidence base in Australia on sexual offender risk management is under-developed. In this paper, we describe a current research project tasked with developing a national sex offender recidivism database to advance the evidence base in Australia. It is argued that a national database would advance knowledge and practice in the field of sex offender risk management in Australia in a multitude of ways. Yet there are many obstacles and difficulties in developing such a database. After putting forward a case for the need for such a database, we outline the issues we have encountered and the approaches we have adopted to develop this database. It is intended that this contemporary comment may not only alert readers to this emerging data resource in Australia but also function as a road map to guide future empirical research on offender population databases in Australia.

Background: Receiving early treatment for aneurysmal subarachnoid hemorrhage (aSAH) is associated with better outcomes for the patient. However, delays in treatment of aSAH are common but the causes are not well understood. We explored predictors of early treatment within 12.5 hours or 24 hours after aSAH. Methods: Consecutive cases of confirmed first-ever aSAH were identified from two Australian tertiary referral centers between 2010 and 2016. We used medical and ambulance records to extract details of participants, including time from onset to definitive treatment of either endovascular coiling or neurosurgical clipping, demographics, severity of aSAH (modified Fisher grade; World Federation of Neurosurgeons Scale [WFNS]), risk factors, pre-hospital care, and presenting symptoms. Factors associated with treatment to secure the aneurysm within 12.5 hours or 24 hours on univariable logistic regression were entered into a multivariable model to identify factors independently associated with (odds ratio [OR], 95% CI) earlier treatment. Results: Among 482 patients (mean [SD] age 54.1 [14.5]; 69.9% female) with aSAH, median (IQR) time to treatment was 19.4 (10.6, 31.0) hours, 30% were treated Conclusions: A substantial proportion of people after aSAH were not treated within timeframes associated with better outcomes. Recognition of the urgency and severity aSAH cases were associated with more timely treatment of aSAH.

Smokers can respond defensively to health risk communication such as on-pack warning labels, potentially reducing their effectiveness. Theory suggests that risk perception together with self-efficacy reduces defensive responses and predicts target behaviours. Currently, tobacco warning labels globally predominantly target risk and do not explicitly consider efficacy. This study explores the effectiveness of combining Australian tobacco warning labels with efficacy content to increase quitting intentions.RCT in 83 smokers over three weeks. After a seven-day baseline phase (smoking from usual tobacco packaging), participants were randomised to one of two adhesive labels groups for the remaining 14 days: standard health warning labels (HWLs) featuring enhanced efficacy messages (experimental group) or unmodified standard HWLs (control group). Participants attached these labels to their tobacco packaging and recorded their cognitions and smoking behaviour once daily using smartphones. Multi-level structural equation modelling was used to test theorised effects of the labels on self-efficacy, risk perception and intentions to quit.There was no effect of exposure to efficacy messages on either self-efficacy, risk perceptions or intentions to quit. However, self-efficacy and risk perceptions were positively associated with quitting intentions at the within-person level.The predictive relationships between self-efficacy, risk perception and intention to quit were supported, however, supplementing standard warning labels with efficacy messages had no effect on these cognitions. Whether this is due to conditioned avoidance of health warning labels, characteristics of the messages, or limitations imposed by format is unclear.Self-efficacy and risk perception predict intentions to quit smoking. Adding efficacy content to tobacco health warnings may have potential to bolster these cognitions but more research is required to determine the contexts in which this would be effective and who would be likely to benefit. The time course by which exposure to efficacy content might influence cessation self-efficacy and downstream quitting intentions also needs to be investigated.

Background and Aim: We explored sex differences in the association between systolic and diastolic blood pressure (SBP), in early adulthood with carotid plaques, carotid IMT and carotid distensibility (CD) in mid-adulthood. Methods: Participants in the Childhood Determinants of Adult Health study at ages 26-36 years were followed-up at ages 39-49 years. Systolic BP and diastolic BP and carotid ultrasound measures (plaques, IMT and CD) were performed in clinics. We used log binomial and linear regression models with risk factor*gender interactions for predicting these carotid measures. Sex-stratified models adjusted for sociodemographic, health-related behavior and biomedical factors were fitted when likelihood ratio tests suggested the effect of risk factors on outcomes differed by sex. Results: Among 1,286 participants (53% women), men, compared to women, had higher prevalence of carotid plaques (17% vs. 10%), thicker carotid IMT (Mean 0.66 ± 0.09 vs. 0.61 ± 0.07) and lower CD (Mean 1.87 ± 0.60 vs. 2.37 ± 0.77). In women, greater SBP in early adulthood was sharply associated with significantly smaller CD (β -0.016 95%CI -0.023, -0.010 vs. β -0.006 95%CI -0.012, -0.001) than men in mid-adulthood adjusted for sociodemographic factors (Figure 1a). In analyses restricted to women, the effect of SBP on CD has decreased after adjusting for age, education, occupation, DBP and use of contraceptives (β -0.009 95%CI -0.019, 0.000) (Figure 1b). Conclusion: CV health was worse in men than women. However, elevated SBP in women put them at greater risk of poorer CV health compared to men, which was partly explained by sociodemographic, biomedical and female-specific factors.

Background Low physical fitness, including muscular strength and cardiorespiratory fitness (CRF), is a risk factor for the metabolic syndrome (MetS). However, it is unknown how physical fitness at different life stages contributes to the development of MetS. Methods Included were 783 Childhood Determinants of Adult Health Study participants who between 1985 and 2019 had measures of physical fitness (muscular strength: dominant grip strength; CRF: 1.6km run or physical work capacity at 170 beats per minute) at three life stages (childhood=7–15 years, young-adulthood=26–36 years, mid-adulthood=36–49 years) and had their MetS status assessed using the harmonised definition in mid-adulthood. The Bayesian relevant life-course exposure model, a novel statistical analytic technique, quantified associations between physical fitness at each life stage with MetS and estimated the maximum accumulated effect of physical fitness across the life-course. Results The contribution of muscular strength at each life stage with MetS in mid-adulthood was equal (childhood=36%, young-adulthood=31%, mid-adulthood=33%), whereas for CRF the greatest contribution was from childhood and mid-adulthood (childhood=41%, young-adulthood=20%, mid-adulthood=39%). A one standard deviation increase in cumulative physical fitness across the life-course was associated with 36–55% reduced odds of MetS (muscular strength: OR = 0.64, 95%Credible Interval=0.40,0.95; CRF: OR = 0.45, 95%Credible Interval=0.30,0.64). Conclusions As physical fitness at each life stage was associated with MetS in mid-adulthood, strategies aimed at increasing both childhood and adult physical fitness levels could improve future health. Key messages Increased participation in both aerobic and muscle-strengthening activities, beginning in childhood and extending into adulthood, could be encouraged to help prevent MetS.

Background: Within-visit SBP variability is associated with age and SBP, but its long-term clinical significance is unknown. We examined the association between child, adult, and life-time within-visit SBP variability with markers of end-organ damage using data from a 31-year longitudinal study. Methods: Within-visit SBP variability was calculated as the standard deviation of three sitting SBP readings among up to 3010 participants aged 6–18 years (childhood) who were re-measured up to seven times to mid-adulthood. Markers of cardiovascular end-organ damage in adulthood were carotid intima--media thickness, brachial flow-mediated dilatation, carotid distensibility, pulse wave velocity, left ventricular mass index, carotid plaque, and coronary artery calcification. Results: The mean (standard deviation) cumulative within-visit SBP variability was 2.7 (1.5) mmHg in childhood, 3.9 (1.9) mmHg in adulthood and 3.7 (1.5) mmHg across the observed life-time. Childhood within-visit SBP variability was not correlated with its subsequent values measured from 3 to 31 years later. With adjustment for age, sex, cumulative SBP, BMI and serum lipids, neither child, adult, or life-time cumulative within-visit SBP variability associated with markers of cardiovascular end-organ damage. However, higher child, adult, and life-time cumulative SBP significantly associated with higher carotid intima--media thickness, higher pulse wave velocity, lower brachial flow-mediated dilatation, lower carotid distensibility in adulthood. Conclusion: Within-visit SBP variability from childhood to adulthood does not provide additional predictive utility over SBP over the same period of the life course.

Objectives Low muscular strength is a risk factor for current and future adverse health outcomes. However, whether levels of muscular strength persist, or track, and if there are distinct muscular strength trajectories across the life course is unclear. This study aimed to explore muscular strength trajectories between childhood and mid-adulthood. Design Prospective longitudinal study. Methods Childhood Determinants of Adult Health Study participants had their muscular strength (right and left handgrip, shoulder extension and flexion, and leg strength measured by hand-held, shoulder and leg-back dynamometers, and a combined strength score) assessed in childhood, young adulthood and mid-adulthood. The tracking of muscular strength was quantified between childhood and mid-adulthood (n = 385) and young- and mid-adulthood (n = 822). Muscular strength trajectory patterns were identified for participants who had their muscular strength assessed at least twice across the life course (n = 1280). Results Levels of muscular strength were persistent between childhood and mid-adulthood and between young- and mid-adulthood, with the highest tracking correlations observed for the combined strength score (childhood to mid-adulthood: r = 0.47, p

Context To the best of our knowledge, no previous studies have examined the role of youth calcium intake in the development of impaired glucose metabolism, especially those with long-term high calcium intake. Objectives To examine whether youth and long-term (between youth and adulthood) dietary calcium intake is associated with adult impaired glucose metabolism and type 2 diabetes (T2D). Design, setting, and participants The Cardiovascular Risk in Young Finns Study is a 31-year prospective cohort study (n = 1134; age, 3 to 18 years at baseline). Exposures Dietary calcium intake was assessed at baseline (1980) and adult follow-up visits (2001, 2007, and 2011). Long-term (mean between youth and adulthood) dietary calcium intake was calculated. Main outcome measures Adult impaired fasting glucose (IFG) and T2D. Results We found no evidence for nonlinear associations between calcium intake and IFG or T2D among females and males (all P for nonlinearity > 0.05). Higher youth and long-term dietary calcium intake was not associated with the risk of IFG or T2D among females or males after adjustment for confounders, including youth and adult body mass index. Conclusions Youth or long-term dietary calcium intake is not associated with adult risk of developing impaired glucose metabolism or T2D.

Background: Understanding the origins of sex differences in cardiovascular diseases (CVD) may help with prevention. We examined sex differences in carotid artery IMT and plaques in adulthood including the contribution of childhood risk factors. Methods: Boys and girls aged 7-15 years old from the Australian Schools Health and Fitness Survey in 1985 were followed up in the Childhood Determinants of Adult Health study at ages 36-49 years between 2014-19. Sex differences in adult carotid IMT and plaques, identified with 2D ultrasound of left and right carotid arteries, were examined with linear and log binomial regression, respectively. Childhood sociodemographic, psychosocial, health-related behavioural and biomedical risk factors that might contribute to sex differences in carotid IMT/plaques were identified with purposeful model building. Results: Among 1,286 men and women with vascular measurements of carotid IMT (53% women, mean carotid IMT 0.63 mm ± 0.09 standard deviation) women had thinner carotid IMT measurements than men (β coefficients -0.053 95% CI -0.063, -0.043). Adjusting for age standardised waist circumference (WC), waist/hip ratio (WHR), waist/height ratio (WHtR) and systolic blood pressure (SBP) in childhood reduced the sex difference of carotid IMT in adulthood (see Figure), but a significant sex-difference in carotid IMT remained. Women had a 42% lower risk of plaques than men (Relative Risk 0.58 95% CI 0.42, 0.79). School achievement levels, endurance/power fitness and SBP in childhood partially explained the sex difference in the prevalence of plaques at adulthood (see Figure) as the sex difference decreased and became statistically insignificant. Conclusion: Various factors in childhood had contributed to thicker carotid IMT and higher prevalence of carotid plaques in men compared to women. These findings suggest that the origins of adult sex differences in CVD may begin in childhood. There may be benefits of sex-specific primary prevention programs starting in childhood.

Background and aims: Rapid access to specialised care improves outcomes after aneurysmal subarachnoid haemorrhage (aSAH) but there is limited evidence on the optimal time-to-treatment. We investigated onset-to-treatment time and hospital discharge destination in aSAH. Methods: Consecutive first-ever aSAH patients were retrospectively identified from multiple overlapping sources in two comprehensive cerebrovascular referral centres between 2010-2016. Onset-to-treatment time (hours from onset of symptoms to treatment to secure aneurysm), clinical characteristics, and neurological complications (NINDS classifications) were extracted by clinical data collectors from medical records. Among survivors, we estimated the effect of continuous onset-to-treatment on hospital discharge destination (i.e. home vs. rehabilitation/other hospital as proxy for functional recovery) using logistic regression with adjustment for gender, treatment type (clipping or coiling), hospital presentation (direct admission or transfer), and severity (World Federation of Neurosurgical Societies scale, modified Fisher scale). Non-linear effects were investigated using natural cubic splines. Results: Among 402 survivors at discharge, there was a strong non-linear effect of onset-to-treatment time on odds of being discharged home compared to discharge to rehabilitation independent of severity, gender, treatment type and transfer (see Figure). The greatest benefit to discharge home was evident with treatment at up to 12.5 hours but the benefit remained at up to 20 hours post-onset. Conclusions: aSAH Treatment occurring within 12.5 hours led to greater discharge to home. Our use of continuous modelling provides clarity around optimal treatment times for aSAH to guide clinical practice.

Introduction: Prolonged childhood passive smoke exposure may affect adult cardiovascular health but there are few studies of cardiac function. Subclinical left ventricular dysfunction detected by global longitudinal strain (GLS) is predictive of the subsequent development of heart failure. We investigated the association of passive smoke exposure during childhood with GLS in adults. Methods: Data were from the Childhood Determinants of Adult Health (CDAH) study 34-year follow-up (2014-19). Three measures of passive smoking (severity of exposure index [SEI], cumulative years of exposure [CYE], total household smokers [THS]) were derived retrospectively from a validated questionnaire. GLS was measured in clinics using a Siemens Acuson SC2000 ultrasound machine and 4V1c transducer with speckle tracking analysis. Linear regression adjusted for confounding factors (age, gender, childhood socioeconomic position, childhood smoking, adult smoking status, parental education level) examined the association between childhood passive smoke exposure and GLS in adulthood. Results: Among 781 participants (mean age 45.2 ± 2.5 SD years, 52.6% females, 54.2% exposed to passive smoking), GLS showed a decrease (β adjusted -0.17% 95% CI -0.32%, -0.02%) per SD of SEI (range: 0-318, mean 24.2 ± 35.8 SD). CYE (range: 0-106, mean 10.4 ± 13.9 SD) was associated with a decrease in GLS (β adjusted -0.18% 95% CI -0.33%, -0.05%) per SD of exposure. For each THS in childhood (range: 0-5, mean 0.9 ± 1.0 SD), there was a decrease in GLS (β adjusted -0.20% 95% CI -0.36%, -0.05%). Conclusion: Childhood passive smoke exposure, independent of own smoking, was associated with a reduction in GLS, a measure of subclinical cardiac dysfunction. Each 1% decrease in GLS has been associated with 12% higher risk of cardiovascular morbidity and mortality in low-risk general population. There are potential long-term consequences to cardiac function from childhood passive smoke exposure.

Background Although low child and adult grip strength is associated with adverse cardiometabolic health, how grip strength across the life course associates with type 2 diabetes is unknown. This study identified the relative contribution of grip strength measured at specific life stages (childhood, young adulthood, mid-adulthood) with prediabetes or type 2 diabetes in mid-adulthood. Methods Between 1985 and 2019, 263 participants had their grip strength measured using an isometric dynamometer in childhood (9–15 years), young adulthood (28–36 years) and mid-adulthood (38–49 years). In mid-adulthood, a fasting blood sample was collected and tested for glucose and glycated haemoglobin (HbA1c). Participants were categorized as having prediabetes or type 2 diabetes if fasting glucose levels were ≥ 5.6 mmol or if HbA1c levels were ≥ 5.7% (≥ 39 mmol/mol). A Bayesian relevant life course exposure model examined the association between lifelong grip strength and prediabetes or type 2 diabetes. Results Grip strength at each time point was equally associated with prediabetes or type 2 diabetes in mid-adulthood (childhood: 37%, young adulthood: 36%, mid-adulthood: 28%). A one standard deviation increase in cumulative grip strength was associated with 34% reduced odds of prediabetes or type 2 diabetes in mid-adulthood (OR 0.66, 95% credible interval 0.40, 0.98). Conclusions Greater grip strength across the life course could protect against the development of prediabetes and type 2 diabetes. Strategies aimed at increasing muscular strength in childhood and maintaining behaviours to improve strength into adulthood could improve future cardiometabolic health. Video abstract

Context The influence of dietary pattern trajectories from youth to adulthood on adult glucose metabolism is unknown. Objective To identify dietary pattern trajectories from youth to adulthood and examine their associations with adult impaired fasting glucose (IFG). Methods Thirty-one-year population-based cohort study among 1007 youths aged 3-18 years at baseline in Finland. Diet intake was assessed in 1980, 1986, 2001, 2007, and 2011. Group-based trajectory modelling was used to identify dietary pattern (identified by factor analysis) trajectories. Adult IFG was measured by the latest available data from 2001, 2007, and 2011. Results Among 1007 participants, 202 (20.1%) developed IFG and 27 (2.7%) developed type 2 diabetes in adulthood (mean follow-up of 30.7 years; mean [SD] age 40.5 [5.0] years). Three dietary patterns were identified at baseline and were retained in 1986 and 2001: “Traditional Finnish,” “High carbohydrate,” and “Vegetables and dairy products.” Three different patterns were identified in 2007, which remained similar in 2011: “Traditional Finnish and high carbohydrate,” “Red meat,” and “Healthy.” Trajectories of increased or stably medium “red meat” pattern scores from youth to adulthood were detrimentally associated with IFG (relative risk 1.46, 95% CI 1.12-1.90 for Medium (M)-stable/M-large increase vs low-stable trajectory) after adjusting for confounders. This association was slightly reduced after further adjusting for long-term dietary fiber intake. Conclusion Trajectories of an increased or stably moderate adherence to a “red meat” dietary pattern from youth to adulthood are associated with higher risk of adult IFG. This association is partly explained by low dietary fiber intake.

Importance Elevated non–high-density lipoprotein cholesterol (non–HDL-C) is associated with the presence of coronary artery calcification (CAC), a marker of heart disease in adulthood. However, the relative importance of non–HDL-C levels at specific life stages for CAC remains unclear. Objective To identify the relative association of non–HDL-C measured at distinct life stages (adolescence, young adulthood, mid-adulthood) with the presence of CAC measured in mid-adulthood. Design, Setting, and Participants The Cardiovascular Risk in Young Finns Study is a population-based prospective cohort study that started in 1980 with follow-up over 28 years. Participants from 3 population centers (Kuopio, Tampere, and Turku in Finland) represent a convenience sample drawn from the 3 oldest cohorts at baseline (aged 12-18 years in 1980). Data were collected from September 1980 to August 2008. Analysis began February 2020. Exposures Non–HDL-C levels were measured at 3 life stages including adolescence (aged 12-18 years), young adulthood (aged 21-30 years), and mid-adulthood (aged 33-45 years). Main Outcomes and Measures In 2008, CAC was determined from computed tomography and dichotomized as 0 (no CAC, Agatston score = 0) and 1 (presence of CAC, Agatston score ≥1) for analysis. Using a bayesian relevant life course exposure model, the relative association was determined between non–HDL-C at each life stage and the presence of CAC in mid-adulthood. Results Of 589 participants, 327 (56%) were female. In a model adjusted for year of birth, sex, body mass index, systolic blood pressure, blood glucose level, smoking status, lipid-lowering and antihypertensive medication use, and family history of heart disease, cumulative exposure to non–HDL-C across all life stages was associated with CAC (odds ratio [OR], 1.50; 95% credible interval [CrI], 1.14-1.92). At each life stage, non–HDL-C was associated with CAC and exposure to non–HDL-C during adolescence had the strongest association (adolescence: OR, 1.16; 95% CrI, 1.01-1.46; young adulthood: OR, 1.14; 95% CrI, 1.01-1.43; mid-adulthood: OR, 1.12; 95% CrI, 1.01-1.34). Conclusions and Relevance These data suggest that elevated non–HDL-C levels at all life stages are associated with coronary atherosclerosis in mid-adulthood. However, adolescent non–HDL-C levels showed the strongest association with the presence of CAC in mid-adulthood, and greater awareness of the importance of elevated non–HDL-C in adolescence is needed.

The role of genetic risk scores associated with adult body mass index (BMI) on BMI levels across the life course is unclear. We examined if a 97 single nucleotide polymorphism weighted genetic risk score (wGRS97) associated with age-related progression in BMI at different life stages and distinct developmental trajectories of BMI across the early life course.2188 Cardiovascular Risk in Young Finns Study participants born pre-1980 who had genotype data and objective measurements of height and weight collected up to 8 times from age 6 to 49 years. Associations were examined using Individual Growth Curve analysis, Latent Class Growth Mixture Modelling, and Poisson modified regression.The wGRS97 associated with BMI from age 6 years with peak effect sizes observed at age 30 years (females: 1.14 kg/mIndividuals with genetic susceptibility to higher adult BMI have higher levels and accelerated rates of increase in BMI in childhood/adolescence, and are at increased risk of having a less favourable life-course BMI trajectory.

Background: Understanding body mass index (BMI) trajectories across the lifecourse may help identify risk of overweight or obesity and strategic points for preventive interventions. We describe BMI trajectories from childhood to adulthood in four population-based cohorts established in the 1970s-80s and their sociodemographic correlates. Methods: Data were from 12,086 participants (45% male) from four cohorts established in Australia, Finland and the US. Participants had ≥3 measures of height and weight, including ≥1 in childhood (6-18 years, mean 9.7 to 11.1 years at first visit) and ≥1 in adulthood (mean 40.0 to 50.9 years at last visit). Latent Class Growth Mixture Modelling estimated BMI trajectory groups. Correlates (age, gender, race, parental education) of BMI trajectories were identified with log multinomial regression. Results: Mean BMI ranged from 17.8-18.3 kg/m 2 at first visit and 26.4-30.2 kg/m 2 at last visit. Six BMI trajectories (Figure) were identified in three cohorts: persistently normal (48-57% of participants), improving from high (1-2%), progressing to overweight (30-39%), progressing to obese (1-8%), late onset obese (2-6%), and progressing to severe obesity (1-3%). One cohort had a seventh group: greatly improving ( Conclusion: Similar BMI trajectories were identified across cohorts, countries and time, despite different BMI distributions. Females and black Americans were most likely to be of high BMI at the end of follow-up. Few participants (≤2%) improved from high BMI. A better understanding of the factors that influence the highest and improving BMI trajectories may help identify risk reduction strategies.

Objectives To estimate and compare tri-ponderal mass index (TMI) and body mass index (BMI) at each age from childhood to young adulthood in the prediction of adulthood obesity-related outcomes. Study design Participants of this observational study (n = 432) were from a 20-year infancy-onset randomized atherosclerosis prevention trial. BMI and TMI were calculated using weight and height measured annually from participants between ages 2 and 20 years. Outcomes were aortic intima-media thickness (at the age of 15, 17, or 19 years), impaired fasting glucose and elevated insulin levels, homeostasis model assessment of insulin resistance index, serum lipids, and hypertension at the age of 20 years. Poisson regressions, Pearson correlation, logistic regression, and area under the curve (AUC) were used to estimate and/or compare associations and predictive utilities between BMI and TMI with all outcomes. Results The associations and predictive utilities of BMI and TMI with all outcomes were stronger at older ages. BMI had significantly stronger correlations than TMI with insulin (at age 16 years), systolic blood pressure (age 5-20 years), and triglycerides (age 18 years). BMI had significantly greater predictive utilities than TMI for insulin resistance (at age 14-16 years; difference in AUC = 0.018-0.024), elevated insulin levels (age 14-16 years; difference in AUC = 0.018 and 0.025), and hypertension (age 16 to 20 years; difference in AUC = 0.017-0.022) but they were similar for other outcomes. Conclusions TMI is not superior to BMI at any ages from childhood to young adulthood in the prediction of obesity-related outcomes in young adulthood.

Debate continues on the limitations of using body mass index (BMI) to assign youth overweight/obesity status. Calculated as weight in kilograms divided by height in meters squared, BMI might not be applicable in youth during periods of rapid growth. Although recent evidence has indicated that triponderal mass index (TMI, calculated as weight in kilograms divided by height in meters cubed) might have better accuracy in estimating youth body fat levels than BMI, its clinical importance in estimating adulthood outcomes has not been examined. Therefore, we assessed whether youth TMI and its combination with BMI or subscapular skin fold thickness (SST), compared with BMI alone, have better utility in estimating adult obesity-related outcomes.

BACKGROUND AND OBJECTIVES: Youth with high BMI who become nonobese adults have the same cardiovascular risk factor burden as those who were never obese. However, the early-life BMI trajectories for overweight or obese youth who avoid becoming obese adults have not been described. We aimed to determine and compare the young-childhood BMI trajectories of participants according to their BMI status in youth and adulthood. METHODS: Bayesian hierarchical piecewise regression modeling was used to analyze the BMI trajectories of 2717 young adults who had up to 8 measures of BMI from childhood (ages 3–18 years) to adulthood (ages 34–49 years). RESULTS: Compared with those with persistently high BMI, those who resolved their high youth BMI by adulthood had lower average BMI at age 6 years and slower rates of BMI change from young childhood. In addition, their BMI levels started to plateau at 16 years old for females and 21 years old for males, whereas the BMI of those whose high BMI persisted did not stabilize until 25 years old for male subjects and 27 years for female subjects. Compared with those youth who were not overweight or obese and who remained nonobese in adulthood, those who developed obesity had a higher BMI rate of change from 6 years old, and their BMI continued to increase linearly until age 30 years. CONCLUSIONS: Efforts to alter BMI trajectories for adult obesity should ideally commence before age 6 years. The natural resolution of high BMI starts in adolescence for males and early adulthood for females, suggesting a critical window for secondary prevention.

Background— Dyslipidemia is a major modifiable risk factor for cardiovascular disease. We examined whether the addition of novel single-nucleotide polymorphisms for blood lipid levels enhances the prediction of adult dyslipidemia in comparison to childhood lipid measures. Methods and Results— Two thousand four hundred and twenty-two participants of the Cardiovascular Risk in Young Finns Study who had participated in 2 surveys held during childhood (in 1980 when aged 3–18 years and in 1986) and at least once in a follow-up study in adulthood (2001, 2007, and 2011) were included. We examined whether inclusion of a lipid-specific weighted genetic risk score based on 58 single-nucleotide polymorphisms for low-density lipoprotein cholesterol, 71 single-nucleotide polymorphisms for high-density lipoprotein cholesterol, and 40 single-nucleotide polymorphisms for triglycerides improved the prediction of adult dyslipidemia compared with clinical childhood risk factors. Adjusting for age, sex, body mass index, physical activity, and smoking in childhood, childhood lipid levels, and weighted genetic risk scores were associated with an increased risk of adult dyslipidemia for all lipids. Risk assessment based on 2 childhood lipid measures and the lipid-specific weighted genetic risk scores improved the accuracy of predicting adult dyslipidemia compared with the approach using only childhood lipid measures for low-density lipoprotein cholesterol (area under the receiver-operating characteristic curve 0.806 versus 0.811; P =0.01) and triglycerides (area under the receiver-operating characteristic curve 0.740 versus area under the receiver-operating characteristic curve 0.758; P Conclusions— The inclusion of weighted genetic risk scores to lipid-screening programs in childhood could modestly improve the identification of those at highest risk of dyslipidemia in adulthood.

Log-likelihood profiling method and R-code for the choice of priors of the changepoint mean. (Îźcp). (DOCX 14 kb)

Annotated RJAGS sample code to fit a type 1 trajectory divergence model with a fully unstructured 4 by 4 covariance matrix for the random growth parameters. (DOCX 14 kb)

Prior sensitivity analyses methods and results. (DOCX 25 kb)

Background Bayesian hierarchical piecewise regression (BHPR) modeling has not been previously formulated to detect and characterise the mechanism of trajectory divergence between groups of participants that have longitudinal responses with distinct developmental phases. These models are useful when participants in a prospective cohort study are grouped according to a distal dichotomous health outcome. Indeed, a refined understanding of how deleterious risk factor profiles develop across the life-course may help inform early-life interventions. Previous techniques to determine between-group differences in risk factors at each age may result in biased estimate of the age at divergence. Methods We demonstrate the use of Bayesian hierarchical piecewise regression (BHPR) to generate a point estimate and credible interval for the age at which trajectories diverge between groups for continuous outcome measures that exhibit non-linear within-person response profiles over time. We illustrate our approach by modeling the divergence in childhood-to-adulthood body mass index (BMI) trajectories between two groups of adults with/without type 2 diabetes mellitus (T2DM) in the Cardiovascular Risk in Young Finns Study (YFS). Results Using the proposed BHPR approach, we estimated the BMI profiles of participants with T2DM diverged from healthy participants at age 16 years for males (95% credible interval (CI):13.5–18 years) and 21 years for females (95% CI: 19.5–23 years). These data suggest that a critical window for weight management intervention in preventing T2DM might exist before the age when BMI growth rate is naturally expected to decrease. Simulation showed that when using pairwise comparison of least-square means from categorical mixed models, smaller sample sizes tended to conclude a later age of divergence. In contrast, the point estimate of the divergence time is not biased by sample size when using the proposed BHPR method. Conclusions BHPR is a powerful analytic tool to model long-term non-linear longitudinal outcomes, enabling the identification of the age at which risk factor trajectories diverge between groups of participants. The method is suitable for the analysis of unbalanced longitudinal data, with only a limited number of repeated measures per participants and where the time-related outcome is typically marked by transitional changes or by distinct phases of change over time. Electronic supplementary material The online version of this article (doi:10.1186/s12874-017-0358-9) contains supplementary material, which is available to authorized users.

Spaghetti plot of the individual trajectories of those with T2DM in adulthood (N = 88) and those who did not develop T2DM in adulthood (N = 2452). Red solid line: loess smoother curve indicating the average longitudinal trend in each group (Figure S1.) and scatterplot of the life-course BMI data (in kg/m2) stratified by sex. Solid lines and gray bands: loess smoothed average trajectories and confidence intervals for each group (adult T2DM vs. non-T2DM group); dashed lines: age-specific averages of BMI levels (Figure S2.) (DOCX 1918 kb)

Low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), and triglycerides (TG) are modifiable risk factors for cardiovascular disease. Several genetic loci for predisposition to abnormal LDL-C, HDL-C and TG have been identified. However, it remains unclear whether these loci are consistently associated with serum lipid levels at each age or with unique developmental trajectories. Therefore, we assessed the association between genome wide association studies (GWAS) derived polygenic genetic risk scores and LDL-C, HDL-C, and triglyceride trajectories from childhood to adulthood using data available from the 27-year European 'Cardiovascular Risk in Young Finns' Study. For 2,442 participants, three weighted genetic risk scores (wGRSs) for HDL-C (38 SNPs), LDL-C (14 SNPs) and triglycerides (24 SNPs) were computed and tested for association with serum lipoprotein levels measured up to 8 times between 1980 and 2011. The categorical analyses revealed no clear divergence of blood lipid trajectories over time between wGRSs categories, with participants in the lower wGRS quartiles tending to have average lipoprotein concentrations 30 to 45% lower than those in the upper-quartile wGRS beginning at age 3 years and continuing through to age 49 years (where the upper-quartile wGRS have 4-7 more risk alleles than the lower wGRS group). Continuous analyses, however, revealed a significant but moderate time-dependent genetic interaction for HDL-C levels, with the association between HDL-C and the continuous HDL-C risk score weakening slightly with age. Conversely, in males, the association between the continuous TG genetic risk score and triglycerides levels tended to be lower in childhood and become more pronounced after the age of 25 years. Although the influence of genetic factors on age-specific lipoprotein values and developmental trajectories is complex, our data show that wGRSs are highly predictive of HDL-C, LDL-C, and triglyceride levels at all ages. Public Library of Science open access

Diatoms possess a silica frustule decorated with unique patterns of nanosize features. Here, we show for the first time from in situ samples that the size of the nanopores present at the surface of the diatom Cocconeis placentula Ehrenb. varies with fluctuating salinity levels. The observed reduction in nanopore size with decreasing salinity agrees with previous laboratory experiments. We also uniquely combined our observations with theoretical considerations to demonstrate that the decrease in the diffusive layer thickness is compensated for by the changes in pore size, which maintain a steady diffusive flux toward the diatom’s cell at different salinities. This process allows diatoms to absorb similar amount of nutrients whatever the salinity and as such to increase their ecological competitiveness in fluctuating environments. These results further suggest that the overall ecological success of diatoms, and their ability to react to environmental changes, may be controlled by the flexibility of the morphological characteristics of their frustules.

Aims: The relationship between life-course body mass index (BMI) trajectories and adult risk for cardiovascular disease (CVD) is poorly described. In a longitudinal cohort, we describe BMI trajectories from early childhood to adulthood and investigate their association with CVD risk factors [Type 2 diabetes mellitus (T2DM), high-risk lipid levels, hypertension, and high carotid intima-media thickness (cIMT)] in adulthood (34-49 years). Methods and results: Six discrete long-term BMI trajectories were identified using latent class growth mixture modelling among 2631 Cardiovascular Risk in Young Finns Study participants (6-49 years): stable normal (55.2%), resolving (1.6%), progressively overweight (33.4%), progressively obese (4.2%), rapidly overweight/obese (4.3%), and persistent increasing overweight/obese (1.2%). Trajectories of worsening or persisting obesity were generally associated with increased risk of CVD outcomes in adulthood (24-49 years) [all risk ratios (RRs) >15, P < 0.05 compared with the stable normal group]. Although residual risk for adult T2DM could not be confirmed [RR = 2.6, 95% confidence interval (CI) = 0.14-8.23], participants who resolved their elevated child BMI had similar risk for dyslipidaemia and hypertension as those never obese or overweight (all RRs close to 1). However, they had significantly higher risk for increased cIMT (RR = 3.37, 95% CI = 1.80-6.39). Conclusion: The long-term BMI trajectories that reach or persist at high levels associate with CVD risk factors in adulthood. Stabilizing BMI in obese adults and resolving elevated child BMI by adulthood might limit and reduce adverse cardiometabolic profiles. However, efforts to prevent child obesity might be most effective to reduce the risk for adult atherosclerosis.

International audience; Background : Picophytoplankton (i.e. cyanobacteria and pico-eukaryotes) are abundant and ecologically critical components of the autotrophic communities in the pelagic realm. These micro-organisms colonized a variety of extreme environments including high salinity waters. However, the distribution of these organisms along strong salinity gradient has barely been investigated. The abundance and community structure of cyanobacteria and pico-eukaryotes were investigated along a natural continuous salinity gradient (1.8% to 15.5%) using flow cytometry. Results : Highest picophytoplankton abundances were recorded under salinity conditions ranging between 8.0% and 11.0% (1.3 x 106 to 1.4 x 106 cells ml-1). Two populations of picocyanobacteria (likely Synechococcus and Prochlorococcus) and 5 distinct populations of pico-eukaryotes were identified along the salinity gradient. The picophytoplankton cytometric-richness decreased with salinity and the most cytometrically diversified community (4 to 7 populations) was observed in the brackish-marine part of the lagoon (i.e. salinity below 3.5%). One population of pico-eukaryote dominated the community throughout the salinity gradient and was responsible for the bloom observed between 8.0% and 11.0%. Finally only this halotolerant population and Prochlorococcus-like picocyanobacteria were identified in hypersaline waters (i.e. above 14.0%). Salinity was identified as the main factor structuring the distribution of picophytoplankton along the lagoon. However, nutritive conditions, viral lysis and microzooplankton grazing are also suggested as potentially important players in controlling the abundance and diversity of picophytoplankton along the lagoon. Conclusion : The complex patterns described here represent the first observation of picophytoplankton dynamics along a continuous gradient where salinity increases from 1.8% to 15.5%. This result provides new insight into the distribution of pico-autotrophic organisms along strong salinity gradients and allows for a better understanding of the overall pelagic functioning in saline systems which is critical for the management of these precious and climatically-stress ecosystems.

International audience; The abundance and community structure of viruses and heterotrophic bacteria were investigated along a natural continuous salinity gradient (18 to 155 PSU) in a South Australian temperate coastal lagoon using flow cytometry. The brackish waters of the lagoon (18 to 25 PSU) were characterised by high viral concentrations (1.3 × 108 to 1.5 × 108 ml–1) and elevated virus to bacteria ratios (11.7 to 15.5), suggesting high viral infection rates and long persistence of viruses in the water. The increase in salinity above 25 PSU resulted in a decrease in viral abundance without a significant modification of bacterial abundance. A concomitant increase in viral and bacterial abundances with salinity was observed from 50 to 150 PSU, where the highest abundances were observed (1.4 × 108 and 2.5 × 108 ml–1, respectively). Prokaryote cytometric richness also varied greatly along the salinity gradient, suggesting a modification of the phylogenetic composition and/or variability in the activity level of the bacterioplankton community along the salinity gradient. The most cytometrically diversified bacterial community (6 to 7 subpopulations) was observed between 50 and 150 PSU. BIOENV analysis identified salinity as the main factor structuring the distribution of bacteria throughout the lagoon. The effect of salinity on viral populations appeared to be more indirect, as the distribution of viruses was mainly driven by host abundance (i.e. bacteria) along the salinity gradient. The complex patterns described here represent the first observation of viral and microbial dynamics along a continuous salinity gradient from 18 to 155 PSU.