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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.

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.

Objectives: Life course exposure to passive smoke may predict health, but there are few validated measures. We tested the reliability and validity of a retrospective life course passive smoking questionnaire. Methods: Participants from the third follow-up of the Childhood Determinants of Adult Health study (2014-2019, ages 36-49 years) retrospectively reported mother/father/other household member smoking when living at home during childhood, including duration (years) and smoking location (never/sometimes/always inside house). The severity of exposure index (SEI; sum of mother/father/other years smoked multiplied by smoking location), cumulative years of exposure (CYE; sum of mother/father/other years), and total household smokers (THS) were derived. The reliability of retrospective passive smoking reports was examined with intraclass correlation coefficients (ICCs) using household smoking reported 34 years earlier in 1985 by participants when aged 7-15 years. Construct validity was examined by correlating retrospective passive smoking with participants’ smoking in adulthood and lung function in childhood and adulthood. Results: Among 2082 participants (mean±standard deviation [SD], 45.0±2.5 years; 55.2% females), THS ranged from 0 to 5 (mean± SD, 0.9±1.0), CYE ranged from 0 to 106 (mean±SD, 10.5±13.9), and SEI ranged from 0 to 318 (mean±SD, 24.4±36.0). Retrospective measures showed moderate agreement with total household smokers reported in childhood (ICC, 0.58 to 0.62). The retrospective measures were weakly but significantly (pConclusions: The retrospective passive smoking questionnaire showed reasonable reliability and validity. This measure may be useful for epidemiological studies.

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.

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.

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.

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.