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Author(s):  
Andrew Haynes ◽  
Joanne McVeigh ◽  
Leanne Lester ◽  
Peter R. Eastwood ◽  
Leon Straker ◽  
...  

2021 ◽  
pp. jech-2021-218039
Author(s):  
Robert Tait ◽  
Rebecca Ivers ◽  
Jennifer L Marino ◽  
Dorota Doherty ◽  
Petra L Graham ◽  
...  

BackgroundRoad traffic crashes (RTC) are a leading cause of mortality and morbidity in young people. Severe mental health and behavioural conditions increase the likelihood of RTC, as do a range of driving-risk activities.MethodWe used data from the Raine Study, a prebirth cohort from Perth, Australia, to assess the relationship between measures of common mental health or behavioural conditions (Child Behavior Checklist Internalising and Externalising scores) at age 17 and subsequent RTC by 27 years, controlling for substance use and driving-risk activities.ResultsBy 27 years of age, of 937 participants, 386 (41.2%) reported zero crashes and 551 (58.8%) reported ≥1 crashes. In the baseline Poisson model, increased Externalising scores (eg, aggression and delinquency) were associated with increased RTC (incidence rate ratio (IRR)=1.02, 95% CI 1.01 to 1.02): increased Internalising scores (eg, anxiety and depression) were associated with fewer RTC (IRR=0.99, 95% CI 0.98 to 1.00). In the fully adjusted model, the mental health measures were not significant (Externalising IRR=1.01, 95% CI 0.99 to 1.02: Internalising IRR=0.99, 95% CI 0.99 to 1.00). Risky driver activities, such as falling asleep while driving (IRR=1.34), more frequent use of a hands-free telephone (IRR=1.35) and more frequent hostility towards other drivers (IRR=1.30) increased the rate of RTC.ConclusionMeasures of mental health scores at age 17 were not predictive of subsequent RTC, after adjusting for measures of driving-risk activities. We need to better understand the determinants of externalising and risky driving behaviours if we are to address the increased risk of RTC.


Spine ◽  
2021 ◽  
Vol Publish Ahead of Print ◽  
Author(s):  
Anne Smith ◽  
Mark Hancock ◽  
Susan O’Hanlon ◽  
Michael Krieser ◽  
Peter O'Sullivan ◽  
...  

2021 ◽  
Vol 138 ◽  
pp. 53-59
Author(s):  
Getinet Ayano ◽  
Ashleigh Lin ◽  
Kim Betts ◽  
Robert Tait ◽  
Berihun Assefa Dachew ◽  
...  

Author(s):  
Elvira V. Bräuner ◽  
Youn-Hee Lim ◽  
Trine Koch ◽  
Trevor A. Mori ◽  
Lawrence Beilin ◽  
...  

Author(s):  
Wrivu N Martin ◽  
Carol A Wang ◽  
Stephen J Lye ◽  
Stephen G Matthews ◽  
Rebecca M Reynolds ◽  
...  

Abstract Context Human and animal studies suggest that hypothalamic-pituitary-adrenal axis (HPA-A) function may be programmed in utero; however, these findings are inconsistent. Given the powerful metabolic actions of cortisol, it is important to clarify the influence of early life on adult HPA-A function. Objective To determine the relationship between fetal growth and HPA-A stress response to a psychosocial stressor in young adults. Design Multigenerational, prospective cohort study (The Raine Study) conducted between 1989 and 1991. Setting King Edward Memorial Hospital, Perth, Western Australia, Australia. Participants 917 participants aged 18 from Gen 2 of the Raine Study. Main Outcome Measures Measures of Hypothalamic-Pituitary-Adrenal-Axis function before and after exposure to the Trier Social Stress Test. Results In fully adjusted models, an inverse linear relationship was observed between birth weight and and plasma measures of 1) baseline cortisol (β = -0.90%, 95% CI: -1.73 to -0.07; p = 0.03); 2) peak cortisol (β = -0.78%, 95% CI -1.51 to -0.06; p=0.03); 3) AUCg (β = -0.89%, 95% CI -1.60 to -0.18; p=0.01); and 4) adrenal sensitivity (β = -1.02, 95% CI: -1.85 to -0.18; p=0.02). Similar results were demonstrated for per cent optimal birth weight. No consistent quadratic relationships were identified. No associations were found between measures of fetal adiposity and HPA-A function at age 18, or fetal growth and HPA-A response pattern. Removal of anticipatory responders from the models substantially attenuated the observed relationships. Conclusion We observed an inverse linear relationship between fetal growth and HPA-A function at age 18. This differs from the inverse parabolic relationship (inverted U curve) reported in adults of advanced age. Altered adrenal sensitivity may underlie this relationship.


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