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Cannabis exposure as an interactive cardiovascular risk factor and accelerant of organismal ageing: a longitudinal study
  1. Albert Stuart Reece,
  2. Amanda Norman,
  3. Gary Kenneth Hulse
  1. School of Psychiatry and Clinical Neurosciences, University of Western Australia, Crawley, Western Australia, Australia
  1. Correspondence to Dr Albert Stuart Reece; sreece{at}bigpond.net.au

Abstract

Objectives Many reports exist of the cardiovascular toxicity of smoked cannabis but none of arterial stiffness measures or vascular age (VA). In view of its diverse toxicology, the possibility that cannabis-exposed patients may be ageing more quickly requires investigation.

Design Cross-sectional and longitudinal, observational. Prospective.

Setting Single primary care addiction clinic in Brisbane, Australia.

Participants 11 cannabis-only smokers, 504 tobacco-only smokers, 114 tobacco and cannabis smokers and 534 non-smokers. Exclusions: known cardiovascular disease or therapy or acute exposure to alcohol, amphetamine, heroin or methadone.

Intervention Radial arterial pulse wave tonometry (AtCor, SphygmoCor, Sydney) performed opportunistically and sequentially on patients between 2006 and 2011.

Main outcome measure Algorithmically calculated VA. Secondary outcomes: other central haemodynamic variables.

Results Differences between group chronological ages (CA, 30.47±0.48 to 40.36±2.44, mean±SEM) were controlled with linear regression. Between-group sex differences were controlled by single-sex analysis. Mean cannabis exposure among patients was 37.67±7.16 g-years. In regression models controlling for CA, Body Mass Index (BMI), time and inhalant group, the effect of cannabis use on VA was significant in males (p=0.0156) and females (p=0.0084). The effect size in males was 11.84%. A dose–response relationship was demonstrated with lifetime exposure (p<0.002) additional to that of tobacco and opioids. In both sexes, the effect of cannabis was robust to adjustment and was unrelated to its acute effects. Significant power interactions between cannabis exposure and the square and cube of CA were demonstrated (from p<0.002).

Conclusions Cannabis is an interactive cardiovascular risk factor (additional to tobacco and opioids), shows a prominent dose–response effect and is robust to adjustment. Cannabis use is associated with an acceleration of the cardiovascular age, which is a powerful surrogate for the organismal–biological age. This likely underlies and bi-directionally interacts with its diverse toxicological profile and is of considerable public health and regulatory importance.

  • Biological age
  • Cannabis and aging
  • Accelerated aging
  • Biomarkers of aging

This is an Open Access article distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/

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Footnotes

  • Contributors ASR designed the study, treated the patients, conducted the PWA studies, analysed the data and wrote the initial draft of the paper. GKH gave advice on study design and data analysis, wrote the paper and assisted with literature review. AN assisted with literature review and wrote the paper.

  • Funding This research received no specific grant from any funding agency in the public, commercial or not-for-profit sectors.

  • Competing interests None declared.

  • Ethics approval Southcity Medical Centre Human Research Ethics Committee.

  • Provenance and peer review Not commissioned; externally peer reviewed.

  • Data sharing statement No additional data are available.

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