Evidence map›Paper›PMID 27821595›Full record

Observational studyBMJ open2016

Cannabis exposure as an interactive cardiovascular risk factor and accelerant of organismal ageing: a longitudinal study.

Albert Stuart Reece, Amanda Norman, Gary Kenneth Hulse

Abstract readObservational Study
In one paragraph

Observational study in BMJ open, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

37 citing papers in PubMed.

  1. Cannabinoid impacts on ethnic modulation of atrial septal defect prevalence USA.Journal of perinatology : official journal of the California Perinatal Association · 2026
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors.

Albert Stuart ReeceSchool of Psychiatry and Clinical Neurosciences, University of Western Australia, Crawley, Western Australia, Australia.
Amanda NormanSchool of Psychiatry and Clinical Neurosciences, University of Western Australia, Crawley, Western Australia, Australia.ORCID 0000-0002-5183-1192
Gary Kenneth HulseSchool of Psychiatry and Clinical Neurosciences, University of Western Australia, Crawley, Western Australia, Australia.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectivesMany 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.

designCross-sectional and longitudinal, observational. Prospective.

settingSingle primary care addiction clinic in Brisbane, Australia.

participants11 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.

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

main outcome measureAlgorithmically calculated VA. SECONDARY OUTCOMES: other central haemodynamic variables.

resultsDifferences 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).

conclusionsCannabis 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.

Indexed as

AdultAgingCannabisCardiovascular DiseasesFemaleHumansLongitudinal StudiesMaleMiddle AgedProspective StudiesPulse Wave AnalysisRadial ArteryRegression AnalysisRisk FactorsVascular StiffnessAccelerated agingBiological ageBiomarkers of agingCannabis and aging

Identifiers

PMID27821595
PMCPMC5129004

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.