Epidemiology of Cannabis

Genotoxicity, Neurotoxicity, Epigenomics and Aging

1st Edition - April 22, 2025
Imprint: Academic Press
Authors: Albert Stuart Reece, Gary Kenneth Hulse
Language: English
Paperback ISBN:
9 7 8 - 0 - 4 4 3 - 1 3 4 9 2 - 0
eBook ISBN:
9 7 8 - 0 - 4 4 3 - 1 3 4 9 3 - 7

Epidemiology of Cannabis: Genotoxicity, Neurotoxicity, Epigenomics and Aging provides a novel and comprehensive exploration of five areas that have previously been associ… Read more

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Epidemiology of Cannabis: Genotoxicity, Neurotoxicity, Epigenomics and Aging provides a novel and comprehensive exploration of five areas that have previously been associated with cannabis use, namely mental health in adults and young adults, pediatric autism, congenital anomalies, cancers, and aging. The book also explores the possibility of how these associations might be reflected in overall disease trends at the population health level. This book surveys these five areas in detail and applies cutting-edge analytical software and geospatial space–time analytical techniques to these questions.

With all this information gathered into one book in an easily readable form, this book is a reference for clinicians, health science and allied health practitioners, public health and basic science researchers and drug and health regulators interested in these topics. It is also suitable for inclusion in course work and study preparation courses at both the undergraduate and postgraduate levels.

Epidemiology of Cannabis
Cover image
Title page
Table of Contents
Copyright
About the authors
Foreword
Foreword—Snake oil seduction or academic truth?
Prologue
Implications for policy
Outline
Assessment
Plan of action
Commentary
Assessment
Plan of action
References
Section A: Mental illness
Chapter 1 Close parallels between cannabis use and deteriorating US Mental Health at four levels supports and extends the epidemiological salience of demonstrated causal mental health relationships: A geospatiotemporal study
Abstract
Keywords
Introduction
Methods
Analysis plan
Statistical considerations
Data availability
Assessing causality
Results
National level
Regional level
State level
Substate level
Considerations of causality
Koch’s postulates
Hills’ causal algorithm
Brain disease pathways and mechanisms
Cannabis and mass violence
Brain
Endocannabinoid system in the brain
Dopamine
Other
Mitochondriology
Immunome
Genomic studies
Cannabinoid-opioid interactions
Conclusion
Mental health general questions and case studies
General questions
Case studies
References
Section B: Autistic spectrum disorder
Chapter 2 Linked rise of cannabis use and autism incidence demonstrated by close three-level geospatiotemporal relationships, USA, 1990–2011
Abstract
Introduction
Methods
Results
Conclusions
Keywords
Introduction
Methodological comment
Assessing causality
Data availability
Results
National level data
Regional level
State level data
Impact of cannabis legal status on autism rates
Causal inference
Discussion
Mechanistic considerations
European neuroteratology studies
Morphogen gradients guide brain development
Retinoic acid
Slit-Robo
Neurexin-neuroligin
DSCAM and DLGAP2
Oligodendrocytes and myelination
Genomic studies
Epigenomic studies
Pediatric poisonings
Conclusion
General questions
Case studies
Case 1
Case 2: Josephine and Andres
Case 3: Lionel
References
Section C: Congenital anomalies
Chapter 3 Geospatiotemporal and causal inferential analysis of United States congenital anomalies as a function of multiple cannabinoid- and substance-exposures: Phenocopying thalidomide and hundred megabase-scale genotoxicity
Abstract
Keywords
Executive summary
Introduction
Methods
Ethics
Results
Cannabis-related defects
Upper quintile threshold discontinuity
Conclusion
Cannabis-related congenital anomalies
Cannabis-related anomalies by geotemporospatial criteria, N = 38
Cannabis-related anomalies by prevalence ratio criteria, N = 44
Cannabis-related anomalies by prevalence ratio criteria, N = 42
Introduction
Methodology
Data sources
Cannabis consumption quintiles
Data analysis
Statistics
Broom-Purrr multimodel assessments
Matrix multiplication
Geospatial modeling
Two phases of data analysis
Spatial error structures
Spatial model specification
Corrections for multiple testing
Assessing causality
Data availability
Ethics
Results
Section one: Drug use by ethnicity and age
Section two: Drugs and congenital anomalies overview
Section three: Chromosomal defects
Section four: Gastroschisis and body wall
Section five: Atrial septal defect (secundum type)
Section six: Cardiovascular defects of interest
Section seven: Hawaiian—American review
Discussion
General considerations
Bivariate analysis
Summary observations
Data summary
Forest plot
Canada
Australia
Mechanistic summary
Multivariable analysis
Multivariable causal analysis
Multivariable causal analysis
Effect of cannabis legalization
Considerations of causality
Geotemporal trimodality
Causality and the hill criteria
Causal inference
Causal assignment
Commonality
Pathways and mechanisms
Genotoxic mechanisms
Morphogen gradients control body formation and patterning
Cannabinoid modulation of other morphogenetic pathways
Specific organ systems
Heart
Respiratory defects
Face
Gastrointestinal tract
Urinary tract
Body wall anomalies
Limbs
Chromosomal defects
Interactions of other major morphogen systems with cannabinoids
Cannabinoid teratology
Chromosomal mechanics and dynamics
Sperm and cannabinoids
Oocytes and cannabinoids
Embryonic development
Conclusion
Directions for future research
Congenital anomalies general questions and case studies
General questions
Case studies
References
Section D: Cancer and heritable cancer
Chapter 4 Geospatiotemporal and causal inferential epidemiological survey and exploration of cannabinoid- and substance-related carcinogenesis in the United States from 2003 to 2017
Abstract
Background
Methods
Results
Conclusion
References
Chapter 4 Geospatiotemporal and causal inferential epidemiological survey and exploration of cannabinoid- and substance-related carcinogenesis in USA 2003–2017
Abstract
Background
Methods
Results
Conclusion
Keywords
Objectives
Introduction
Methods
Assessing causality
Results
Section I—General introduction and overview of All Cancers
Tobacco-linked cancers
Total cancers
Substance use
Ethnicity
Bivariate associations of cancer
Introductory analysis—Bivariate exposure trends
Regression tables
Compiled comparative tables by substance
Tables of dichotomous categorical contrasts
Bivariate correlation plots
Significance overview
Section II—28 Individual cancer types
Total cancer rates and trends
Acute lymphoid leukemia
Acute myeloid leukemia
Bladder cancer
Brain cancer
Breast cancer
Cervical cancer
Chronic lymphoid leukemia
Chronic myeloid leukemia
Colorectal cancer
Esophageal cancer
Hodgkins lymphoma
Kaposi sarcoma
Kidney cancer
Liver cancer
Lung cancer
Melanoma
Melanoma and latitude
Multiple myeloma
Non-Hodgkins lymphoma
Oropharyngeal cancer
Ovarian cancer
Pancreas cancer
Penis cancer
Prostate cancer
Stomach cancer
Thyroid cancer
Vaginal and vulval cancers
Section III—Selected geotemporospatial models
All Cancers
Acute lymphoid leukemia
Acute myeloid leukemia
Bladder cancer
Brain cancer
Breast cancer
Cervical cancer
Chronic lymphoid leukemia—Two temporal lags
Colorectal cancer
Esophageal cancer at four temporal lags
Hodgkins disease at one temporal lag
Kaposi sarcoma
Kidney cancer
Liver cancer lagged to 6 years
Lung cancer
Melanoma
Non-Hodgkins lymphoma
Oropharyngeal cancers
Ovarian cancer
Prostate cancer
Stomach cancer at six temporal lags
Thyroid cancer
Vulvovaginal cancer at four temporal lags
Tobacco models
Cervical cancer
Lung cancer
Penile cancer at one spatial and four temporal lags
Section IV—Summary of geospatial model fitted values analysis
Section V—Summary of geotemporospatial matrix multiplication modeling
Cigarette analysis
Section VI—Comparisons with known carcinogens
Tobacco
Alcohol
Obesity
Cannabis
Cannabidiol
Overall comparisons
Legal status
Affected numbers of patients
Section VII—Summary of summaries
Bivariate relationships
Regression summaries
Panel models
Geospatial models
Causal-geospatial analytical synthesis
Section VIII—Discussion
Main results
Comparison with epidemiology of cancer in Europe
Causal assignment
Pathways and mechanisms
Gametes
Comparison of genomics of cancer with cannabinoid epigenomics
Pan-cancer
Acute myeloid leukemia
Medulloblastoma
Pancreatic cancer
Overall
Epigenetic overview
Methylation of DNA
Cancer epigenetics
Reduction in histones and post-translational modifications
Proteins
Epigenomics and bioenergetics
Interactions with specific pathways
Metabolome
Lactate and lactylation
Lactate in hepatocarcinogenesis
Lactylation enforces glycolytic metabolism, cell Stemness, and differentiation block
Metabolic inhibitors induce teratogenesis
2 Hydroxyglutarate (2HG)
Isocitrate dehydrogenase
Epitranscriptomics
Sarcopaenia in aging and cancer
Novel immune pathways to cell death
Mitochondriology
Microbiome
Immunome
Memory is encoded epigenetically
Inflammation drives the senescent phenotype of aging
General immune studies
Cancer cachexia
Transposable elements
cGAS-STING
Actin
Genetic biology of cancer
Specific cancers
Head and neck squamous cancer
Hematological cancer
Pancreatic cancer
Renal cancer
Breast cancer
Prostate cancer
Bladder cancer
Non-Hodgkins lymphoma
Chromatin looping in cancer
Overcoming replicative block
Generalizability
Strengths and limitations
Conclusion
General questions
Case studies
Valerie
Alexander
John
References
Section E: Epigenetics and aging
Chapter 5 Multivalent cannabinoid epigenotoxicities and multigenerational aging
Abstract
Keywords
Introduction
Definitions
Epigenetic layers
Hallmarks of aging
Methodology
Data
Computations
Ethical permission
Results and discussion
Historical studies
Mitochondrial inhibition
Important earlier epigenomic studies
Longitudinal human sperm study
Detailed analysis of longitudinal sperm study results
Perturbation of fundamental epigenomic machinery
Stem cell genes
Age-related immunometabolic genes
Chromosomes, centrosomes, and kinetochores
DNA repair
Epigenomics
Epigenomics of cannabinoid teratology
Brain
Cannabinoid neurotoxicity
Cannabinoid epigenomic neurotoxicity
Summary of cannabinoid neurotoxicity
Cardiovascular system
Other organs and systems
Chromosomal anomalies
Uronephrology
Body wall
Teratological summary
Epigenomics of cannabinoid-related cancers
Epigenomics of aging
Overview of conceptual aging paradigm
Aging is driven by a loss of epigenetic information
Epigenomics
Overall pattern of cannabis toxicity
Hallmarks of cannabinoid accelerated aging
Epigenomic—genomic overlap in aging syndromes
Heterochronic parabiosis
Haemopoietic stem cells
Heterochronic CSF circulation
Movement in fibroblasts
Ovarian aging
Mouse aging
Epigenomics and pathobiology of aging
Inflammation and stem cells
Cardiovascular disease
Hematopoietic stem cells
Skeletal muscle
Summary genomic-epigenomic tables
Summary of cannabinoid aging acceleration
Overall summary of multivalent cannabinoid epigenotoxicities
Case studies—Epigenetics and aging
Leonard
Case questions
Q multiple choice
References
Chapter 6 Conclusion
References
Index

Albert Stuart Reece

Dr. Stuart Reece has been a registered medical practitioner in Australia since 1982. He has worked with a special interest in addiction medicine since 1997 when he was introduced to naltrexone medicine in Perth. He has worked in a variety of hospital and community-based environments in Australia, UK, France, and Papua New Guinea. In addition to his basic medical qualification, Dr Reece holds surgical fellowships from the Royal College of Surgeons of Edinburgh and the Royal College of Physicians and Surgeons of Glasgow, a Fellowship of the Royal Australian College of General Practitioners, and a Doctorate of Medicine in liver transplantation. Dr Reece was appointed as Associate Professor of Medicine at the University of Western Australia in 2010, and an adjunct Professor of Medicine at both the University of Western Australia and the Edith Cowan University in 2018.

Affiliations and expertise

Professor, University of Western Australia, Australia and Professor, Edith Cowan University, Australia

Gary Kenneth Hulse

Professor Gary Hulse has worked in the area of problem alcohol and drug use for the past 30 years, For the past fourteen years he has held an academic appointment as ‘Coordinator of Alcohol and Drug Education and Training’ within the Faculty of Medicine, University of Western Australia, based at Sir Charles Gairdner Hospital Perth. Research and clinical activities have been primarily directed at developing evidence- based information which will enhance clinical practice. Between 1992-2009, Professor Hulse chaired the Committee on Alcohol and Drug Education in Medical Schools on behalf of the Committee of Deans Australian and New Zealand Medical Schools. Professor Hulse has published in excess of 150 peer review publications. He is Chief Editor of two evidence based clinical alcohol and drug texts published by Oxford University Press which have been adopted as the standard text for medical training by the Australian Medical Schools [Committee of Deans].

Affiliations and expertise

Professor, University of Western Australia, Australia and Professor, Edit Cowan University, Australia

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