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Should we legalise cannabis?

by BMJ Article and Rapid Responses, posted 04 07 2019

Fiona Godlee, editor in chief

Author affiliations

fgodlee@bmj.com
Follow Fiona on Twitter @fgodlee

In any public debate there may come a point when the evidence for a shift in direction clearly outweighs that against. Has this point been reached for drug policy reform?

Several UK medical bodies have decided it has. The Royal College of Physicians of London, the Faculty of Public Health, and the Royal Society for Public Health all now support decriminalising non-medical use of drugs such as cannabis, cocaine, and heroin. In this they agree with the World Health Organization and the UK government’s own independent Advisory Council on the Misuse of Drugs. The other medical royal colleges and the BMA have no official position. In 2016 the BMA’s annual representative meeting called for legislation to prioritise treating rather than criminalising drug users, but a motion in 2018 to publicly support decrimina­­­lisation was defeated. The BMJ has called for a regulated legal market in currently illegal drugs for any use (doi:10.1136/bmj.k2057; doi:10.1136/bmj.i6067; bmj.com/war-on-drugs).

Of the royal colleges with no official position, three might be said to represent doctors working at the sharpest end of the war on drugs: those of general practitioners, emergency medicine, and psychiatrists. Their views therefore hold particular sway, especially the psychiatrists, and especially among politicians, whose fear of public opinion on this issue was recently reaffirmed when Conservative leadership candidates rushed to endorse the current law despite their own admissions of previous drug taking (https://blogs.bmj.com/bmj/2019/06/19/drugs-are-decriminalised-in-the-uk-if-you-are-a-white-privileged-mp). So a debate held this week at the annual meeting of the Royal College of Psychiatrists on whether cannabis supply should be legalised is an important event. We carry both sides of the debate (doi:10.1136/bmj.l4468).

It’s interesting to see where the battle lines are drawn. Both sides agree on the greatly increased risk of psychosis from daily use of high potency cannabis, of the sort that is widely available in the UK. But what would be the effect of legalisation? Molly Meacher and colleagues cite evidence that low potency cannabis can be consumed safely and conclude that a state controlled, regulated market would protect health as well as raising tax revenues. They would set age and potency limits and ban advertising. Robin Murray and Adam Grindley concede that legalisation wouldn’t necessarily increase use and potency, but they want to wait and see what happens in the US and Canada. In the meantime they support decriminalisation of people who take drugs.

Perhaps the Royal College of Psychiatrists will take courage from this and follow suit.

 

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Re: Should we legalise cannabis?  

18 July 2019
Albert S Reece
Physician
University of Western Australia
35 Stirling Hwy, Crawley

Cannabis Threatens Oocytes, a Non-Renewable National Genomic Resource – and Implications of Prostacyclin Vasodilation and Anti-thrombogenesis

The classic experiments of Morishima reported by NIDA in 1984 leave very little to the imagination in relation to the genotoxic effects of cannabis on developing oocytes. Morishima showed that 20% of oocytes were lost after just the first cell division following cannabis exposure, and the news got worse in subsequent divisions 1. Apparently the oocytes were not able to cope with the genotoxic stress induced by cannabis exposure. Cannabis is known to induce DNA damage by several mechanisms including damage to chromosomes at the time of cell division, dramatic reductions in histone formation which form the core of the nucleosomes around which DNA is twined and are crucially involved in signalling to the transcription and epigenetic machinery to regulate gene expression, alteration of DNA methylation and many other processes 2-6. And genotoxic stress of many types is known to trigger DNA checkpoints and interfere with the normal process of meiotic and mitotic cell division; and are also known to trigger ageing and cellular senescence pathways.

The implications of stimulated senescence in human gametes have not been clearly thought out.

A momentary consideration of the differing biology of gametic reproduction in the two sexes is pertinent. Every medical student is taught that infant females are born with 1,000,000 oocytes in their ovaries, a number which falls to 400,000 by the time of menarche and she loses 20-50 with each menstrual cycle until ovarian exhaustion some time before menopause. This monotonic decline in the oocyte pool caused by their non-replacement directly implies that any genotoxic damage suffered by the developing oocyte would be FIXED in place, and just as we learned through studying mechanisms of chromothripsis and epigenomics, any cells not fatally damaged – which many would be - could pass on these effects to subsequent cell divisions, and potentially the developing embryo. In males the biology is very different, with 1500 sperm formed each second and an estimated 3 million million over a 60 year reproductive lifetime. Genotoxic damage sustained by males 4 7 would therefore have to be passed on by mechanisms involving cell division – of which there are many including chromosomal fragmentation, oxyradical DNA adduct formation particularly of the base guanine, and extensive DNA methylation and epigenomic damage of many types.

Can oocytes repair DNA damage? The answer to this question is not straightforward. It was classically taught that human oocytes have deficient DNA repair mechanisms related to the dramatically reduced availability of DNA repair proteins in contrast to oocytes of other species such as mice and monkeys 8-11. If so this implies that genomic damage would necessarily be passed along. However more recent studies suggest that oocytes have more DNA repair capacity than previously thought 12. However by analogy with epigenomic and chromothripsis studies it seems most unlikely that human oocytes can completely repair their genomic / epigenomic damage particularly in the context of Morishima’s work demonstrating extensive and severe genotoxicity, chromosomal bridging, chromoplexy and obvious macroscopic chromosomal damage.

Such considerations lead to the appalling conclusion that oocytes suffering the very considerable genotoxic / epigenotoxic damage imposed by cannabinoids – including cannabidiol 7 – can be irreversibly damaged and some of these damaged gametes will pass their genetically scrambled misinformation to subsequent embryos. Similar considerations apply to males albeit by well described mechanistic pathways which include cell division.

In this sense oocytes in particular can be conceptualized as a non-renewable genomic resource, and a key component of our national gene-environmental interactive heritage.

One of the less appreciated findings of the stunning paper on the genotoxic effects of cannabis on mice and human sperm by Murphy et. al. was the finding that cannabis exposure in both species reduces prostacyclin by epigenetic mechanisms 4. The thromboxane – prostacyclin axis has been known for several decades to control the balance between vasoconstriction and platelet adhesiveness on the one hand and vasodilatation and platelet disaggregation on the other. Both are highly potent agents active at the nanomolar level and tightly control vasomotor tone and the coagulation state or “stickiness” of the blood. Prostacyclin is a key vasodilator and regulator of microvascular integrity. It is known to have a powerful and potent effect on maintaining the patency of vessels of sub-millimeter diameter.

Dr Nora Volkow, Director of NIDA has expounded on the links between cannabis use and the cardiovascular disorders of myocardial infarction and stroke in adults 13 14. Cannabinoids acting via type 1 cannabinoid receptors (CB1R’s), the dominant cannabinoid receptor in the body, have been shown to strongly induce proinflammatory including arteritic states 15 16. Cannabis has also been shown to upregulate thromboxane at the proteomic level 17. The recent demonstration that cannabis epigenetically suppresses prostacyclin production offers a further major mechanistic basis for cannabinoid vasotoxicity. It also establishes a major point of cross-talk between cannabinoid and prostaglandin proinflammatory signalling which is clinically relevant.

This becomes of clinical significance when the association of cannabis with gastroschisis and multiple other cardiovascular disorders is considered 6 18-22. The links between maternal cannabis use and gastroschisis have been described elsewhere 6 20-22. Fascinatingly geographical microclusters of gastroschisis in Canada, California and Australia have also been described 23-26 suggesting that some environmental exposure is occurring within a tight geographical radius which is damaging foetal development.

If cannabis is linked with both vasospasm and a thrombogenic state then the fate of embryonic anterior abdominal wall closure, which normally occurs about the tenth or twelfth week of foetal development, would seem to be inevitably imperiled.

Were cannabis to be linked just with mental illness, just with autistic spectrum disorder, just with 28 congenital defects or just with a 50% rise in TOTAL pediatric cancers then there should be no debate on any measures which increase its use, access or availability. That it has been linked with all four areas, in the context of its many other known harms – respiratory, driving, impaired developmental trajectory, reduction in IQ, hippocampal shrinkage, brain disconnection and immunopathies - implies directly that the cannabis legalization debate itself is non-viable and profoundly and inherently misleading.

What is required is improved public education to dispel the widespread myths, and set the truth at liberty and give it legs to set the world’s people free wherever they reside in the beautiful way the truth has always done. Can we rise to the challenge??

References

1. Morishima A. Effects of cannabis and natural cannabinoids on chromosomes and ova. NIDA Res Monogr 1984;44:25-45.
2. Tahir SK, Zimmerman AM. Influence of marihuana on cellular structures and biochemical activities. Pharmacology, biochemistry, and behavior 1991;40(3):617-23.
3. Tilak SK, Zimmerman AM. Effects of cannabinoids on macromolecular synthesis in isolated spermatogenic cells. Pharmacology 1984;29(6):343-50. [published Online First: 1984/01/01]
4. Murphy SK, Itchon-Ramos N, Visco Z, et al. Cannabinoid exposure and altered DNA methylation in rat and human sperm. Epigenetics 2018 doi: 10.1080/15592294.2018.1554521
5. Reece A. S., Husle G.K. Cannabis Teratology Explains Current Patterns of Coloradan Congenital Defects: The Contribution of Increased Cannabinoid Exposure to Rising Teratological Trends Clinical Pediatrics 2019;In Press
6. Reece AS, Hulse GK. Chromothripsis and epigenomics complete causality criteria for cannabis- and addiction-connected carcinogenicity, congenital toxicity and heritable genotoxicity. Mutat Res 2016;789:15-25. doi: 10.1016/j.mrfmmm.2016.05.002
7. Russo C, Ferk F, Misik M, et al. Low doses of widely consumed cannabinoids (cannabidiol and cannabidivarin) cause DNA damage and chromosomal aberrations in human-derived cells. Archives of toxicology 2018 doi: 10.1007/s00204-018-2322-9
8. Mihalas BP, Redgrove KA, McLaughlin EA, et al. Molecular Mechanisms Responsible for Increased Vulnerability of the Ageing Oocyte to Oxidative Damage. Oxid Med Cell Longev 2017;2017:4015874. doi: 10.1155/2017/4015874
9. Feng R, Sang Q, Kuang Y, et al. Mutations in TUBB8 and Human Oocyte Meiotic Arrest. New England Journal of Medicine 2016;374(3):223-32. doi: doi:10.1056/NEJMoa1510791
10. Pfender S, Kuznetsov V, Pasternak M, et al. Live imaging RNAi screen reveals genes essential for meiosis in mammalian oocytes. Nature 2015;524(7564):239-42. doi: 10.1038/nature14568
11. Wang X, Liu D, He D, et al. Transcriptome analyses of rhesus monkey preimplantation embryos reveal a reduced capacity for DNA double-strand break repair in primate oocytes and early embryos. Genome Res 2017;27(4):567-79. doi: 10.1101/gr.198044.115
12. Stringer JM, Winship A, Liew SH, et al. The capacity of oocytes for DNA repair. Cell Mol Life Sci 2018;75(15):2777-92. doi: 10.1007/s00018-018-2833-9
13. Volkow ND, Baler RD, Compton WM, et al. Adverse Health Effects of Marijuana Use. New England Journal of Medicine 2014;370(23):2219-27. doi: doi:10.1056/NEJMra1402309
14. Volkow ND, Compton WM, Weiss SR. Adverse health effects of marijuana use. N Engl J Med 2014;371(9):879. doi: 10.1056/NEJMc1407928
15. Menahem S. Cardiovascular Effects of Cannabis Usage. In: V.R. P, ed. Handbook of Cannabis and Related Pathologies: Biology, Pharmacology and Treatment. New York: Academic Press 2017:481-85.
16. Pacher P, Steffens S, Hasko G, et al. Cardiovascular effects of marijuana and synthetic cannabinoids: the good, the bad, and the ugly. Nat Rev Cardiol 2018;15(3):151-66. doi: 10.1038/nrcardio.2017.130
17. Wang J, Yuan W, Li MD. Genes and pathways co-associated with the exposure to multiple drugs of abuse, including alcohol, amphetamine/methamphetamine, cocaine, marijuana, morphine, and/or nicotine: a review of proteomics analyses. Molecular neurobiology 2011;44(3):269-86. doi: 10.1007/s12035-011-8202-4
18. Reece A. S., Hulse G.K. Cannabis Teratology Explains Current Patterns of Coloradan Congenital Defects: The Contribution of Increased Cannabinoid Exposure to Rising Teratological Trends Clinical Pediatrics 2019;In Press
19. Reece AS, Hulse G.K. Impacts of Cannabinoid Epigenetics on Human Development: Reflections on Murphy et. al. “Cannabinoid Exposure and Altered DNA Methylation in Rat and Human Sperm” Epigenetics 2018; 13: 1208-1221. Epigenetics 2019;In Press
20. Reece A.S. Chronic Toxicology of Cannabis. Clinical Toxicology 2009;In Press(Accepted 28/05/09.)
21. Reece AS. Known Cannabis Teratogenicity Needs to be Carefully Considered. British Medical Journal 2018;362:k3357. [published Online First: 4th August 2018]
22. Reece AS, Norman A, Hulse GK. Cannabis exposure as an interactive cardiovascular risk factor and accelerant of organismal ageing: a longitudinal study. BMJ Open 2016;6(11):e011891. doi: 10.1136/bmjopen-2016-011891
23. Anderson JE, Cheng Y, Stephenson JT, et al. Incidence of gastroschisis in california. JAMA Surgery 2018 doi: 10.1001/jamasurg.2018.1744
24. Bassil KL, Yang J, Arbour L, et al. Spatial variability of gastroschisis in Canada, 2006-2011: An exploratory analysis. Canadian journal of public health 2016;107(1):e62-7. doi: 10.17269/cjph.107.5084
25. McMillan M. Birth Defects Exceed NSW Average. Northern Star Newspaper, 3rd June 2011. Lismore: Northern Star, 2011.
26. Expert Review Panel Appointed to New South Wales Health. Review of Gastroschisis on the NSW North Coast. In: From New South Wales Health Department Center for Record Linkage DC, Dr Lee Taylor, ltayl@doh.health.nsw.gov.au ,, ed. Sydney: New South Wales Health Department,
, 2011:1-11.

Competing interests: No competing interests

 

Re: Should we legalise cannabis?

08 July 2019
JK Anand
Retired doctor
Free spirit
Peterborough, England

I do not know if we should. And in these days of globalisation, perhaps it is wrong of me to adopt a parish pump attitude.
But I ask: Why does the Great British Public need so many mind altering drugs?
Sir Walter Raleigh brought in tobacco. You might say it is not likely to cause delusions, illusions, hallucinations. But it has a dependency producing effect.
Cannabis has been growing wild in the tropics since the year dot.
I have seen it growing by the road-side ( alf a century ago) in North West India.
Never saw anyone “run amok”. There were rare cases though.

Back to my “parish”.
There must be something wrong with the British psyche of today. The Brits did not go overboard with all the drugs half a century ago.
Can the psychologists please tell us what has gone wrong and how it can be put right?

Thank you

Competing interests: No competing interests

 

Re: Should we legalise cannabis?

07 July 2019
Kalpana Elizabeth Dein
Consultant Forensic Psychiatrist
HMP Thameside (Oxleas NHS Trust)
HMP Thameside, Griffin Manor Way, London SE28 0HE

In her editorial, Fiona Godlee, draws our attention to points raised by Meacher et al (1) as to why the Royal College of Psychiatrists should join the BMJ’s position in legalising cannabis. Godlee (2) also recommends the legalisation of cocaine and heroin, but in this response, I will focus on cannabis, which is often considered “harmless” (3), in comparison to cocaine or heroin.

As psychiatrist Prof Robin Murray and “recovered cannabis-user” Adam Gridley (1) point out, the use of cannabis impacts mental health services disproportionately. Besides issues of dependence, the development of psychosis, schizophrenia, the loss of liberty through psychiatric detention, use of hospital beds through involuntary admissions; there is also the strong association with violence (Coid et al, 2017), and the consequent risk of incarceration for the user. This is no small matter for psychiatry.

Unlike many of our colleagues in the medical sub-specialities, we cannot miss the enormous impact that cannabis use has on the mental health, life and liberty of our patients.

As a forensic psychiatrist working in England, it would be amiss of me not to highlight the significant relationship between violence and substance misuse in the UK (4). Any savings for the police from decriminalisation will be likely replaced by a surge in violent crime (3), and the use of police time in escorting individuals who become mentally unwell (8) after using cannabis.

Given the recent increase in knife crime (5), the rise of homicides (6), the upsurge of mental health problems among young people in UK (7) against the backdrop of cuts in healthcare and policing (8), the unknown impact of Brexit on the NHS and the economy; this is surely not the time to conduct an expensive social experiment?

When it comes to legalising cannabis, Murray and Gridley (1) point out to the opportunity for the UK to watch and learn from the mistakes of others across the pond.

What can we learn from the British experience so far? The legal status of the best-known drug of abuse, namely alcohol, poses a significant burden on health and public safety despite health campaigns to ameliorate its negative impact. Alcohol is the most dangerous drug in the UK (9) because it is legal. Do we need cannabis to displace it from its prime position (3)? Can we afford the luxury?

The very nature of addiction means that those who become dependent will develop tolerance to milder forms of cannabis and begin to abuse stronger and more potent iterations as evidence from the US suggests (3).

Any illusion that decriminalising can help streamline access is immediately dispelled as I begin my weekly psychiatric clinic in prison, where my almost inevitably poor patients, the majority of whom accept that cannabis is harmful, will sell out their soul for a puff.

While it is tempting to pander to the greed of corporations desperate to capitalise on this industry, and doctors and politicians who want their piece of cannabis cake, without any fear of reprisal, let us consider the real price. The impressionable young, those vulnerable to develop psychosis, or become violent, will find their future potential reduced to a mental health and/or crime statistic. Cannabis legalisation will hurt the poorest and the most vulnerable in our society, disproportionately. How can we agree to that?

1. Meacher M, Nutt D, Liebling J, Murray RM, Gridley A. Should the supply of cannabis be legalised now?. BMJ. 2019 Jul 3;366:l4473.

2. Godlee, F., 2019. Should we legalise cannabis?.

3. Berenson A. Marijuana is more dangerous than you think. WSJ. Jan 4, 2019 https://www.wsj.com/articles/marijuana-is-more-dangerous-than-you-think-...

4. Coid J, Hu J, Kallis C, Ping Y, Zhang J, Hu Y, Bui L, Ullrich S, Bebbington P. A cross-national comparison of violence among young men in China and the UK: psychiatric and cultural explanations. Social psychiatry and psychiatric epidemiology. 2017 Oct 1;52(10):1267-79.

5. Knife and Offensive Weapon Sentencing Statistics, England and Wales – 2018. Ministry of Justice. March 14, 2019. https://assets.publishing.service.gov.uk/government/uploads/system/uploa...

6. Crime in England and Wales: year ending September 2018. ONS. 25 April 2019. https://www.ons.gov.uk/peoplepopulationandcommunity/crimeandjustice/bull...

7. Pitchforth J, Fahy K, Ford T, Wolpert M, Viner RM, Hargreaves DS. Mental health and well-being trends among children and young people in the UK, 1995–2014: analysis of repeated cross-sectional national health surveys. Psychological medicine. 2019 Jun;49(8):1275-85.

8. Dodd V. Police 'picking up pieces of mental health system', says watchdog. The Guardian. 27 Nov 2018. https://www.theguardian.com/society/2018/nov/27/police-mental-health-sys...

9. Nutt, D.J., King, L.A. and Phillips, L.D., 2010. Drug harms in the UK: a multicriteria decision analysis. The Lancet, 376(9752), pp.1558-1565.

Competing interests: No competing interests

 

Re: Should we legalise cannabis?

07 July 2019
Albert S. Reece
Physician
University of Western Australia and Edith Cowan University, Perth, Western Australia
35 Stirling Hwy., Crawley, Western Australia

Cannabis Debates and Cannabis Debacles:
Serious Downstream Implications of Cannabis Neurotoxicity and Genotoxicity

The piece by Dr Godlee reminds us on the one hand that weighty decisions are being made on the basis of flawed and incomplete evidence and on the other that much of what we have seen till now in relation to the epidemiology of cannabis has occurred in a low cannabis use environment, a protected situation which is directly due to cannabis’s hitherto illegal status, which bears little resemblance to the high-use high-potency products and consumption patterns which are presently emerging on both sides of the 49th parallel in North America.

Our research group has taken a novel approach which looks for correlates at the population health level of findings which have been made in important and repeated epidemiological studies. As shown below numerous and emphatic confirmations of such laboratory and study findings in relation to cannabis have been found at the population health level. Such repeated confirmations imply careful pause at the national and international policy level.

The 2019 World Drug Report from the United Nations office of Drugs and Crime demonstrates in detail that the presently emerging cannabis epidemic in USA is one of increased intensity of use more than increased numbers of users. The National Survey of Drug Use and Health (NSDUH) shows a rise in lifetime use of cannabis 2006-2017 of 9% compared to an 80% rise in those using cannabis daily or almost daily. When combined with the high potency forms of cannabis and hashish oil presently widely available in North America, this portends a tsunami of serious downstream sequelae. Most published cannabis epidemiology is only marginally relevant to this new high-use high-potency era.

NSDUH quantifies several parameters of mental health including any mental illness, serious mental illness and suicidal thinking against national drug use across both time and space. Close temporospatial association has been demonstrated in unpublished explorations of all three indices with cannabis use and cannabinoid exposure. Such findings confirm at the level of population health the many published studies linking cannabis consumption to numerous measures of serious mental health outcomes including depression, bipolar disorder, anxiety and schizophrenia.

It was recently shown that the autism epidemic in USA is rising exponentially related to the increased use of cannabis whilst the use of most other drugs has fallen (NSDUH) and that the incidence of autism is predicted to be 60% higher in cannabis liberal states than states where cannabis is not legal by 2030 1 2. Such findings imply that the adverse mental health outcomes well described in adults are even more serious in children and confirm epidemiologically the many experimental studies showing interference with brain development by multiple pathways. Such children will likely never have the opportunity to develop normally – as they never were.

Colorado is known as one of the US leaders in cannabis liberalization. It is less well known that an extra 11,753-20,152 major congenital abnormalities occurred din Colorado from 2000-2014 (depending on whether one uses the September 2018 Colorado birth defects data or the October 2018 data), and particularly features 104% rise in spina bifida, 71% rise in microcephalus and 123% rise in atrial septal defect, 45% rise in all cardiovascular defects, 35% rise in major central nervous system defects and 34% rise in chromosomal anomalies including a 25% rise in Down’s syndrome 3. Indeed the emergence of very elevated rates of atrial septal defect in Kentucky, Colorado, Hawaii and many US cannabis-liberal states suggests the emergence of yet another cannabis related congenital defect (CDC data). This in turn suggests our presently described list of over 20 cannabis-associated birth defects is itself incomplete and likely to expand dramatically in coming years.

All seven studies to examine the relationship between cannabis use and gastroschisis have been positive with an odds ratio of about 3.0 4. A recent important CDC study documented impressive racial differences in gastroschisis incidence 5. If one assigns the baseline incidence of gastroschisis in children of African-American teenager mothers (9.0/100,000 live births) to unity, then the incidence of gastroschisis in infants born to non-Hispanic white mothers is twice as common (17.1) and in American Indian / Alaska Natives is three times as common (26.0). These relativities disappeared quickly at older maternal ages consistent with a differential environmental teenage exposure rather than a truly genetic explanation. These changes directly parallel the historical rates of teenage cannabis use in these racial groups as quantified by the Youth Risk Behaviour Survey, the Monitoring the Future Survey and the National Longitudinal Alcohol Survey in USA. A mechanism was recently described whereby interference in late gestational uterine blood flow around the time of birth can cause preeclampsia in the mother and other external sequalae 6.

Cannabis use in parents has been previously linked with childhood leukaemias and sarcomas which are some of the major cancers of childhood 7. Unsurprisingly then one notes a 52% rise in all childhood cancer from 1975-2017 based in CDC Surveillance Epidemiology and End Results (SEER) data. As noted above the use of other drugs has fallen across this time. Cannabis has been shown to be reproductively toxic by many routes including interfering with cell division and mitosis and damaging to many parts of the epigenomic machinery 8 9. Indeed the presence of DNA fragments in the cytoplasm has been shown to be potently stimulating to the innate immune system in a cell autonomous manner which in turn damages the genome. This explains the frequently cited increase in the degree of malignancy of cannabis related cancers, and their occurrence in much younger patients, which were previously not understood. Again the rates of all pediatric cancer in African-Americans is about 60% that occurring in Americans of Caucasian heritage, which again parallels lower rates and lower intensity of cannabis use in African-American communities – a situation which is presently in a state of flux.

Four of four studies examining the relationship between testicular cancer and cannabis use have all been strongly positive with an odds ratio of around 3 7 10. Unsurprisingly there has been a 66% rise in the rate of all-age testicular cancer from 3.8 to 6.3 cases /100,000 (CDC SEER Data).

Dr Godlee’s call to watch carefully the unfolding milieu in North America is timely and salient. However we need to do so with open eyes and carefully and impartially evaluate what we are really seeing judged against the important metrics of earlier eras when cannabis use was less prevalent. Detailed and sophisticated space-time investigations are required. We find it paradoxical – and probably unjustifiable – that at a time when scientific knowledge is so advanced and epidemiological methods are so complex that confusion reigns supreme in this area and the field is overripe with disinformation.

We welcome the call for continued careful surveillance but feel that while so many concerning findings continue to be uncovered studious caution is the only responsible approach. Sophisticated spatial geostatistical investigations are urgently mandated. Public education on cannabis is obviously paramount. Cannabis disinformation is our greatest threat.

References

1. Reece A. S., Hulse G.K. Effect of Cannabis Legalization on US Autism Incidence and Medium Term Projections. Clinical Pediatrics: Open Access 2019;4(2):In Press. doi: DOI: 10.24105/2572-0775.4.154 . [published Online First: May 3rd 2019]
2. Reece A. S., Hulse G.K. Epidemiological Associations of Various Substances and Multiple Cannabinoids with Autism in USA. Clinical Pediatrics: Open Access 2019;4(2):In Press. doi: 10.24105/2572-0775.4.155 [published Online First: May 3rd 2019]
3. Reece A. S., Husle G.K. Cannabis Teratology Explains Current Patterns of Coloradan Congenital Defects: The Contribution of Increased Cannabinoid Exposure to Rising Teratological Trends Clinical Pediatrics 2019;In Press
4. Reece A. S., Hulse G.K. Cannabis Teratology Explains Current Patterns of Coloradan Congenital Defects: The Contribution of Increased Cannabinoid Exposure to Rising Teratological Trends Clinical Pediatrics 2019;In Press
5. Short TD, Stallings EB, Isenburg J, et al. Gastroschisis Trends and Ecologic Link to Opioid Prescription Rates - United States, 2006-2015. MMWR Morb Mortal Wkly Rep 2019;68(2):31-36. doi: 10.15585/mmwr.mm6802a2
6. Robertson SA. Preventing Preeclampsia by Silencing Soluble Flt-1? N Engl J Med 2019;380(11):1080-82. doi: 10.1056/NEJMcibr1817501
7. Reece A.S. Chronic Toxicology of Cannabis. Clinical Toxicology 2009;In Press(Accepted 28/05/09.)
8. Reece AS, Hulse G.K. Impacts of Cannabinoid Epigenetics on Human Development: Reflections on Murphy et. al. “Cannabinoid Exposure and Altered DNA Methylation in Rat and Human Sperm” Epigenetics 2018; 13: 1208-1221. Epigenetics 2019;In Press
9. Reece AS, Hulse GK. Chromothripsis and epigenomics complete causality criteria for cannabis- and addiction-connected carcinogenicity, congenital toxicity and heritable genotoxicity. Mutat Res 2016;789:15-25. doi: 10.1016/j.mrfmmm.2016.05.002
10. Reece A. S., Hulse G.K. Explaining Contemporary Patterns of Cannabis Teratology. Clinical Pediatrics 2019;4(1):1000146. doi: 10.4172/2572-0775.1000146 [published Online First: 20th February 2019]

Competing interests: No competing interests

 

Re: Should we legalise cannabis?

07 July 2019
Peter J Hitchens
Journalist
2 Derry Street W8 5TS
@ClarkeMicah

It is shocking to see medical bodies representing doctors - whose first responsibility is to do no active harm- even discussing the legalisation of marijuana, a drug whose use is strongly and meaningfully correlated with incurable mental illness and criminal violence. The evidence against it has been accumulating rapidly in recent years. The argument that open sale will somehow lead to lower strengths has already been disproved in Colorado, where continuing competition from the illegal market (thriving because of heavy taxation) has ensured that strengths remain high. Modern professionals seem oddly spellbound by the slender case for marijuana legalisation. If any other product with such grave health implications were seeking legalisation they would recognise that this was just another ugly greed lobby, backed by big money, hoping to make profits out of human misery.

Competing interests: No competing interests

 

Re: Should we legalise cannabis?

05 July 2019
M.A. Aleem
Emeritus Professor of Neurology * Visiting Specialist in Neurology ** Consultant Neurologist ***
The Tamilnadu Dr.M.G.R. Medical University * Dhanalakshami Srinivasan Medical College ** ABC Hospital ***
Chennai 600032* Perambalure 621212** Trichy 620018*** Tamilnadu India
@drmaaleem

Need Legalisation for certain epileptic syndromes

Cannabis medicines for specific conditions such as in some intractable epileptic syndromes should be legalised .

Competing interests: No competing interests