Get a Clue - Weed

Details: Published: 19 October 2023; Hits: 823

T.H.C – The Human Consequences: Why legalisation is a public and personal health nightmare.

Details: Published: 05 October 2023; Hits: 846

A look at the association between cannabis use and schizophrenia, as well as the need for comprehensive public health policies and education.

September 25, 2023 Victor Ajluni, MD

The increasing acceptance and legalization of cannabis use worldwide has underscored the need to understand its potential health implications. One area of significant concern is the association between cannabis use and schizophrenia, a severe mental disorder characterized by thought and emotional disturbances. This association is particularly important, given the global burden of schizophrenia, which affects more than 20 million individuals worldwide, according to the World Health Organization.¹

A Mendelian randomization study by Vaucher, et al, provided observational evidence of an increased risk of schizophrenia associated with cannabis use.² Rentero, et al, highlighted the importance of differentiating between cannabis-induced psychosis and schizophrenia for therapeutic purposes.³ Ortiz-Medina, et al, emphasized the need for more research to fully understand the relationship between cannabis use and psychosis.⁴

Urits, et al, found that about 1 in 4 patients with schizophrenia are also diagnosed with cannabis use disorder (CUD), indicating a strong association between cannabis use and psychological disorders.⁵ Marconi, et al, reported a dose-response relationship between the level of cannabis use and the risk of psychosis, suggesting that higher levels of cannabis use could lead to long-lasting psychotic disorders.⁶

García Álvarez, et al, explored the impact of cannabis use on cognitive impairment in schizophrenia and first-episode psychosis, providing further evidence of the potential risks associated with cannabis use.⁷ Cohen, et al, discussed both the positive and negative effects of cannabis and cannabinoids on health, including their association with cognitive alterations, psychosis, and schizophrenia.⁸

In a comprehensive review published in The Lancet, Jauhar, et al, discussed the etiological and therapeutic challenges of schizophrenia, including the role of cannabis as a potential causative factor. They highlighted that cannabis and childhood adversity are areas of debate as causative factors for schizophrenia, emphasizing the need for further research in these areas.⁹

In their review, Lowe, et al, emphasized the need to gauge the potential impact of cannabis legalization on vulnerable populations, such as those with mental illnesses including schizophrenia. They discussed the potential for cannabis to induce long-term psychiatric effects, including the exacerbation of symptoms in individuals with preexisting psychiatric conditions like schizophrenia.¹⁰

Lastly, Hamilton discussed the complex interaction between cannabis, psychosis, and schizophrenia. He highlighted the need for a credible contribution to public health in light of increasing cannabis legalization. His study provided evidence of a dose-response relationship between cannabis use and the risk of psychosis, emphasizing that the risk increases with the frequency of use and the potency of cannabis.¹¹

In conclusion, although the acceptance and legalization of cannabis continue to grow, it is crucial to consider the potential risks associated with cannabis use. The association between cannabis use and schizophrenia underscores the need for comprehensive public health policies and education to mitigate these risks. Further research is needed to fully elucidate the complex interaction between cannabis use, psychosis, and schizophrenia

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Details: Published: 04 October 2023; Hits: 749

Cannabis use disorder and adverse cardiovascular outcomes: A population-based retrospective cohort analysis of adults from Alberta, Canada

Aim: To measure the association between cannabis use disorder (CUD) and adverse cardiovascular disease (CVD) outcomes.

Participants: We identified participants with CUD diagnosis codes and matched them to participants without CUD codes by gender, year of birth and time of presentation to the health system. We included 29 764 pairs (n = 59 528 individuals in total).

Conclusions: Canadian adults with cannabis use disorder appear to have an approximately 60% higher risk of experiencing incident adverse cardiovascular disease events than those without cannabis use disorder.

(Research: https://onlinelibrary.wiley.com/doi/10.1111/add.16337 )

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Details: Published: 06 September 2023; Hits: 770

(Summary: the following demographics should completely ABSTAIN from cannabis use:

People aged 0-28 years of age (children and adolescents – developing brain)
Pregnant women
People with mental illness or vulnerable to such
Drivers/Driving (one could also assume, anyone operating a vehicle of any kind)

Whilst there are only some minor benefits from some cannabis derivatives, they come with adverse side effects and there is no curative properties in cannabis. More clinical, double-blind, placebo accounted for trials are required to further understand limitations, risks and potential benefits of cannabis. Dalgarno Institute)

Abstract:

Objective: To systematically assess credibility and certainty of associations between cannabis, cannabinoids, and cannabis-based medicines and human health, from observational studies and randomised controlled trials (RCTs).

Searches and inclusion criteria: We conducted an umbrella review of meta-analyses of observational studies(i.e., case-control and cohort studies) and randomised controlled trials that reported on any outcome associated with cannabis and cannabinoids use in humans.

Conclusions: Convincing or converging evidence supports that cannabis use is associated with poor mental health and cognition, increased the risk of car crashes, and can have detrimental effects on offspring if used during pregnancy. Cannabis use should be avoided in adolescents and young adults (when neurodevelopment is still occurring), when most mental health disorders have onset and cognition is paramount for optimising academic performance and learning, as well as in pregnant women and drivers. Conversely, cannabidiol could be considered a potential beneficial treatment option in epilepsy across age groups to reduce seizures. Cannabis based medicines could also be considered for chronic pain across different conditions, such as multiple sclerosis, spasticity in multiple sclerosis, for nausea and vomiting in people with mixed conditions and for sleep in cancer. However, clinical relevance must be considered before a possible incorporation into clinical guidelines; for example, including numbers needed to treat for benefit, risk to benefit ratios, comparative efficacy and safety with existing treatment options, and development of patient information concerning potential adverse events. Cannabidiol appears to be safe regarding psychiatric symptoms, but more research needs to be conducted before this drug can be recommended for the treatment of any psychiatric disorder. The remaining associations between cannabis and health outcomes are not supported by converging or convincing evidence.

Law and public health policy makers and researchers should consider this evidence synthesis when making policy decisions on cannabinoids use regulation, and when planning a future epidemiological or experimental research agenda, with particular attention to the tetrahydrocannabinol content of cannabinoids. Future guidelines are needed to translate current findings into clinical practice, while involving stakeholders.

(Source: https://www.bmj.com/content/382/bmj-2022-072348

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Details: Published: 06 September 2023; Hits: 952

Subtle but pervasive changes can occur between uses.

Understanding THC’s interaction with the brain’s important natural cannabinoid chemistry and physiology will now make sense of the impact that overly frequent cannabis use has on the brain and mental functioning.

Because THC stimulates our brain’s natural cannabinoid receptors (CB1) far more strongly and longer than the endogenous cannabinoid neurotransmitters anandamide and 2-AG, cannabis use throws brain chemistry out of balance temporarily, usually to people’s enjoyment. This loss of chemical equilibrium lasts an average of 4 hours when cannabis is inhaled and 8 hours when ingested orally before the liver metabolizes the THC and it is eliminated in the feces (55%) and urine (20%).

Most occasional cannabis users feel little or no effect the following day, but an interesting experiment reveals a subtle impact 24 hours after smoking a single joint. Private licensed pilots with over 200 hours of flight experience had their baseline skills measured in a flight simulator, then were provided a joint containing 10 or 20 mgs of THC to smoke. This was considered the equivalent of a moderate social dose in the mid-1980s.

A variety of pilot actions during routine landings were impaired 24 hours after smoking the joint, including the number and size of adjustments to stabilize the plane, distance off center on landing, and vertical and lateral deviation on approach to landing. Pilots showed no awareness of these impairments. Performance returned to baseline 48 hours after being high.

When the task became more complex by introducing turbulent weather conditions calling on pilots to react in real time to avoid trouble, responses were slower and less well organized than their baseline performance. In other words, the pilots’ response to novel events was altered (see the post How Cannabis Makes Everything So Interesting for clarification on the role our internal cannabinoid system plays in the experience of novelty.)

When THC stimulates CB1 receptors in the amygdala, cannabinoid tone increases, lowering the bar for any stimulus being imbued with a sense of novelty. Novelty draws our attention to unexpected stimuli. This phenomenon is largely responsible for cannabis making everything more interesting. But this is not the end of the story.

Whenever neurons containing CB1 receptors are over-stimulated by THC’s stronger and longer activation, a homeostatic response follows in an effort to rebalance the brain. The phrase “over-stimulated” means only that THC’s stimulation of CB1 receptors exceeds normal physiologic levels, leading to greater than normal negative feedback on the neuron’s release of transmitters with each firing. THC quells neuronal activity not by reducing the rate of nerve cell firing, but rather the amount of transmitter released each time the neuron fires.

As a result, neurons immediately react to THC’s over-stimulation by reducing the number of CB1 receptors. This reduction of receptors is called downregulation. A variety of mechanisms, including pulling receptors inside the cell so they are no longer available to be stimulated, begins with a single exposure to cannabis. By downregulating CB1 receptors, neurons partially regain some balance. Fewer receptors reduce the amount of negative feedback produced by cannabinoid stimulation and a more physiologic balance is re-established.

After THC has been metabolized and eliminated, CB1 receptors begin upregulating back to their normal level of availability. Upregulation after a single or occasional dose of cannabis occurs rapidly. Most people feel unaffected the following day.

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