Cannabis, Boomers, And Violence

Almost all drugs used by humans recreationally are derivatives of compounds found in plants which mimic chemicals native to the human body. Methamphetamine is descended from ephedrine, which is close to epinephrine. Entheogenic psychedelics such as mescaline are structurally close to phenethylamine. Heroin is an adaptation of morphine, attaching to the same receptors as enkephalins and endorphins. Tryptamines such as psilocybin are remarkably similar to the regulator serotonin.

Your brain has receptors (like locks, or ports) which naturally bind with chemicals in your body (keys) to control mood, pain, and other functions. The drug fits into the receptor like a fake key, triggering the same response as your natural brain chemicals. Your brain normally recycles ("re-uptakes") used chemicals quickly. Some drugs "dam up" this recycling process, so the natural chemicals stay active longer in the space between brain cells. This blocking causes a massive release of natural chemicals like putting a dam in a river, producing a "high": the natural chemicals (like dopamine, serotonin, etc.) build up instead of flowing away normally. This is the theory behind how antidepressant medication is designed to work.

Hitchens has repetitively banged the drum of blaming cannabis use for violence, but he is in scientific error from basic pharmacological misunderstanding of what the endocannabinoid system is, and how it functions. Yes, there is a link to psychosis; yes, synthetics are linked to violence, whereas natural modulated cannabis is not. There is a massive gulf of difference between how these chemicals work, which must be understood for mature, responsible drug policy to be formulated.

Critics such as this have a layman's thumbnail resolution of pharmacology. Libertarian advocates have none at all: synthetic cannabis is exceptionally dangerous.

To understand why Boomers - the advocates of these types of chemicals back in their vacuous twenties - so fundamentally misunderstand anything to do with drugs at all, and why we need to go back to a science-based approach to the social problems they cause, we have to return to the murky depths of GCSE Science.

The Human Endocannabinoid Mystery

"Endo" means endogenous, or "native." The endocannabinoid system (ECS) is a widespread regulatory network in the human body which helps maintain homeostasis (the body's internal balance.) It influences mood regulation, memory formation, appetite control, pain sensation, immune response, and sleep cycles, and operates through retrograde signaling: endocannabinoids are released from postsynaptic neurons and travel backward to bind with receptors on presynaptic neurons, modulating neurotransmitter release. This creates a feedback mechanism which can either enhance or dampen neural activity as needed.

The system includes endocannabinoids themselves (naturally produced cannabinoid-like molecules), cannabinoid receptors (primarily CB1 and CB2), and enzymes which manufacture and break down endocannabinoids. The two primary molecules are anandamide and 2-arachidonoylglycerol (2-AG), which are produced on-demand from membrane lipids rather than being stored in vesicles like traditional neurotransmitters.

CB1 receptors are abundant in the central nervous system, particularly in the brain regions controlling movement, memory, pain perception, and reward processing. They're also found in peripheral tissues including the digestive system and reproductive organs. CB2 receptors are primarily located in immune cells and peripheral tissues, playing important roles in inflammation and immune response modulation.

Cannabis: A Sophisticated Plant

Cannabis (Hemp) belongs to the Cannabaceae family and is generally classified into three main species or subspecies: Cannabis sativa, Cannabis indica, and Cannabis ruderalis. Extensive crossbreeding has blurred these distinctions significantly; modern cannabis varieties are typically hybrids combining traits from different lineages. The plant is dioecious, meaning individual plants are either male or female, with female plants producing the resin-rich flowers containing the highest cannabinoid concentrations.

The plant produces aromatic compounds called terpenes which contribute to strain-specific effects and flavours, giving it a characteristically pungent smell. Myrcene, limonene, and pinene are common examples. The "entourage effect" theory suggests these compounds work in tandem with cannabinoids to produce the plant's overall effects, though scientific evidence for this remains limited.

100+ natural cannabinoids are produced in specialised structures called trichomes - tiny, mushroom-shaped glands covering the flowers and surrounding leaves. The plant manufactures cannabinoids as carboxylic acid precursors (like THCA and CBDA) which are non-psychoactive. These acid forms convert to their active counterparts (THC and CBD) through decarboxylation, a process which occurs naturally over time or rapidly when heated through smoking, vaporising, or cooking.

THC ((−)-trans-Δ9-tetrahydrocannabinol or (6aR,10aR)-6,6,9-Trimethyl-3-pentyl-6a,7,8,10a-tetrahydro-6H-benzo[c]chromen-1-ol) is the primary psychoactive compound responsible for cannabis's intoxicating effects. CBD (cannabidiol) is non-intoxicating and often comprises the second-highest concentration. CBG (cannabigerol) serves as a precursor to other cannabinoids and is sometimes called the "mother cannabinoid." CBC (cannabichromene) and CBN (cannabinol) are other notable compounds, with CBN typically forming as THC degrades over time. The plant produces dozens of additional major cannabinoids in smaller quantities, including THCV (tetrahydrocannabivarin), which may have appetite-suppressing effects, and CBDA (cannabidiolic acid), which shows promise for anti-inflammatory applications. Delta-8 THC, structurally similar to regular delta-9 THC but with reportedly milder effects, occurs naturally in trace amounts.

Modern breeding has created distinct chemotypes based on cannabinoid profiles - high-THC varieties for recreational use, high-CBD strains for medical applications, and balanced ratios for specific therapeutic purposes. Hemp varieties are legally defined as containing less than 0.3% THC by dry weight.

Our best understanding to date suggests the plant, like Coca, evolved these compounds millions of years ago as sophisticated defense mechanisms. THC may protect the plant from ultraviolet light, with studies showing cannabis plants exposed to UVB rays produced more THC than unexposed plants, suggesting a protective function against DNA damage from solar radiation. Cannabinoids act as natural pesticides, similar to caffeine and nicotine in other plants, deterring insects and herbivorous animals from eating the plant. They have insecticidal properties, and the sticky resinous trichomes create a double defense against predatory bugs.

Since plants lack immune systems like animals, they produce chemical cocktails to guard against infections. Studies show cannabinoids including THC have anti-microbial properties, helping protect against bacterial and fungal pathogens. Trichomes (the structures containing cannabinoids) help prevent overheating in dry climates and provide insulation during frost in colder environments.

Cannabis didn't evolve cannabinoids with the mammalian endocannabinoid system in mind - the fact they interact with our CB1 and CB2 receptors is just a happy coincidence. Our endocannabinoid system evolved long before cannabis even existed to help maintain homeostasis using our own naturally-produced compounds like anandamide. The cannabis plant essentially developed a sophisticated chemical defense system over millions of years which happened to perfectly mimic our brain's natural regulatory molecules - which is why cannabinoids affect us so profoundly despite being produced by a plant for entirely different purposes.

Natural THC vs CBD Modulation

While both compounds interact with the endocannabinoid system, they do so differently. THC directly activates CB1 receptors, producing its characteristic psychoactive effects. CBD has low affinity for CB1 receptors but can act as a negative allosteric modulator - essentially changing the receptor's shape to make THC bind less effectively. This doesn't block THC entirely but can reduce its potency.

CBD can significantly reduce THC's psychoactive intensity and duration: many users report cannabis strains with higher CBD content produce less anxiety, paranoia, and cognitive impairment compared to high-THC, low-CBD varieties. This tempering effect appears to work through multiple pathways rather than simple receptor competition.

CBD may also slow THC metabolism by competing for the same liver enzymes (particularly CYP2C9 and CYP3A4) which break down cannabinoids. This could theoretically extend THC's duration while simultaneously reducing its peak intensity, creating a more gradual, sustained effect profile.

Some research suggests CBD might influence how quickly CB1 receptors become desensitised to THC, potentially preventing the receptor downregulation which contributes to tolerance development. This could help maintain therapeutic benefits over time while reducing the escalating doses often seen with THC-only products. Medical cannabis products increasingly use specific THC:CBD ratios to optimise therapeutic effects while minimising adverse reactions. Common ratios like 1:1, 2:1, or even 20:1 (CBD:THC) allow patients to access cannabis's medical benefits with reduced psychoactivity. Some users specifically seek balanced strains to avoid THC's more intense psychological effects. Taking CBD before THC appears more effective at reducing psychoactive intensity than taking them simultaneously or CBD afterward.

The Science Of Getting High

When cannabis is smoked or vaporised, THC enters the lungs where it rapidly diffuses across the thin alveolar membranes directly into the bloodstream. This creates an almost immediate effect: users typically feel initial changes within 30 seconds to 2 minutes. The THC-rich blood travels straight to the heart and then to the brain, where it quickly crosses the blood-brain barrier due to its fat-soluble properties. Peak effects occur within 15-30 minutes, creating an intense but relatively short-lived experience lasting 2-3 hours.

Eating cannabis creates a dramatically different experience. THC must first survive the acidic stomach environment, then pass through the small intestine into the portal circulation leading to the liver. Here, liver enzymes convert THC into 11-hydroxy-THC, a metabolite which is actually more potent and longer-lasting than the original compound. This process takes 30-90 minutes, sometimes longer depending on stomach contents and individual metabolism. The resulting high is typically more intense, more body-focused, and can last 4-8 hours or more.

Regardless of consumption method, once THC reaches the brain it immediately begins binding to CB1 receptors throughout the central nervous system. These receptors are densely concentrated in the hippocampus (memory), prefrontal cortex (executive function), cerebellum (coordination), and basal ganglia (movement). The compound essentially hijacks the brain's natural endocannabinoid signaling system, which normally provides precise, localised, short-term regulation of neural activity.

THC's receptor binding triggers a cascade of neurotransmitter disruptions. In the hippocampus, it interferes with acetylcholine release, immediately impairing the ability to form new memories (explaining why people often can't remember what they were just talking about while high.) In dopamine-rich reward circuits, THC stimulates increased dopamine release, creating euphoria and reinforcing the desire to repeat the experience.

As THC concentrations peak, users experience characteristic alterations in consciousness. Time perception becomes distorted as the brain's internal timing mechanisms malfunction. Sensory processing intensifies - colours appear more saturated, sounds more layered, and physical sensations more pronounced. This occurs because CB1 receptors in sensory processing areas become overstimulated, amplifying normal input signals.

The body responds with observable changes as peripheral CB1 receptors activate. Heart rate increases by 20-50 beats per minute as cardiovascular CB1 receptors trigger sympathetic nervous system responses. Blood vessels in the eyes dilate, causing the telltale redness. Saliva production decreases through receptor activation in salivary glands, creating dry mouth. Blood pressure may initially spike then drop as vascular systems adjust.

During peak intoxication, working memory becomes severely impaired while long-term memory retrieval may actually enhance, creating the paradox where users can vividly recall distant events but can't track ongoing conversations. Motor coordination suffers as cerebellar CB1 receptors disrupt fine motor control. Executive function declines, making complex decision-making and planning difficult.

Smoked cannabis produces a sharp peak followed by gradual decline, while edibles create a slower build to a sustained plateau. The 11-hydroxy-THC from edibles tends to produce more sedating, body-focused effects compared to the more cerebral high from smoking. Vaporising falls between these extremes, offering rapid onset with slightly less respiratory irritation.

The high's intensity and character vary dramatically between individuals based on tolerance (regular users need higher doses), body composition (THC stores in fat tissue), genetics (variations in cannabinoid receptor density and metabolism), and psychological state (anxiety can amplify negative effects while relaxation enhances positive ones). As THC levels decline, the brain's homeostatic mechanisms gradually restore normal neurotransmitter balance. However, even after subjective effects fade, subtle cognitive impairments in attention, memory, and reaction time may persist for hours, particularly with edibles where active metabolites continue circulating long after the user feels "normal" again.

Synthetics Are Not Cannabis

The synthetic cannabinoid landscape represents a complex evolution of 1000+ laboratory-created compounds which attempt to mimic cannabis effects while often producing dramatically different and more dangerous outcomes. Put shortly: these chemicals affect the same CB1 and CB2 system, but they are not cannabis.

New generations like the MDMB and ADB compounds are appearing faster than regulatory agencies can respond. The potency continues to increase while safety profiles become even less predictable.

The fundamental difference is natural cannabis evolved over millions of years with built-in safety mechanisms and balanced effects, while synthetic cannabinoids are artificial molecules designed to activate specific receptors with maximum potency and minimal regard for human safety. They represent a cautionary tale of how academic research tools can become dangerous street drugs when removed from their intended scientific context.

The story begins with legitimate scientific research. The HU series was developed by Israeli researcher Raphael Mechoulam and Hebrew University colleagues in the 1980s and 1990s. HU-210, one of the most potent, was created to study cannabinoid receptors and proved to be 100-800 times more potent than natural THC. These compounds were never intended for human consumption but rather as research tools to understand how the endocannabinoid system functions.

Around the same time, American researcher John W. Huffman at Clemson University began developing the JWH series (named after his initials) in the 1990s. Compounds like JWH-018, JWH-073, and JWH-200 were designed as research chemicals to map cannabinoid receptor activity. Huffman has repeatedly expressed dismay his academic research tools became recreational drugs.

The AM series emerged from pharmaceutical research, particularly through Alexandros Makriyannis at Northeastern University. Compounds like AM-2201 and AM-694 were developed as potential therapeutic agents, exploring whether synthetic cannabinoids could provide medical benefits without psychoactive effects. The CP series came from Pfizer's research programs investigating pain management applications.

By the mid-2000s, these research chemicals began appearing in underground markets. Entrepreneurial chemists realised academic papers detailing synthesis methods could be used to create novel psychoactive substances which weren't yet illegal. The first commercial "Spice" products appeared around 2004-2008, initially containing JWH compounds sprayed onto plant material.

The synthesis of JWH-018 ("Spice", (Naphthalen-1-yl)(1-pentyl-1H-indol-3-yl)methanone) is publicly available from Huffman's research and industrially trivial: 1-Naphthoyl chloride + Indole + 1-Bromopentane.

As governments banned specific compounds, manufacturers simply switched to new analogs. When JWH-018 was scheduled, they moved to JWH-073. When that was banned, they shifted to AM compounds, then to newer generations. The SGT series (like SGT-263 and SGT-151) and various other novel structures emerged during this period as chemists stayed ahead of legislation.

Most synthetics are full CB1 receptor agonists, meaning they completely activate the receptor, while THC is only a partial agonist which produces a ceiling effect. This distinction explains why synthetic overdoses can be life-threatening while cannabis overdoses are typically just unpleasant.

Natural THC has relatively balanced activity at both CB1 and CB2 receptors and interacts with other systems including serotonin and glycine receptors. Most synthetics show extreme CB1 selectivity with little CB2 activity, eliminating the anti-inflammatory and immunomodulatory effects which provide some of cannabis's therapeutic benefits. Many synthetics are 10-100 times more potent than THC, making precise dosing nearly impossible.

THC metabolism is well-understood, producing predictable metabolites like 11-hydroxy-THC and THC-COOH. Synthetic cannabinoids often metabolise through different pathways, creating unknown metabolites which may be active and potentially toxic. Some metabolites are more potent than the parent compound, leading to unpredictable duration and intensity.

Unlike cannabis, which contains CBD and other compounds which moderate THC's effects, synthetic products typically contain single, highly potent compounds with no natural buffering agents. The absence of the "entourage effect" means users experience pure, unmodulated receptor activation without the safety mechanisms evolution built into the cannabis plant.

The full agonist activity of synthetics can cause severe medical emergencies rarely seen with natural cannabis: seizures, kidney damage, psychosis, and cardiovascular crises. Emergency departments report cases of synthetic cannabinoid users requiring intensive care, mechanical ventilation, and dialysis - outcomes virtually unknown with natural cannabis use.

CB1, CB2, And Violence

The relationship between cannabinoid use and violence is complex and nuanced, with significant differences between natural cannabis and synthetic compounds, and important distinctions between correlation, causation, and mediating factors like psychosis.

The contrast with alcohol is particularly illuminating: alcohol consistently shows strong associations with violent behaviour across cultures and study designs, with clear dose-response relationships and plausible biological mechanisms involving disinhibition and aggression-promoting neurochemical changes. Cannabis lacks these pharmacological properties and shows opposite associations in most research.

The cannabis-psychosis link is well-established, with meta-analyses showing heavy cannabis use, particularly high-THC varieties used during adolescence, approximately doubles the risk of developing psychotic disorders. The relationship appears dose-dependent and is strongest for early-onset, frequent use. However, the absolute risk remains relatively low - even among heavy users, most do not develop psychosis.

Large-scale epidemiological studies generally show either no association or a negative correlation between cannabis use and violent behaviour. The National Longitudinal Study of Adolescent Health found cannabis users were actually less likely to engage in violent behaviour compared to alcohol users. However, some studies have identified specific contexts where associations may exist, particularly involving heavy use, early onset, or pre-existing psychological vulnerabilities.

CB1 receptors are densely distributed in brain regions which regulate aggression and impulse control, including the amygdala, prefrontal cortex, and hypothalamus. Animal studies suggest CB1 activation generally reduces aggressive behaviour through several mechanisms: dampening amygdala reactivity to threatening stimuli, reducing stress hormone release, and impairing the formation of fear-based memories which can trigger defensive aggression. This neurobiological evidence supports the observation natural cannabis typically has calming rather than aggression-inducing effects.

CB1 receptors throughout the brainstem and peripheral nervous system become overwhelmed, disrupting basic physiological regulation. Heart rate can spike dramatically (sometimes over 200 beats per minute), blood pressure fluctuates wildly, and temperature regulation fails. This autonomic instability creates a state of physiological panic which compounds psychological distress and can trigger fight-or-flight responses even in non-threatening situations.

While cannabis use can contribute to psychosis risk, and psychotic individuals show elevated rates of violent behaviour, establishing a direct causal chain from cannabis to violence through psychosis remains problematic. Most cannabis-induced psychotic episodes are temporary and resolve with abstinence. Moreover, the vast majority of people with cannabis use disorders never engage in violent behaviour, and most violent crimes are committed by individuals without psychotic symptoms.

Cannabis users often differ from non-users in numerous ways which independently correlate with violence risk: socioeconomic status, concurrent substance use (particularly alcohol), personality traits, environmental factors, and legal system interactions. When these confounding variables are controlled for, the cannabis-violence association typically diminishes substantially.

Acute cannabis intoxication generally reduces rather than increases aggression through several mechanisms: muscle relaxation, sedation, impaired motor coordination, and altered time perception making sustained aggressive behaviour difficult. The cognitive impairments associated with being "high" - including reduced working memory and impaired executive function - typically make complex violent planning less likely, though they might theoretically reduce impulse control in predisposed individuals.

Cannabis withdrawal can produce irritability and mood disturbances, particularly in heavy users. However, cannabis withdrawal syndrome is generally mild compared to other substances and rarely involves the severe agitation seen with alcohol or benzodiazepine withdrawal. The irritability is typically more akin to caffeine withdrawal than the potentially dangerous agitation associated with substances more clearly linked to violence.

The synthetic cannabinoid literature tells a starkly different story. Case reports consistently describe extreme agitation, unpredictable violent outbursts, and dangerous behaviour. The full CB1 agonist activity, combined with unknown metabolites and potential contaminants, can produce severe psychiatric symptoms including paranoid delusions, hallucinations, and loss of behavioural control. Emergency responders report synthetic cannabinoid users often require multiple personnel to restrain and may continue aggressive behaviour even under heavy sedation.

The severe behavioural effects stem from synthetic cannabinoids essentially breaking the brain's fundamental regulatory systems simultaneously: removing inhibitory control, overwhelming excitatory systems, disrupting basic physiology, and eliminating higher-order behavioural regulation. It's analogous to simultaneously cutting the brake lines, jamming the accelerator, and disconnecting the steering wheel of the brain's behavioural control systems.

Full CB1 agonists like synthetic cannabinoids activate receptors at 100% capacity, unlike THC which only achieves partial activation (around 20-40% maximum response). This complete receptor saturation creates sustained, overwhelming signals which flood neural circuits. The brain's CB1 receptors normally receive brief, precisely-timed endocannabinoid signals lasting seconds to minutes. Full agonists maintain this activation for hours, essentially jamming the brain's regulatory frequency.

CB1 receptors are heavily concentrated on GABAergic interneurons - the brain's primary "brake pedal" cells which prevent excessive neural activity. When synthetic cannabinoids fully activate these receptors, they dramatically reduce GABA release, removing the brain's ability to calm overexcited circuits. This disinhibition is particularly dangerous in the amygdala and prefrontal cortex, where loss of GABAergic control can unleash primitive fear and rage responses without higher-order modulation.

The disrupted GABA system allows glutamate - the brain's primary excitatory neurotransmitter - to run unchecked. This creates a hyperexcitable state where normal stimuli trigger exaggerated responses. In limbic circuits controlling emotion and threat detection, this glutamate excess can produce paranoid ideation, extreme anxiety, and hair-trigger aggressive responses to perceived threats which may not exist.

Full CB1 agonism causes massive, sustained dopamine release in reward circuits, but unlike natural rewards, this activation doesn't terminate normally. The result is not pleasure but a dysphoric hyperdopaminergic state associated with paranoia, agitation, and psychosis. This mirrors the dopamine excess seen in acute schizophrenic episodes, explaining why synthetic cannabinoid users often present with paranoid delusions and bizarre behaviour.

The prefrontal cortex - responsible for executive function, impulse control, and rational decision-making - contains dense CB1 receptor populations. Full agonist activity essentially shuts down this region's normal function, eliminating the brain's ability to override primitive emotional responses with rational thought. Users lose the capacity for behavioural planning, consequence evaluation, and impulse inhibition which normally prevent violent outbursts.

CB1 receptors normally help regulate the hypothalamic-pituitary-adrenal (HPA) axis, the body's primary stress response system. Full agonist activity disrupts this regulation, causing either excessive cortisol release (creating agitation and hypervigilance) or complete suppression (preventing normal stress adaptation). Either extreme can contribute to behavioural instability and inappropriate responses to environmental stimuli.

The combination of reduced GABAergic inhibition and excessive glutamate activity lowers the brain's seizure threshold. While not all users experience clinical seizures, many exist in a subclinical hyperexcitable state where normal neural firing patterns become chaotic. This electrical instability can manifest as erratic, unpredictable behaviour and may contribute to the "superhuman strength" sometimes reported in agitated synthetic cannabinoid users.

Prolonged full agonist exposure forces CB1 receptors to desensitise and internalise, but this process is imperfect and uneven across brain regions. The result is a chaotic mix of hyperactivation in some circuits and hypoactivation in others, eliminating the coordinated neural activity necessary for organised behaviour. Users may simultaneously exhibit sedation and agitation, or alternate between extreme states unpredictably.

People with underlying psychiatric conditions, adolescent brains with immature regulatory systems, or genetic variations in cannabinoid metabolism may be particularly susceptible to these effects. The same full agonist dose which causes mild agitation in one person might trigger complete behavioural decompensation in another.

Those with pre-existing antisocial personality traits, bipolar disorder, or genetic predispositions to psychosis may experience exacerbated symptoms. However, these represent a small subset of users, and the cannabis use may be better understood as triggering underlying vulnerabilities rather than directly causing violent behaviour.

The weight of evidence suggests natural cannabis use is not directly causally linked to violent behaviour and may actually reduce aggression in most users. Any associations found in population studies appear largely explained by confounding variables, selection effects, and the small subset of users who develop serious psychiatric complications. The relationship is better characterised as cannabis potentially exacerbating violence risk in already susceptible individuals rather than creating violent tendencies de novo.

Synthetic cannabinoids represent a clear exception, with substantial evidence for direct causation of aggressive and violent behaviour through their extreme pharmacological effects. The distinction between natural and synthetic cannabinoids is crucial for policy and clinical considerations.