Hallucinogens and Marijuana Use, Effects, Myths, and Realities

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Hallucinogens and Marijuana Use, Effects, Myths, and Realities

Abnormal Psychology · Chapter 18: Substance-Related Disorders: Understanding Addiction and TreatmentSection 18.3 · lesson 68 of 9717 min · free with a free account

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In this lesson

Effects, myths, and realities - with the evidence stated at its true strength.

  • Describe the hallucinogen class and its clinical concerns
  • Assess therapeutic research claims critically
  • State the cannabis evidence - use disorder, cognition, psychosis - accurately
  • Correct common myths, and describe the policy debate

Transcript

Everything said in the video, section by section (2,156 words). Read along, or search it.

Substance-Related Disorders: Understanding Addiction and Treatment

Hallucinogens and Cannabis

This section covers hallucinogens and cannabis. Their effects, the myths around them, and the realities. It is a section where evidence is often overstated in both directions, so the aim throughout is to state each finding at its true strength. We cover the hallucinogen class, therapeutic research, cannabis and its contested link with psychosis, common myths, the policy debate, and two composite cases.

Before You Begin

Pharmacology, Evidence, and Policy Only

As before, this material is educational, and not a basis for diagnosing yourself or anyone else. If you are concerned about your own or another person's use, please speak with a qualified professional. These conditions are treatable, and recovery is a common outcome. This section covers pharmacology, evidence, and policy. It contains no quantities, no routes, and no preparation content. Nothing in it is guidance about use. It also contains no description of any altered state as an experience. That is deliberate. Descriptive accounts of altered states work as promotional material, whatever the intent. The clinical categories are what the material needs.

The Hallucinogen Class

Defined by Receptor Action

Hallucinogens are a pharmacological grouping of compounds whose primary action is to alter perception, cognition, and mood, through mechanisms distinct from depressants and stimulants. The classical hallucinogens act mainly as agonists at a particular serotonin receptor subtype. That shared receptor action is what defines the group, not origin or legal status. The label covers a chemically diverse set of compounds, some from plants and fungi, some synthesized. That diversity carries no implication about safety. The clinical effect categories are named flatly. Perceptual, cognitive, and emotional alteration. Dissociative compounds are a separate group, acting mainly at a different receptor system. Their mechanism informs one of the explanatory accounts of psychosis covered in the next chapter.

Table 18.3.1

Different Classes, Different Questions

Here are the three groupings side by side. The classical hallucinogens raise concerns about acute adverse reactions, a persisting perception disorder, and precipitating difficulty in vulnerable people. The dissociative compounds raise concerns about acute adverse reactions, and their mechanism informs a psychosis account. Cannabis raises entirely different concerns. A recognized use disorder with a withdrawal category, a contested association with psychosis, and concerns about adolescent onset. These are often discussed together, as though they raised the same questions. The clinical issues have almost nothing in common.

Hallucinogens: Clinical Concerns

Low Dependence Is Not Low Risk

Three clinical concerns belong to the hallucinogen class. Acute adverse reactions are a recognized clinical category, requiring supportive medical care. No management content is given here, because guidance framed as risk reduction works as use guidance. Hallucinogen persisting perception disorder is a condition in which perceptual disturbances that arose during intoxication continue, or recur, after use has stopped, causing distress or impairment. It is rare. But it matters more than its frequency suggests. It can be persistent, and it directly contradicts the belief that this class produces no lasting difficulty. Third, dependence liability in the classical hallucinogens is low. That is a genuine pharmacological finding, and it needs an immediate qualification of equal weight. Low dependence liability does not mean low risk. The acute psychological risks are real. The safety risks from altered perception and judgment are real. And a compound that produces no dependence can still cause serious harm on a single occasion. Dependence liability measures one thing. It is not a summary of risk.

Therapeutic Research

Supervised Trials - Not Personal Use

Certain compounds in this class, and certain cannabinoid compounds, are being investigated as treatments for specific conditions. That is research in controlled clinical settings, under medical supervision. Four points are what you should take from it. First, the status is preliminary. Early findings in psychiatry have a poor record of surviving replication at scale. Second, blinding is a serious problem. Participants generally know whether they received an active compound, so expectation cannot be separated from effect by the usual means. Third, the intervention is not the compound alone. Trials involve intensive preparation, supervision throughout, and structured follow-up with trained clinicians. The results cannot be attributed to the compound in isolation. Fourth, participants are selected and screened. Trials exclude people at higher risk of adverse outcomes, so study populations differ from the general population. And so this research provides no basis for personal use. Unsupervised use carries precisely the risks the research settings are designed to exclude.

Cannabis

Not a Single Substance

Cannabis acts mainly at the endocannabinoid system, a receptor system widely spread through the brain, including regions for memory, coordination, and reward. The plant contains multiple active compounds, and two prominent ones have different, in some ways opposing, actions. So the composition of a product determines its effects. Talking about cannabis as a single substance is inaccurate. Regulation has changed substantially, ranging from prohibition to general legal availability. Product diversity has grown. And, stated in words only, the potency of available products has increased over time. So evidence gathered in earlier decades describes exposure that differs from current exposure, which limits how far older findings transfer. A cannabis use disorder is recognized in the classification, and assessed across the same four domains as any other. That corrects a common, confidently held belief that cannabis cannot produce a use disorder. It can. A withdrawal category exists, and people present for treatment. The belief persists because dependence liability is lower than for some substances. But lower than something is not the same as absent.

Cognition and Adolescence

Established, Contested, and Plausible

On cognition, two questions must be kept separate. During use, effects on attention, working memory, and forming new memories are well established. After stopping, the evidence is genuinely contested. Some studies find residual differences. Others find the differences resolve with abstinence. The confounds are substantial. People who use differ in education, socioeconomic position, other substance use, and pre-existing cognitive differences. Studies measuring cognition before use begins are the informative design, and they are scarce. The defensible summary is that acute effects are established, persistence is contested, and the evidence for persistence is strongest for adolescent-onset use. More generally, earlier onset of use is associated with poorer cognitive, educational, and mental health outcomes. Adolescence is a period of major neural reorganization, which makes that plausible. But association is not causation. Early use is also associated with adversity, family circumstances, existing difficulties, and other substance use. The mechanism strengthens the case, without settling it.

The Cannabis-Psychosis Question

A Robust Association, an Open Question

Now the most contested question in this section. The association between cannabis and psychosis. It is presented here with the association at full strength, and the causal question explicitly open. The association is robust. Cannabis use and psychotic outcomes co-occur more often than chance, across many studies and settings. Two features are often cited as strengthening the causal case. A dose-response pattern, in which heavier and earlier use goes with a greater elevation in outcome. And genetic interaction findings, in which the association appears stronger in people carrying particular genetic variants. Both are consistent with causation. Neither establishes it, because both are also compatible with the alternatives.

Figure 18.3.3

4 Accounts of the Same Association

Here are four competing accounts of the same association. In the first, cannabis use causes psychosis. In the second, the arrow runs the other way. The earliest stage of the condition comes first, and use follows it. In the third, a shared vulnerability raises the likelihood of both use and psychosis. And in the fourth, other confounding factors drive both. The point is that this question is empirically approachable, not just a matter of opinion. Each account makes a different prediction, and each has a design that could test it. None of the four has yet been ruled out.

The Honest Position

Neither Alarmist Nor Dismissive

Reverse causation deserves particular attention, because it is the account most often dismissed too quickly. The prodromal period can precede a first episode by months or years. During it, a person may be distressed, withdrawn, and experiencing attenuated symptoms. Use beginning then would appear to come before onset, while actually following the condition's earliest stage. Establishing the order precisely enough to exclude this is genuinely difficult. So here is the honest position. The causal question is not settled. The claim that cannabis simply causes psychosis goes beyond what the design of the evidence can establish. The claim that the association is entirely artifact ignores its robustness, the dose-response pattern, and the plausible mechanism. A clinician should be able to state the association accurately, state that causation is contested, and state what would settle it. And overstating risk is not a safe error. A person who checks an overstated claim will discount everything else you said, including what was accurate.

Medical Cannabis

3 Distinctions Do Most of the Work

On medical cannabis, three distinctions do most of the work. First, where evidence exists. Certain cannabinoid preparations have evidence for specific, narrowly defined indications, and some have regulatory approval on that basis. Second, where claims outrun the evidence. Cannabis is promoted for a very wide range of conditions, and for most of them the evidence is absent, preliminary, or negative. The breadth of those claims is itself a reason for caution. Genuine treatments rarely work for everything. Third, a regulated medical product is not general availability. A preparation of known composition, prescribed for a defined indication with clinical oversight, differs from a product of unknown composition obtained without any of that. Conflating the two is the most common error in this area.

Table 18.3.4

Myths - and Why They Persist

Here are six common beliefs, set against the evidence. Natural means safe. But origin has no bearing on pharmacological effect or risk. Non-addictive means harmless. But dependence liability measures one property, and the other risks are independent of it. Legal means low-risk. But legal status reflects policy and history, not pharmacology. The class with the largest mortality burden is legal in most places. Hallucinogens cannot cause lasting difficulty. But persisting perception disorder is recognized. Cannabis cannot cause dependence. But a use disorder and a withdrawal category are recognized. And research shows these substances are beneficial. But that research is preliminary, screened, and supervised, and gives no basis for personal use. Notice that each myth has an understandable origin. A belief with a reason behind it is not corrected by contradiction alone. The reason has to be addressed.

Public Policy

Liberalization: Both Cases at Full Strength

Liberalization is a live policy debate, presented here with both positions at their strongest, and neither endorsed. The case for it. Criminal records harm employment, housing, and immigration, imposed unequally across social and ethnic groups, often beyond the harm of the use itself. Prohibition has not eliminated availability. Regulation allows quality control and known composition. Legal markets can be taxed to fund treatment. And criminalization deters help-seeking, which is a direct clinical harm. The case against it. Availability drives use at population level, and more use means more harm, even if the harm per person is unchanged. Commercial promotion follows legalization, and the legally available classes show what that produces. Poor regulation can combine the disadvantages of both approaches. And liberalization is hard to reverse. Outcomes in places that have liberalized are mixed, and the observation periods are short. Neither position is established, and this course does not resolve the debate.

Case Vignette 1 (Composite)

Jonah: A First Episode, Use Present

Now two composite cases, constructed for instruction. Jonah is twenty-one. His family brings him to an emergency setting with a psychotic presentation. He has no previous mental health contact, and a cousin with a psychotic condition. His family describe a change over roughly eight months, with marked deterioration in the last three weeks. He left his course, withdrew from friends, and has not been working. He has used cannabis for some years. Three possibilities are live. A substance-induced psychosis. A primary psychotic condition with co-occurring use. Or a primary condition brought forward by use. The presentation itself does not distinguish them. The family's timeline places his functional decline before the recent deterioration. That may be the prodromal period, which makes reverse causation a real possibility. So immediate management follows the presentation and the medical risk. The diagnostic question is recorded as open, and an observed abstinence period is arranged, with support. Persistence would point to a primary condition, and resolution to a substance-induced one. His family history raises the prior probability of a primary condition, without settling anything on its own. And both a substance use disorder and a primary condition may need treatment.

Case Vignette 2 (Composite)

Marianne: Assessed Like Any Use Disorder

Marianne is twenty-nine. She attends after her partner raised concern about a change over two years. She has moved from full-time to part-time, then to occasional work. She has given up two activities that mattered to her, and describes a recurring argument at home. Work through the domains. Impaired control, with failed attempts to cut down and use beyond her intentions. Social impairment, in her work, her activities, and the conflict at home. Risky use needs assessment, and is not yet established. And pharmacologically, she needs more for the same effect, and has difficulty on stopping. So a cannabis use disorder is assessed exactly like any other, across the same four domains. Nothing about quantity, product, or experience entered the assessment. Marianne says cannabis is not addictive, so this cannot be what is happening. That is the myth from the table. The clinical response is to address the reason behind it, lower dependence liability heard as none, rather than contradicting her flatly. Expect that belief to be part of the presentation, not an obstacle to it.

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FAQ

Questions students ask us

About Hallucinogens and Marijuana Use, Effects, Myths, and Realities

What is hallucinogen persisting perception disorder?
Hallucinogen persisting perception disorder is a condition in which perceptual disturbances that first arose during hallucinogen intoxication continue or recur after use has stopped, causing distress or impairment. It is rare, but it can be persistent. It matters because it contradicts the common belief that hallucinogens cannot cause lasting difficulty, and it shows that the low dependence liability of classical hallucinogens does not mean low risk.
Can you develop a cannabis use disorder?
Yes, cannabis use disorder is a recognized diagnosis, assessed across the same four domains as any other substance use disorder: impaired control, social impairment, risky use, and tolerance or withdrawal. A cannabis withdrawal category also exists, and people do present for treatment. The belief that cannabis is not addictive persists because its dependence liability is lower than that of some substances, but lower is not the same as absent.
Does cannabis cause psychosis?
The association between cannabis use and psychosis is robust, but whether cannabis causes psychosis is still contested. A dose-response pattern and genetic interaction findings are consistent with causation, yet four accounts remain open: cannabis causes psychosis, early prodromal symptoms lead to use, a shared vulnerability drives both, or other confounding factors drive both. An accurate statement names the association, notes that causation is unsettled, and avoids overstating risk.
Do psychedelic therapy studies show hallucinogens are safe to use?
No, clinical trials of certain hallucinogens provide no basis for personal use. The findings are preliminary, blinding is difficult because participants usually know whether they got an active compound, and the treatment includes intensive preparation, supervision, and follow-up, not the compound alone. Trials also screen out people at higher risk, so unsupervised use carries exactly the risks these research settings are designed to exclude.

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