I’m afraid that “repeating word-of-mouth information until it’s disproven” isn’t how the scientific method works, and wouldn’t be considered rigorous in the research community. I look forward to your findings.

Just to review, your arguments that I’m labeling as non-evidence-based are:

1. LSD is stored in body fat
2. LSD can be released after the initial trip is over
3. When the LSD is released it can trigger a “flashback” during which the person is “tripping-out”
4. Because of this risk, anyone who has used LSD should be banned from operating a vehicle

You chose to quote an abstract from a 40-year-old lit review, and even though it doesn’t support your point, you’re declaring this “case closed.” You’re either arguing in bad faith or you’re not putting much effort into finding the truth. Either way I think you know your case is weak.

“Delayed, intermittent phenomena (“flashbacks”) and LSD-precipitated functional disorders that usually respond to treatment appropriate for the non-psychedelic-precipitated illnesses they resemble, round out this temporal means of classification.”

Strassman is summarizing the range of post-LSD experiences that have been reported. Delayed, intermittent psychosis is at one end of the range and mild, short-term symptoms at the other. He doesn’t validate those reports, and goes on to say that no causal relationship had been established, and the etiology of “flashbacks” was at that time controversial.

A more recent 2021 review by David Nutt et al. (Nutt is by most accounts the most credentialed and respected psychedelic researcher today) says:

A common perception linked to psychedelics is that they induce ‘flashbacks’ of the drug experience long after its acute effects have subsided. Although transient drug-free visual experiences resembling the effects of hallucinogens have been documented in psychedelic users (e.g. 40–60% of users; Baggott et al., 2011; Carhart-Harris and Nutt, 2010), they are not hallucinogen-specific, as they can also be caused by other psychoactive substances, for example, alcohol or benzodiazepines (Holland and Passie, 2011), and can occur in healthy populations (Halpern et al., 2016). In most cases, these side effects are mild and diminish in duration, intensity and frequency with time (Strassman, 1984).

If these symptoms are prolonged and distressing, the syndrome is known as HPPD. The DSM-V (American Psychiatric Association (APA), 2013) reports a prevalence rate for HPPD as 4.2% in hallucinogen users (Baggott et al., 2011) based on a single online questionnaire. Other studies have documented much lower prevalence rates of the disorder, some as low as 1/50,000 (Grinspoon and Bakalar, 1979). Furthermore, if approximately 1/25 users experience HPPD as suggested by Baggott et al. (2011), then it would be a near statistical certainty that some participants in the current era of psychedelic research, which has collectively included thousands of participants in trials since 2000 (Carhart-Harris et al., 2021; Ross et al., 2016), would have experienced HPPD by now; however, this has not been the case.

However, the emergence of large online fora dedicated to the discussion of HPPD on websites, such as Reddit (e.g. https://www.reddit.com/r/HPPD/, which has > 7000 members), suggests that cases can be identified at the population level, even if the prevalence is too low to be captured in clinical trials that typically use small sample sizes. While the large-scale data collection of online fora is helpful to gain insights into wider populations, samples are self-selected and likely to be biased, limiting the conclusions that can be drawn.

The incidence of HPPD appears to be much lower in the clinical context, perhaps as a result of efficient screening and preparation (Cohen, 1960; Johnson et al., 2008). Although Halpern and Pope (2003) suggest that there may be no identifiable risk factors for HPPD, a subsequent study of 19 individuals who developed HPPD found that all recalled anxiety and/or panic reactions during the triggering episode (Halpern et al., 2016). Thus, HPPD symptoms could potentially be conceived as a form of trauma response, similar to PTSD, or a form of health anxiety evoked by residual symptoms of the original experience.

I will say again that your original arguments are not supported by current research. I won’t spend any more time debating this with you because we don’t seem to have the same definitions of “evidence” and “misinformation.”

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