Urban legends

The second half of the claim was once standard neuroscience. Charles Gross, reviewing the history in 2000, wrote that for over a century the field assumed that "new neurons are not added to the adult mammalian brain".[1]

The first half was told above all about alcohol. In 1993 two Danish researchers opened their paper by noting that "it is commonly believed that chronic alcohol abuse results in loss of neocortical neurons", and that the assumption "has not been properly tested".[2]

They tested it. Jensen and Pakkenberg counted neurons in the neocortex of 11 alcoholic men and 11 matched controls after death. The "total mean neocortical neuron numbers in the two groups did not differ".[2] What the drinkers had lost was white matter: "chronic alcoholics lose white matter", the authors wrote, and they argued this damage may be reversible with abstinence.[2]

The same paper is also why the result matters. Its authors stated that "lost neocortical neurons cannot be replaced".[2] For most of the cortex, that half of the legend holds.

The hippocampus is different. In 1998 Eriksson and colleagues found newly divided neurons in the brains of adult patients and concluded that "the human hippocampus retains its ability to generate neurons throughout life".[3] A 2013 study dated neurons by the carbon-14 left from nuclear bomb tests and estimated that "700 new neurons are added in each hippocampus per day".[4]

The point is disputed. In 2018 Sorrells and colleagues found no young neurons in adult hippocampi and concluded that neurogenesis there "does not continue or is extremely rare in adult humans".[5] The same year Boldrini and colleagues examined hippocampi from people aged 14 to 79 and reported "thousands of immature neurons in the DG" at every age.[6]

The slogan fails on the case it was built on, since the best-known count in heavy drinkers found no lost cortical neurons.[2] Its second half is right for the cortex and too absolute for the hippocampus.[2][4]

Warnings that strangers poison trick-or-treat sweets are older than the drug version. The sociologist Joel Best has tallied newspaper reports of tampered Halloween treats in the United States and Canada since 1958.[1]

The drug form has a documented case in Detroit in 1970. Best records that "five year old Kevin died after eating heroin supposedly hidden in his Halloween candy". Then, as Best puts it, "less heavily publicized was a follow up story": the boy had found the heroin in a relative's home.[1]

Best has reviewed press coverage back to the late 1950s. He writes that he has been "unable to find a substantiated report of a child being killed or seriously injured by a contaminated treat" collected while trick-or-treating.[1]

Hospital records point the same way. Best's review of case reports found that "the medical literature does not offer any reports of children poisoned or otherwise harmed by treats" received at the door.[1]

The deaths that were blamed on Halloween candy turned out to have other causes. Besides the Detroit heroin case, Best lists a 1974 Texas cyanide death in which the candy came from the boy's own father, and three later deaths traced to illness.[1]

Each new drug has had its turn. In 2014, when recreational cannabis went on sale in Colorado, Denver police warned about THC sweets, though "there were no reports of that actually having happened". In 2015 a Facebook warning about ecstasy pills handed out as candy spread after "the police department in Jackson Mississippi relayed it".[1]

In 2022 the DEA warned about brightly coloured fentanyl pills, and Republican Party chair Ronna McDaniel "linked rainbow fentanyl to Halloween" on Fox News. After the holiday Best wrote that he was "not aware of any U.S. reports of children receiving" fentanyl-tainted treats that year.[1] Two days after Halloween, Vice News could not find "a single report of candy mixed with fentanyl". Buffalo police, answering posts that blamed local deaths on laced candy, said they "have no reports of incidents at this time".[2]

Best concludes that "Halloween sadism is best seen as a contemporary legend": a story told as true with little or no evidence behind it.[1]

The claim had a scientific peak on 27 September 2002, when Science published a paper by George Ricaurte's group at Johns Hopkins. It reported that "Nonhuman primates exposed to several sequential doses of MDMA" developed severe damage to dopamine neurons, and warned that "recreational MDMA users may unwittingly be putting themselves at risk" of later brain disorders.[1]

In September 2003 the authors retracted the paper. The monkeys had not received MDMA. Nature reported that the group had "accidentally injected monkeys with methamphetamine" from mislabelled vials.[2] PubMed now lists the paper as retracted.[1]

What human imaging does show is narrower than holes. A 2010 PET study of 49 regular ecstasy users found serotonin transporter binding "significantly decreased throughout all cerebral cortices", tied to how much they had used. The same study's MRI scans "revealed no overall regional volume differences between groups".[3] Lower transporter binding is a real finding worth taking seriously. It is a change in a marker, not missing brain tissue.

The retraction travelled less far than the paper. A 2021 study of the 50 largest American newspapers found that of the 26 that covered the 2002 paper, "only 14 (54%) covered its retraction".[4]

On 18 March 2015 the DEA sent a nationwide alert about fentanyl to US law enforcement. Its press release said the agency had warned officers that "fentanyl can be absorbed through the skin and accidental inhalation of airborne powder can also occur".[1]

In June 2016 the DEA released a roll call video for police under the headline "Fentanyl Exposure Kills". Acting Deputy Administrator Jack Riley said on it that "a very small amount ingested or absorbed through your skin can kill you". Two New Jersey detectives exposed to a small amount appeared on the video. One said, "I thought I was dying".[2]

The best-known case came in May 2017 in East Liverpool, Ohio. Patrolman Chris Green collapsed after "brushing a small amount of white powder from his shirt" following a drug search, and was given naloxone at the station and in hospital.[3]

In 2017 the American College of Medical Toxicology and the American Academy of Clinical Toxicology reviewed the risk. They concluded that "the risk of clinically significant exposure to emergency responders is extremely low" and that "incidental dermal absorption is unlikely to cause opioid toxicity". They wrote: "we have not seen reports of emergency responders developing signs or symptoms consistent with opioid toxicity from incidental contact".[4]

The airborne risk is also small. The same statement notes that "the vapor pressure of fentanyl is very low", so powder does not give off a gas. Even at the highest airborne level measured in workers at fentanyl factories, an unprotected person "would require nearly 200 min of exposure to reach a dose of 100 mcg of fentanyl".[4]

A 2022 case report describes a worker who spilled a large volume of pharmaceutical fentanyl solution onto broken skin. There were "no clinical effects of opioid exposure observed".[5]

The toxicologists also advised that naloxone be given for objective signs such as slowed breathing, and "not for vague concerns such as dizziness or anxiety".[4]

A 2020 study tracked news coverage of overdose from casual fentanyl contact between 2015 and 2019. It found that "relevant content appeared in 551 news articles spanning 48 states", with the misinformation "amplified by erroneous government statements". Corrections were shared far less.[6]

The belief stuck. In 2021 researchers interviewed 23 police leaders and officers from five agencies. Nearly all "wrongly believed that dermal exposure to fentanyl was deadly".[7] The STAT report on East Liverpool repeated the DEA video's message that "even incidental contact with the drug could result in a fatal overdose".[3]

There is one documented case behind the story. In his book LSD: My Problem Child, Albert Hofmann described "a case in the late sixties of strychnine being found in an LSD sample that was a white powder".[1]

By 1985 the claim was in print as history. Acid Dreams, by Martin Lee and Bruce Shlain, blamed part of the decline of Haight-Ashbury on "samples of LSD showing up laced with amphetamines and strychnine". Erowid later noted the authors gave no source, and filed the claim as a myth "without a reference or additional data to back it up".[2]

On Usenet it was already a running argument. A 1992 post to alt.drugs said "the most likely place to find strychnine is in myths posted to alt.drugs".[1]

The chemist Alexander Shulgin wrote that he had looked at a large number of illicit street samples and "never detected the presence of strychnine" in them. He added that "strychnine is not needed to bond LSD to blotter paper", and that it is not a breakdown product of LSD either.[1]

Street-drug testing programs agree. Published analyses by PharmChem and the Los Angeles County street drug analysis program are described as ones "which likewise never found any strychnine".[1] George Root, who ran Florida's anonymous street drug testing program from 1972 to 1977, wrote: "I recall no instances of samples of actual LSD being combined with strychnine".[1]

The arithmetic rules it out for blotter. A standard 5 mm square weighs about 2 mg. Even "if the paper itself was made completely out of pure strychnine", the dose would sit at the very bottom of its range of activity.[1] Erowid puts it plainly: "It is virtually impossible to fit enough strychnine to have any effect" in most LSD preparations.[3] The 1960s were different only in form, since then "LSD was sold primarily in tablet form" and a tablet is easier to fake.[2]

Strychnine does turn up as an adulterant, in other drugs. A 2011 review of adulterant studies lists it in heroin and notes that the amounts found, "such as strychnine in heroin, are not life-threatening".[4]

The body load has other explanations. Cramps and nausea are reported with LSD itself, and "poorly synthesized LSD might have other ergot derivatives in it".[1]

The first version came from Santa Barbara. On 19 May 1967 the New York Times ran an Associated Press item saying "the vision of four users of LSD has been impaired for life" after they stared at the sun. Its only source was an unnamed spokesman for a local ophthalmological society.[1] Reviewing the coverage in 1994, Snopes noted that "nowhere in this entire article is a single name mentioned".[1]

The famous version came from Pennsylvania in January 1968. Norman Yoder, the state commissioner for the blind, said six college students had taken LSD, lain in a clearing and stared at the sun, and that "the retinas of their eyes were destroyed". He would not say where: "Yoder had refused to identify the college or name the students".[2] Newsweek described them as "all nice kids, not hippies", found "all totally, permanently and helplessly blind".[1]

Governor Raymond Shafer ordered an inquiry, and "within a week the hoax was revealed".[3] The state attorney general said inconsistencies in the "case records apparently doctored to fit the story" led investigators to question Yoder "until he admitted the incident was false". Yoder was suspended, and a state official said he had been sent to a psychiatric hospital in Philadelphia.[2] Newsweek later printed a correction saying it had "ran the story in good faith".[1]

Sun-gazing on LSD can still hurt. The pharmacologist David Nichols points to "two documented cases of eye damage" in the medical literature.[1] One is a 1973 report titled "Solar retinopathy from sun-gazing under the influence of LSD".[4] The other describes a 23-year-old man who "sustained severe macular damage by sun gazing" while on a hallucinogen.[5] Each is one patient with a burned macula, not a group of students struck blind.[4][5]

The story travelled because officials and the national press carried it. It reached readers through the Associated Press and Newsweek before anyone checked it.[2][1]

The story was being passed around and argued about by 1999. On a Straight Dope Message Board thread about acid flashbacks, one poster blamed stories of trips set off by exercise for "the myth that LSD can be stored in your system" and "later released by heavy activities".[1]

Erowid's page on the myth describes the spinal version directly: people claim that "LSD has been found in spinal fluid years after the last time LSD was taken".[2]

LSD does not stay. In a 2017 study, healthy volunteers took 100 or 200 micrograms by mouth. "The plasma half-life was 2.6 h", and the drug showed "first-order elimination up to 12 h".[3]

Spinal fluid is not a store. A review of its physiology states that "CSF is renewed about four times every 24 hours".[4] A drug dissolved in it would be washed out, not kept.[4]

Nobody has shown LSD there years later. Erowid says of the claim: "There is no support for this claim." It asks to hear of any study that has "looked at spinal fluid of LSD users for LSD".[2]

Flashbacks are a separate and real thing. A 2003 review of 20 studies from 1955 to 2001 found that the word flashback "is defined in so many ways that it is essentially valueless". The persistent visual form, hallucinogen persisting perception disorder, "appears to be a genuine but uncommon disorder".[5] A 2014 review says its mechanisms "are largely unknown" and that "low-level visual processing may play an important role".[6] None of the proposed causes is a dose of LSD waiting in the spine.[2][6]