Last week, I attended the Contra Costa County Coroner’s inquest into the death of Anthony Banta, Jr., the hairdresser who was shot and killed by Walnut Creek police during a confrontation in his Creekside Drive apartment December 27, 2012.
In their testimonies, the four officers involved in the confrontation testified and presented a scenario in which they fired on Banta in self-defense. As I reported for the news website News 24-580, the officers had heard 911 calls that Banta had suddenly burst into his roommate’s bedroom just after 3 a.m. and starting choking him.
“I think maybe he’s sleepwalking,” the roommate’s girlfriend told dispatchers. In subsequent exchanges between the girlfriend and dispatchers, officers learned that Banta was armed with a knife and was trying to break down a bedroom door, behind which the roommate and the girlfriend had barricaded themselves. The girlfriend later told police Banta was looking “like a zombie.”
When officers entered the apartment, they found the 22-year-old Banta at the top of the stairs, “agitated,” “wild-eyed.” He refused repeated demands to throw down a large 10-inch knife officers saw him holding, at one point saying “Just shoot me,” before leaping or hurling himself down the stairs. Police opened fire in self-defense, they said. An 11-member jury found Banta’s cause of death to be “accidental.”
What’s been perplexing to Banta’s family and friends, and even to authorities, is that the 5-foot-4 inch Banta was known to everyone, including his roommate and the roommate’s girlfriend, as a polite, non-violent, hard-working young man. He had no history of mental illness or emotional breakdowns and never displayed the kind of behavior witnesses said he displayed that morning.
Forensic pathologist Andy Josselson, testifying at the coroner’s inquest, offered the interesting theory that Banta’s behavior was either the result of an undiagnosed mental illness or of marijuana psychosis. Evidence presented at the inquest showed that Banta had a small amount of THC, the main, mind-altering ingredient in marijuana, in his system, and that there was “moderate marijuana use” in the apartment.
The marijuana psychosis theory is interesting. And, as noted by Josselson, there is much in medical literature about a possible connection between the use of marijuana and the onset of psychosis—the mental state in which someone loses contact with reality.
However, there’s much debate about this phenomenon, especially as it pertains to teens. Health writer Alice G. Walton, writing on Forbes.com, says marijuana has been found to reduce anxiety in some people—an effect we’re all pretty much aware of, through personal experience or otherwise. In others, though, in can induce anxiety and psychosis, she says. There is also debate over whether pot-smoking actually causes people to develop schizophrenia. In another post, she sums up the debate:
The connection is especially important to understand in young people, whose brains are still wiring themselves, a process that continues right up through one’s 20s. Some researchers have framed the issue as a chicken-or-egg conundrum, wondering whether pot smoking leads to psychosis or whether underlying psychosis makes one more likely to smoke pot.
In this post, she cites a Dutch study in which researchers, after following more than 2,100 teens, found “a bidirectional relationship.” After teens were questioned about their pot use over the years and questioned about their social relationships, feelings of loneliness, attention, and thought problems, the team found that kids who at 16 smoked pot were more likely to have psychotic symptoms at 19. At the same time, kids who at 16 showed psychotic symptoms were more likely to smoke pot. Walton says:
So researchers conclude that the “self-medication” and the “damage” (that is, brain damage) hypotheses both hold water – and they both make sense intuitively. For example, the authors say that a person with psychotic symptoms might use marijuana to “improve their mood or to control one’s feelings, boredom, social motives, improving sleep, anxiety and agitation.” … On the flipside, pot smoking could also damage the developing brain, since the teen-age is a “particularly vulnerable period for the effects of cannabis.”
Of course, who really knows whether any of this applies to Banta? Toxicology tests couldn’t be conclusive about when he ingested the marijuana, Josselson said. One screen suggested as few as five hours before his death, but another could only determine it was within 30 days of his death. The sophisticated tests performed on Banta also couldn’t show whether he had newer classes of designer drugs in his system.
One Banta family member agreed it’s possible he had some underlying health issue that caused his behavior that night. That family and friends never saw any signs of mental illness doesn’t necessarily mean he didn’t have something like that going on. Some people with mental illnesses have a hard time reaching out because they are ashamed or they themselves have trouble making sense of thought disorders or breaks with reality. It should also be said that the early 20s is the age at which symptoms of disorders, such as schizophrenia or bipolar disorder. first reveal themselves. Or the symptoms may start earlier, but this is the age at which people are first diagnosed.
The position of the Banta family, as explained by their attorney, Larry Peluso, is that even if Banta suddenly began acting the way police said he did—and for whatever reason—he didn’t have to die. They have filed a federal lawsuit, alleging that police panicked and could have handled the confrontation differently.
One thought on “Did marijuana psychosis kill Anthony Banta, Jr.?”
This is absurd. When a drug like marijuana is used by literally millions of people on a daily basis throughout the world, without any violent or “psychotic” behaviors attached, how does one single it out as the possible culprit for incidents like this, when “designer drugs” aka bath salts, are well known to cause these types of incidents with regularity, and are easily accessible? The tests weren't able to single out designer drugs, but the behavior matches that of many users. Wouldn't it be more viable to start with the more glaring similarities between his actions and those common of other bath salts users than trying to decide if correlation means causation on a statistical minute number of people out of millions?