Recreational drug users call it “Special K.” Large, frequent doses of the anesthetic ketamine can give users vivid hallucinations, but a recently published study hints that the drug may have a medicinal use: temporarily treating depression brought on by bipolar disorder.
The small, proof-of-concept study appears in the journal Archives of General Psychiatry. National Institutes of Health researchers randomly gave 18 depressed patients ketamine or a placebo on two different days, two weeks apart. They used a much smaller dose of the drug than the amount used for recreation or anesthesia, but within 40 minutes 71 percent of the patients who received ketamine showed a significant improvement in mood, which lasted for three days, as measured using a psychiatric depression rating scale.
The quick response time is unusual for the drugs typically used to treat bipolar disorder’s depression, such as lithium or antidepressants like Prozac, and many of the study’s patients had failed to respond to other treatments. On average, the study participants had tried seven antidepressants and 55 percent of participants had failed to respond positively to the extreme measures of electroconvulsive therapy (ECT)–seizures brought on by electrical current. Ketamine’s apparent success may have to do with the neurotransmitter, glutamate:
Around the United States, state governments are rushing to enact bans on K2, the hot new (and still mostly legal) drug made with synthetic cannabinoids: lab-created compounds designed to mimic the effects of THC, the active ingredient in marijuana.
Often marketed as incense, K2 — which is also known as Spice, Demon or Genie — is sold openly in gas stations, head shops and, of course, online. It can sell for as much as $40 per gram. The substance is banned in many European countries, but by marketing it as incense and clearly stating that it is not for human consumption, domestic sellers have managed to evade federal regulation [The New York Times].
Missouri is the most recent state to move against K2, the origin of which dates back to the work of Clemson University scientist John Huffman, who was developing these synthetic compounds in the 1990s. Scientifically, the chemicals are interesting for their potential to mimic some of the pain-relieving aspects of marijuana, which advocates of medical marijuana legality point to, without the negative health effects that come with setting a plant on fire and inhaling the smoke. The chemical used in most varieties of K2 is called JWH-018.
Huffman was interviewed by The Guardian last year when K2 was spreading around Europe. Now in his late 70s, he seems to understand something that many politicians can’t seem to get through their heads: Risk-taking teenagers will go to about any length, legal or illegal, to get high. Huffman says he wouldn’t oblige the numerous enterprising types who asked him how to make his substances, and that the substances are always labeled not for human consumption. But he figured someone was going to figure it out sooner or later, especially considering the chemical doesn’t show up on drug tests.
Poke a snail with a stick and it remembers for a day. Poke a snail with a stick after you’ve given it methamphetamine and it remembers for much longer.
Getting gastropods hooked on meth perhaps sounds cruel, but Barbara Sorg and her team are among those scientists trying to figure out how the drug works in the brain to produce intense connections that feed the addiction cycle. In a study forthcoming in the Journal of Experimental Biology, the scientists show that, in snails at least, meth makes it hard to forget things that happened while on the drug.
Here’s the test: The snails Sorg studied can breathe two ways, through their skin underwater and also through a breathing tube they can deploy when they surface. The team kept two groups of snails—one on meth, one not—in separate tanks of shallow water. And if the snails tried to surface and breathe that way, the scientists would poke them.
Who needs poppy plants to produce morphine? Last month scientists said they’d isolated the genes those plants use to synthesize the narcotic chemical and made it themselves in a lab. Now, in a study in the Proceedings of the National Academy of Sciences, another team has suggested that we mammals might possess the pathway to create our own morphine.
Because we have receptors for the opiate in our brains (which makes it such an effective and addictive painkiller), and because morphine traces show up in our urine, scientists had long wondered if animals could produce the drug themselves. But studies using living animals yielded inconclusive results because of possible contamination from external sources of morphine in their food or in the environment [Nature]. In addition, the body breaks down and changes morphine, which complicates the task.
Do you often feel the need for a sweet sugar rush or a moment of bacon-induced bliss? A new study offers evidence that that surge of pleasure is similar to a heroin high, and that eating junk food regularly can significantly change the brain’s chemical make-up, creating junk food addicts who are driven to overeat.
Lead researcher Paul Kenny says it had previously been unclear whether extreme overeating was initiated by a chemical irregularity in the brain or if the behavior itself was changing the brain’s biochemical makeup. The new research by Kenny and his colleague Paul Johnson, a graduate student, shows that both conditions are possible [Scientific American].
For the study, published online in Nature Neuroscience, Kenny and colleagues headed to the grocery store. “We basically bought all of the stuff that people really like — Ding-Dongs, cheesecake, bacon, sausage, the stuff that you enjoy, but you really shouldn’t eat too often,” he said [Reuters]. One set of lab rats was allowed unfettered access to these high-calorie foods, while another rat group was allowed just one hour of access to the junk food per day. Both sets of rats also had the option of eating standard healthy lab rat fare. Finally, a control group of rats were kept on a healthy diet.
For millennia, humans have used the codeine and morphine of the poppy plant as painkillers—or recreational drugs. For the last half-century, says Peter Facchini, biologists have tried to unlock just how the plant produces these powerful chemicals, and wound up frustrated. But now, in a study in Nature Chemical Biology, Facchini’s team says it has isolated the two genes that are the key to this process, which scientists could use to create some of medicine’s most valuable chemicals without the fields of poppy plants that give rise to the trade of illegal narcotics, especially heroin.
Both of the genes produced enzymes that helped to convert precursor chemicals. One, thebaine 6-O-demethylase (T60DM), had a role in the production of codeine. The other, codeine O-demethylase (CODM) transformed codeine into morphine [Press Association]. Lead author Jillian Hegel, Facchini’s grad student, studied four different poppy relatives and sifted through a library of 23,000 genes to find these two. She put these genes into E. coli bacteria that sat overnight in a flask with a chemical called thebaine that’s present in poppy seeds to see if the bacteria would synthesize the painkillers. “When she came back the next morning, the thebaine was all gone,” says Facchini. “That’s when her eyes got big…. Finding it all had been turned into morphine — that gives a grad student a great sense of power, when they can make morphine” [Science News].
Finally, some potentially hopeful news for military veterans coming home with the lingering psychological scars associated with post-traumatic stress disorder. In a paper for this week’s edition of the New England Journal of Medicine, a team reports finding that troops wounded in Iraq who were treated with morphine right away were less likely to develop PTSD as a result of the incident.
The study of 696 members of the Army, Navy and Marine Corps, all wounded in Iraq from 2004 to 2006, found that 61 percent of those who eventually developed PTSD had been given morphine, usually within an hour after being wounded. But 76 percent of those who did not develop PTSD had been given morphine [Reuters]. Neither the size of the morphine dose nor the severity of injury appeared to make a difference in the morphine effect, the study says.
Addiction researchers constantly wade through the ways that drugs like cocaine change your brain, and a new study in Science has pointed to a new epigenetic factor. Cocaine, the researchers say, can scramble the way genes turn on and off in a key brain region associated with pleasure and reward.
Ian Maze said his team gave one group of mice repeated doses of cocaine and other group repeated doses of saline with just one blast of cocaine at the end to study the differences. The team paid particular attention to a protein called G9a, whose behavior in the nucleus accumbens region of the brain seems to be altered by cocaine use. The role of the protein appears to be to shut down genes that shouldn’t be on. One-time use of cocaine increases levels of G9a. But repeated use works the other way, suppressing the protein and reducing its overall control of gene activation [TIME]. The researchers found that the overactive genes caused brain cells in the region to grow more connections to each other. The growth of such neural connections can reflect learning. But in the case of addiction, that may involve learning to connect a place or a person with the desire for more drugs [TIME].
Despite their tiny size and short lifespan, fruit flies are familiar test subjects in labs because they can show us a lot about ourselves, particularly in terms of genetics. And in a study for Current Biology, a team led by Anita Devineni found that the insects have another thing in common with people—they like alcohol, sometimes a little too much.
The scientists started by giving their test subjects a choice. Flies held inside vials could sip from thin tubes holding either liquid food spiked with 15 percent ethanol or plain liquid food. The researchers measured the descent of the liquids inside each tube to get a readout of which food the flies preferred [Science News]. It was no contest: The flies preferred the alcohol-spiked food, and the more they had it, it seems, the more they craved it—the flies’ tipples grew more frequent over time [National Geographic News].
Cocaine combined with capsaicin, an active ingredient in pepper spray, can be deadly, if research in mice is any indication.
In the early 1990s, anecdotes of people dying after being doused with pepper spray puzzled researchers, until autopsies revealed many were on cocaine at the time. To look for a link between the two substances, a research team injected cocaine, capsaicin or both at once into the abdomens of several groups of about 30 mice. Injections allowed them to control the dose of capsaicin the mice received, which wouldn’t have been possible if the mice were simply sprayed [New Scientist]. Equal doses of cocaine plus capsaicin killed about half the mice, compared to cocaine alone, which killed just a few. And a dose of cocaine high enough to kill half the mice on its own killed up to 90 percent when combined with capsaicin.