Learn about why just because you want something doesn’t mean you like it; why Esperanto is the world’s most successful universal language; and a gene therapy injection in one eye that improved vision in both.
Learn about why just because you want something doesn’t mean you like it; why Esperanto is the world’s most successful universal language; and a gene therapy injection in one eye that improved vision in both.
Just because you want something doesn't mean you like it — and that has implications for addiction by Kelsey Donk
Esperanto Is the World's Universal Language by Reuben Westmaas
Gene therapy injection in one eye surprises scientists by improving vision in both by Cameron Duke
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Find episode transcript here: https://curiosity-daily-4e53644e.simplecast.com/episodes/wanting-and-liking-are-different-to-your-brain
CODY: Hi! You’re about to get smarter in just a few minutes with Curiosity Daily from curiosity-dot-com. I’m Cody Gough.
ASHLEY: And I’m Ashley Hamer. Today, you’ll learn about why just because you want something doesn’t mean you like it; why Esperanto is the world’s universal language; and why a gene therapy injection in one eye improved vision in both.
CODY: Let’s satisfy some curiosity.
This is going to sound counterintuitive, but just because you want something doesn't mean you like it. It’s true, and it has big implications for addiction.
Until very recently, scientists and the general public assumed that if a person wanted something, it must be because they like it. But now, scientists are starting to doubt the truth behind that assumption. And they’re also starting to doubt another assumption: that dopamine is the hormone that drives both wanting and liking.
This idea was first proposed as a sort of thrown-together solution to some confusing study results in the 1990s. Researcher Kent Berridge noticed that when he removed dopamine from rats’ brains, they stopped looking for their favorite sugary foods. That made it seem like dopamine is what made them like sugar. But when he actually gave them sugar, the rats without dopamine still seemed to like the sugary foods: they made the same pleasurable facial expressions they would normally. So then Berridge did the opposite: he increased the dopamine in the rats’ brains. The rats ate four times as much sugar, but they didn’t seem to like it any more than they had before. Something was off.
Berridge developed a hypothesis. Maybe wanting and liking are two separate things that reside in different parts of the brain. And maybe dopamine doesn’t have anything to do with liking — it just relates to wanting.
In another experiment, Berridge learned even more about dopamine’s relationship to wanting. He attached a stick to the rat cage that delivered a minor electric shock when touched. A normal rat would learn to stay away from the stick when shocked. But by making the rat's dopamine system more sensitive, Berridge could make the rat obsessed with the stick. The rat would keep coming back time and time again, despite the minor shock. It’s like when you crave candy during a movie but can’t enjoy it because you’re already full from a big dinner. You get the candy anyway and suffer through it, because your body tells you you want it.
This research has super important implications for how we think about addictions to drugs, alcohol, gambling, and food. For people struggling with addiction, the dopamine system becomes linked to certain cues, like parties, spoons, or syringes. And wanting never goes away, even if liking does. The goal now for addiction researchers should be to figure out if they can tweak the dopamine system to give people relief from their desires. It took a long time for scientists to accept the difference between liking and wanting. But now that it’s accepted, it can hopefully be used to help people recover.
The diversity of languages in the world is something to celebrate. But sometimes, don’t you wish we could all speak one universal language? In fact, people have tried creating a universal language for centuries. None of them have been universally adopted, obviously, but the one that’s gotten the closest is a language called Esperanto.
The story of Esperanto starts way back in 1887, in a part of Poland where residents spoke not one, not two, not three, but four different languages. A physician named Dr. L.L. Zamenhof [ZAM-min-hoff] felt his neighbors would get along a lot better if they all shared a common language. But he worried that defaulting to an already existing language would make non-native speakers into second-class citizens. Thus, he set out to create a single language that would be easy to read, easy to speak, and most importantly, easy to learn.
That means that Esperanto has no more than 16 rules, and none of those rules have any exceptions. It’s also entirely phonetic, meaning that every letter is always pronounced the same way. Dr. Zamenhoff based his language on several languages in the Indo-European family, including English, German, French, and Spanish, and he named Esperanto after the word for "hope" to signify the role he thought it would play in bringing the world together.
Want to hear a few words? "Hello" is "Saluton" [sah-LOO-tone], "Goodbye" is "Ĝis la revido," [JEESE lah reh-VEE-doh] and "Uno bieron, mi petas" [OOH-noh byer-AHN, mee PAY-tass] is the all-important phrase “One beer, please.” And remember: everything is always pronounced the same way, which is what makes Esperanto so easy to learn.
Buuuuut I’m gonna go out on a limb and guess that you probably don't know anybody who speaks Esperanto. Sadly, Dr. Zamenhoff's vision never came to fruition. That may be because language is more than a way to communicate — it's a way to experience another country, try new food, and learn about a new culture, and Esperanto doesn’t have any of that. Still, among invented languages,it's definitely the most successful. William Shatner once starred in a science fiction movie written entirely in Esperanto. Leo Tolstoy spoke it fluently, and was even named honorary president of the Esperanto Vegetarian Association. Today, practitioners of the Baha'i faith are strongly encouraged to learn it, and eight Nobel laureates are Esperantists. Maybe there is hope for Esperanto after all.
Something very unexpected recently happened when scientists were testing a new gene therapy for vision improvement. The scientists found that their therapy not only works, it actually seems capable of improving vision in both eyes even when used on only one.
The gene therapy in question is intended to treat Leber [like Labor] Hereditary Optic Neuropathy, or LHON. It affects 1 in 30,000 people, mostly men between the ages of 20 and 30. LHON is a genetic condition that affects a particular type of nerve in your eye called a retinal ganglion cell. These cells transmit visual messages from your eyes to your brain along the optic nerve, and LHON damages these cells. It’s a devastating condition that causes serious visual impairment within weeks of the first symptoms.
LHON is caused by a faulty gene in the mitochondrial genome. The therapy I’m talking about involved building an engineered virus that could deliver a working version of that gene to the mitochondria. If successful, this would literally overwrite the faulty gene and cure the condition. Pretty exciting stuff. Gene therapies like this could one day cure diseases previously thought to be incurable — not just LHON, but many, many more.
To find out if this therapy actually works like should, the scientists ran a clinical trial. 37 participants with vision loss due to LHON received an injection of the experimental gene therapy in one eye and a placebo injection in the other. The scientists then tracked any changes in their vision for the next two years.
The good news is that the gene therapy seemed to work. 68 percent of the participants had improved vision at the end of the trial. But it didn’t just work in the treated eye. The majority of these participants had their vision improve in the untreated eye, too.
The researchers aren’t sure why this happened, but there are a couple of interesting hypotheses. The first one deals with the plasticity of the brain. Maybe as one eye improves, the brain reorganizes to compensate for the other eye. The second hypothesis suggests that mitochondria containing the edited gene may be able to pass from one nerve cell to another. Although they haven’t tested this in humans, studies in nonhuman primates suggest that the cells of the right and left optic nerve are actually capable of exchanging cell parts at the point where the optic nerves cross.
Either way, it’s amazing. The human body still has some surprises up its sleeve.
Let’s recap the main things we learned today
[ad lib optional]
CODY: Today’s stories were written by Kelsey Donk, Reuben Westmaas, and Cameron Duke,, and edited by Ashley Hamer, who’s the managing editor for Curiosity Daily.
ASHLEY: Scriptwriting was by Cody Gough and Sonja Hodgen. Today’s episode was produced and edited by Cody Gough.
CODY: Join us again tomorrow to learn something new in just a few minutes.
ASHLEY: And until then, stay curious!