Why is Pepto-Bismol pink? (McGill OSS)

3 minute read

It’s minty, chalky, unpleasantly viscous, and useful for a wide range of stomach ailments, but why is Pepto-Bismol so vibrantly pink?

The active ingredient in Pepto is bismuth subsalicylate. Once in the stomach, bismuth subsalicylate breaks down into two products—bismuth and salicylic acid—the latter of which is rapidly absorbed into the bloodstream. Salicylic acid is the active ingredient in many anti-acne and wart products and is closely related to acetylsalicylic acid, better known as Aspirin. Bismuth is a metal with somewhat unique properties, including notably its low melting point of just 271.5 ˚C. As such, it finds use as a lead replacement in various contexts. One important one is in lead bullets, the use of which has been highly discouraged, or even outlawed in some places, due to its toxicity. If you have a free day, a bottle of bismuth subsalicylate and some laboratory equipment, you can even extract the bismuth from Pepto-Bismol—it’s iridescent and quite pretty!

Bismuth in the stomach is very poorly absorbed and combines with other compounds present to form various bismuth salts. These salts have antimicrobial activity and prevent bacteria from binding and growing on the mucosal cells of the stomach, as well as increasing fluid reabsorption and decreasing intestinal secretions and inflammation. In these ways, bismuth subsalicylate can help with a wide range of digestive issues, including nausea, diarrhea, stomach ulcers, heartburn, and even cholera.

Contrary to what you may be thinking, it is not bismuth subsalicylate that gives Pepto-Bismol its carnation colouring. That compound is beige. It turns out that Pepto is pink simply because Procter and Gamble dye it pink!

According to Pepto-Bismol, the doctor who developed their pink medicine in the early 20^th century chose pink, but no one really knows why. They keep it pink because you don’t mess with success, and who can blame them? The practically neon hue of their product is instantly recognizable, even when their products are in chewable tablet or pill form. Even generic preparations of bismuth subsalicylate tend to stick to the pink colour palette.

In 1992, a Procter and Gamble spokesperson told the LA Times that the doctor chose pink to appeal to children, but as Pepto-Bismol is not recommended for kids under 12, that seems questionable. This recommendation is due to concerns that bismuth subsalicylate could contribute to a rare condition called Reyes syndrome in children. It’s for this exact reason that Aspirin (acetylsalicylic acid) is not approved for children under 12.

You shouldn’t worry about Pepto-Bismol turning you pink, but there is a slight chance it could turn your tongue, or your poop, dark black. This happens due to a reaction between the bismuth metal and sulfur in your mouth or digestive tract, producing bismuth sulfide. This might happen if you’ve recently eaten a lot of sulfur-rich foods—like cruciferous vegetables (broccoli, cabbage, kale etc.) or alliums (onions, garlic, leeks, etc.)—taken a high dose of a sulfur-containing medication (like sulfonamide antibiotics) or live somewhere with high sulfur concentrations in the water. Don’t panic; it’s only temporary and totally benign.

While the doctor who developed Pepto-Bismol and chose its hot pink shade probably didn’t know, the colour of a medication may have surprising impacts on how patients perceive its effects or rate its effectiveness. A couple of studies have found that patients are more likely to perceive warmly coloured medications (red/orange/pink/etc.) as stimulants or antidepressant drugs versus an association with tranquillizers or depressants for cool-coloured (blue/purple/green) meds.

When studied, the marketing of medications echoes this colour coding, implying a feedback loop between buying medications of a particular colour and associating that colour with that type of medication. Interestingly, studies have also shown that the colour of a drug can influence how bitter patients think it will taste and how strong they believe it is. Specifically for children, there’s a belief that red or pink medications make them look sweeter or more palatable to kids. So maybe the inventor of Pepto-Bismol was trying to invoke the idea of a strawberry milkshake!

This article was written for the McGill Office of Science and Society. View the original here: https://www.mcgill.ca/oss/article/you-asked/why-pepto-bismol-pink

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What Does Snake Venom Do to the Human Body? (McGill OSS)

2 minute read

There are more than 3000 species of snakes on Earth, ranging from the Barbados threadsnake at roughly 10 cm long (about the same as a deck of cards) to the reticulated python at around 6 m in length (almost as tall as an adult male giraffe!). Luckily, only about 600 are venomous, and only around 200 are venomous enough to seriously harm or kill a human.

Despite the existence of hundreds of venoms, nearly all snake venoms fall into one of three categories, depending on how they affect us: neurotoxins, cytotoxins or myotoxins.

Neurotoxins are common to the Elapidae family of snakes, which include cobras, mambas, coral snakes, and copperheads. They work on the nervous system by disrupting the electrical impulses that our nerves and muscles use to function.

Neurotoxins can mess with our neurons in a few different ways. Imagine your neurons like a lamp plugged into an electrical socket. For the lamp to function normally, it should be able to turn on and off at different times. With α-neurotoxins, it’s as if someone put a babyproof cover on the socket, preventing us from plugging our lamp in at all. The result? No light. On the other hand, with dendrotoxins, the lamp is plugged in, but no electricity flows from the socket to our lamp. Again, no light. But with fasciculins, it’s like the lamp’s plug is stuck in the wall. Constantly activated with no off switch, even though we want to go to bed.

Vipers favour the use of cytotoxins—venoms that directly damage cells. Some common types include phospholipases, which disrupt cell walls, and hemotoxins, which affect the circulatory system. Some hemotoxins trigger the destruction of red blood cells, while others affect the clotting factor of blood—either by making blood too clotted and thick to flow or too thin to ever clot and stop external bleeding.

Myotoxins are less common in serpent physiology but are found in certain species of rattlesnakes. They contain basic peptides (chains of amino acids too short to be considered proteins) that directly disrupt the flow of charged molecules our muscles rely on to contract.

With such a wide range of venom types and mechanisms of action, it’s no surprise that nearly every snake species needs a tailor-made antivenom. Luckily, Canada only has four native species of venomous snakes.

Nonetheless, it can be pretty tricky to identify snakes reliably in the wild. So, if you’re ever on the receiving end of a snake bite, seek medical attention immediately! Do not try to catch the snake to bring with you—some help for your doctors in identifying your attacker is not worth a second (or third, or fourth) bite.

This article was written for the McGill Office of Science and Society. View the original here: https://www.mcgill.ca/oss/article/environment-you-asked/how-does-snake-venom-kill-human

The Potential for Caffeine-Free Coffee via Crispr/CAS9 or Crossbreeding (McGill OSS)

5 minute read

Our current methods for decaffeinating coffee are far from ideal. There are a few different methods, all with their own nuanced details, but they all shake out to using some kind of solvent to dissolve and remove caffeine from green coffee beans before roasting. This extra processing means costs to produce decaf are higher, profit margins lower, and production times longer. An even bigger problem is that even the best methods for decaffeination take some aromatic compounds away along with the stimulant molecule, affecting the taste and smell of the resulting coffee.

What if, instead of removing the caffeine from coffee beans, we could grow naturally caffeine-free coffee? Doing just that might be closer on the horizon than we expected.

To know how to stop a coffee plant from producing caffeine, it’s important first to recognize why it’s making it in the first place. Caffeine is a very bitter compound (one of the reasons coffee is a bitter drink), and just as we don’t tend to enjoy overly bitter things, neither do bugs. Coffee plants are believed to produce caffeine in their leaves mainly as a pesticide to defend against being eaten by pests like the coffee berry borer, Hypothenemus hampei.

Interestingly, ancestors of the modern coffee species were probably much lower in caffeine or entirely caffeine-free. The caffeine defence is believed to have developed in central and west Africa, where the coffee berry borer is native. This is where the highest caffeine species of coffee, like Coffea arabica and Coffea canephora, are found. These two species account for nearly 100% of the world’s coffee production.

A fascinating potential method for developing caffeine-free coffee plants involves the subject of the 2021 Nobel Prize in Chemistry: CRISPR/Cas9. Often referred to as “molecular scissors,” the CRISPR/Cas9 tool is inspired by bacterial defence mechanisms against viruses and allows the very precise cutting of an organism’s DNA. In this way, a gene can be targeted and deactivated. A review paper from 2022 took a look at the feasibility of using these molecular scissors to disrupt the biosynthesis of caffeine in coffee plants.

As caffeine is a relatively complex molecule, it isn’t built in just one step. Several enzymes are responsible for precise chemical changes to the proto-caffeine molecule en route to its final form. This is good news for scientists looking to disrupt the synthesis process, as they have multiple enzymes to aim for. The authors of the 2022 review identified an enzyme called XMT as a prime target. XMT is responsible for converting xanthosine into 7-methylxanthosine during step 1 out of 4 in the caffeine synthesis pathway. By targeting the very first step in the process, the subsequent enzymes have no molecules to work on. Debilitating XMT would lead to a build-up of xanthosine, but a different enzyme that can degrade it exists, so it shouldn’t be a problem.

Another potential target is called DXMT. This enzyme is responsible for the penultimate step in caffeine synthesis, converting theobromine into caffeine. Theobromine is quite similar to caffeine structurally and shares some properties with it, like being bitter and toxic to cats and dogs. Importantly, however, theobromine does not have the stimulating effect of caffeine. Targeting and disabling DXMT would lead to a build-up of theobromine in coffee beans, which may actually be a good thing! The bitterness of caffeine is part of the flavour of coffee, meaning that a C. arabica bean without caffeine may still taste different than a C. arabica bean with caffeine, even if they’re otherwise the same. The authors of the study postulate that the increased theobromine content of a DMXT-disabled bean could compensate for the missing bitterness from caffeine.

Genetically engineered caffeine-free coffee could represent a better way of getting our java without the jolt of stimulation, but it will undoubtedly face societal hurdles. While backlash to genetically modified organisms has calmed down recently, anti-GMO sentiments are still present in consumers and regulators. The regulations for getting such a product approved in Europe are particularly stringent and pose a significant barrier.

Even if CRISPR/Cas9 coffee isn’t commercially viable, using these molecular scissors to disable specific genes can help us better understand the complex biosynthesis pathways in coffee plants. So-called knock-out mice, named for having a gene’s function stopped (knocked out), have been pivotal in our understanding of physiology and biology. Want to know what a particular gene does? Knock out its function and see what happens. Much of our understanding of complex diseases like Parkinson’s, cancer or addiction is built upon the findings from knock-out mice.

Another approach to making delicious coffee without the kick may lie with modern species of coffee that naturally produce little or no caffeine. For example, Coffea charrieriana is a caffeine-free variety endemic to Cameroon. C. pseudozanguebariae is native to Tanzania and Kenya, C. salvatrix and C. eugenioides to eastern Africa. Unfortunately, these species of coffee all produce beans that would make a cup of joe that tastes decidedly different from what we’re used to. Still, one potential way to make coffee the same as our usual beans, just without caffeine, is by crossbreeding them with C. arabica plants.

There’s one big problem, though—Where the vast majority of coffee plants are diploid, meaning they have two sets of chromosomes (like humans), C. arabica is tetraploid and has four. Unfortunately, breeding between organisms with different ploidy is typically not successful. Recently, however, several low-caffeine varieties of C. arabica have been discovered in Ethiopia. Crossbreeding between the low- or high-caffeine types of C. arabica may result in a caffeine-free bean that is otherwise the familiar morning starter we know and love.

For the caffeine-sensitive among us, there are interesting new caffeine-free coffee possibilities on the horizon. Even if the methods I’ve outlined here don’t pan out, CRISPR/Cas9 will hopefully enable discoveries regarding caffeine and coffee plants. And we never know what the future may hold.

Why Is Diet Coke So Fizzy? (McGill OSS)

1 minute read

Whether you’re buying ingredients for an at home “Coke and Mentos” demonstration, asking a flight attendant for a beverage, or just trying to pour a can of soda into a glass before hockey comes back on, you may have noticed something: Diet sugar-free sodas fizz more than regular sugar-rich sodas when opened.

The degree of carbonation or “fizziness” of a soda is partly a function of how easily carbon dioxide bubbles can form in the sugary flavour water we call pop. When it’s easier for bubbles to form, you get more of them and therefore an increased “fizziness”.

When a liquid has a high surface tension, it means that the bonds between the liquid’s molecules are very strong. Surface tension is why some spiders can walk on water—the spider’s weight isn’t enough to break apart the water molecules! In a substance with high surface tension, bubbles will not form very easily.

Surfactants are chemicals that decrease the surface tension of a liquid. They will therefore make it a bit easier for bubbles to form. Regarding Diet Coke, aspartame, and potassium benzoate (a preservative) are surfactants! Caffeine as well, but it has much less of an effect due to its low concentration.

Bubbles of gas will struggle to form in very viscous liquids, like maple syrup or waffle batter. Diet soda actually has a slightly higher viscosity than sugary soda, which slightly diminishes its fizzing potential. However, a slightly higher viscosity means that when bubbles do form, they’re a bit more stable. This explains why Diet Coke not only fizzes more than classic Coke, but the foam also lasts longer!

Originally posted here- https://www.mcgill.ca/oss/article/did-you-know/why-diet-coke-so-fizzy