Coffee and matters of the heart

I’ve already written about how coffee, specifically the caffeine content, can improve liver function. And now, as you may have heard on morning news, it can help your heart too!

Public Domain (Author: edm-vgg, 2014)

OK, this news isn’t really new, it does seem like a bit of interesting trivia that morning news rolls out from time to time to make mornings much easier to deal with, and when one thinks of ‘mornings,’ they think ‘coffee.’ What makes this update is that now there’s a mechanism involved – we know that it’s good, but the authors of this week’s Featured Article have proposed and tested out a hypothesis of why it’s good. This week’s article is rather heavy on specialized vocabulary, so I may have to get that out of the way first. We may be casual around here, but we’re also aiming to be accurate. Think of us here as smart casual.

Public Domain (Author: Raditya Febrian, 2013)

Anyway, all this has to do with a protein called cyclin-dependent kinase inhibitor 1B, or CDKN1B (for short, it’s p27 – let’s go with that from now on, shall we?). Like any protein, it’s how genes are expressed in the human body and sent around. After all, genes are essentially instructions. It normally slows down cell division, so it’s no surprise that maybe it should help keep cancer – essentially cell death and division gone wild – in check. However, caffeine can bring the p27 gene out of the nucleus where it normally is and into the mitrochondria, which has its own DNA. This is important as mitochondria are often considered as the ‘powerhouse of the cell‘ as it produces energy through chemical reactions. One would think that muscles would have more mitochondria because of what they do (like, oh, I don’t know, move that body!?), and your heart – which is a muscle – contains quite a lot of it.

So why would p27, which keeps cells from dividing (making sure your heart stays, you know, working), be helpful to heart muscle? The authors suggest that it has to do with ‘fibroblasts,’ cells that secrete the kind of proteins that keep connective tissue such as muscles together. This definitely comes into play when you sustain some kind of muscle injury – a heart attack would be a good example of that – and could do with some healing. However, fibroblasts have a rather curious ability to ‘differentiate,’ or suddenly take up a specialty depending on the conditions they’re in. Think of it as if you, who is probably good at quite a few things, decided that you’re going to get really good at this one thing because of some need, or you really just have a knack for it. Good at baking, but you have kids with celiac disease? Try your hand at gluten-free cookies!

Public Domain (Author: Christine Kramer, 2016)

Jiu-jitsu player with long legs? Why not try getting good at triangle chokes?

Flickr/Public Domain (Author: Matt Hecht, 2015)

You get the idea. Anyway, heart injuries, especially due to a recent heart attack? Get good at building muscle instead! Fibroblasts that specialize in repairing muscle are called myofibroblasts, and they can even act like muscles themselves. Good for closing up wounds, yeah?

So how did Ale-Agha et al. test out this hypothesis? Simple – all you need is some caffeine, a bunch of mice, and several geneticists on hand! I won’t bore/horrify (bore-rify?) you with the details since I think we all know what happens to mice at the end of a lot of genetics experiments anyway (so instead here’s an earlier blog post on human cannibalism), but they wanted to test what p27, in the mitochondria rather than in the nucleus, does to heart muscle cells. In addition, they wanted to compare how caffeine affects the presence of p27 in the cell by adding enough caffeine in their drinking water so that the amount of caffeine in their blood is similar to that of a human after four cups, which is the number you probably caught in the morning news. Bunch of lightweights.

And what did they find? They found that heart muscle with p27 in the mitochondria had better cell respiration, meaning that it’s better at processing materials to create energy (what we think of ‘breathing’ isn’t technically respiration, but let’s not dwell on that here, keep it casual). Not only that, the p27 hearts were actually stronger, as they had thicker walls than the mice who didn’t get this genetic treatment. By comparing mice without this gene to ‘wild types,’ they found that the lack of this gene makes for less-efficient respiration, and not even caffeine can bring it up to par – in other words, caffeine alone won’t make the heart grow stronger, one needs the p27 along with it. With a bit more lab work, the authors found that caffeine increased p27 in the mitochondria of heart muscle cells of the older mice in their sample. There are people out there who believe, albeit jokingly, that coffee is indeed the fountain of youth. What say you now, at least in terms of the heart?


Before we get ahead of ourselves, we may need to bear in mind that this was done on mice. We can safely assume we’re not built the same way, so it may not be so simple. Considering that I do human subjects research (it’s chemical education, relax, it’s pretty much psychology), I have an idea of what kind of ethical minefield one has to cross to collect human tissue. I’m sure there’s a way to do this without having to sacrifice an actual person (although there’s some argument as to why we have to do the same thing to mice), but I don’t know of anyone who would willingly, say, give up a small sample of heart muscle, no matter how many Starbucks gift cards one would give them. But hey, there are other ways to detect patterns in human health that may not require cutting someone open.

Thoughts? Comments? Let me know in the space below, and you don’t need to be a WordPress member to do it! If you’re not doing so already, please follow (if you’re into scientific research with snarky commentary from an overly-caffeinated blogger-scientist) and thanks again for stopping by.

Featured Article: Ale-Agha N, Goy C, Jakobs P, Spyridopoulos I, Gonnissen S, Dyballa-Rukes N, Aufenvenne K, von Ameln F, Zurek M, Spannbrucker T, Eckemann O, Jakob S, Gorressen S, Abrams M, Grandoch M, Fischer JW, Köhrer K, Deenen R, Unfried K, Altschmied J, Haendeler J. (2018). CDKN1B/p27 is localized in mitochondria and improves respiration-dependent processes in the cardiovascular system – New mode of action for caffeine. PLoS Biology 16(6): e2004408. DOI: 10.1371/journal.pbio.2004408.

Featured Image: Public Domain (Author: marja71, 2015)

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