Tag Archives: science

Clearing out old news

I have lost my interest in CVs.

I am so close to beginning university, and I have lost my interested in preening my online presence to pre-emptively please people I haven’t even decided to please yet. This past summer, I have been focused on my choice between my UK university offer and my application to Norwegian universities – a choice that ended up an easy one, seeing as my UK place remains the only offer I have received in either country. And that was enough dwelling on the future without a CV to think of.

But I have not lost my interest in medicine. No, I have been bookmarking interesting articles with the potential to become a post, forming a to-do list in my browser that I have successfully procrastinated from for months. And as I approach Freshers’ Week, I feel the need to clear it out. I can’t say that any of this is news, because some of it is from ages ago. But that doesn’t stop it being interesting.

Do you want to read about the responsible parents who leave their babies outside in winter? Or how about the interesting debate on cosmetic tattoos on the NHS? Then there’s also a thing or two about epigenetics that will defo tweak your imagination. Sound good?

Image from BBC article about babies in sub-zero temps

Image from BBC article about babies in sub-zero temperatures

The babies who nap in sub-zero temperatures: Scandinavian parents and day-care centres put prams outdoors at naptime all through winter. Well, it’s one way to show appreciation for fresh air and safe streets. Fresh air is perceived to be essential to babies’ sleep and health, and of course, there’s the cultural mindset encapsulated in this Nordic saying: there’s no such thing as bad weather, only bad clothing.

How Meditation Affects The Brain: I was surprised. The fMRI scans show the opposite of what I expected. The website is brilliant, by the way – check it out.

Why Women Are Stripey: a video from Veritasium’s channel – a brilliant channel, I’ll add. He begins by explaining the basics of genetics, then goes into X inactivation. X inactivation is one of the coolest, most complex things I’ve ever learned that the body can do, and Veritasium uses some ace animations that lay it out clearly.

Cesarean Delivery May Cause Epigenetic Changes In Babies DNA: more on epigenetics! As cesarean delivery is on the rise worldwide, research is trying to discern the consequences of beginning life like this. If you want a more on epigenetics, I wrote about it a while ago. Seriously, this topic is mind-blowing.

Myalgic Encephalomyelitis is not fatigue, or ‘CFS’: this thorough and enlightening paper is quite an eye-opener. Have you heard of ME? It’s an illness with an uncertain cause. If you have heard of ME or CFS, I’d guess that you associate them with fatigue, or tiredness. (If you haven’t, read this summary.) This article will open your eyes to the real complexity of this illness, and make you reconsider the stereotypes.

Image from Guardian article about cosmetic tattoos

Image from Guardian article about cosmetic tattoos

Should cosmetic tattoos be available on the NHS? I had no reason to believe the answer could be ‘yes’. I had no idea about the role of cosmetic tattooing in aiding recovery, at least psychological recovery, from major illnesses, including cancer. Another eye-opener.

Well that’s my reading list cleared out. Here’s to passion for the subject – after a long apathy to the CV.

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Take naps, not notes

motorcortexLearning is more important than sleep when you’re a student. Coffee shots, dubstep music and panic calls to classmates at 3am are a part of basic revision. Who’s been there?

Fools! Sleep is the best. You know it.

Sleep is more than a mood-booster or a dream-world. Your whole body reboots itself, repairing cells and mopping up waste toxins left over from the day – including in the brain. It is not news that sleep is also important for memory, as shown in various experiments (want examples? Have three articles) that test how sleep affects a human’s abilities.

The news this week is that now we have neurological evidence for this. Wen-Biao Gan and his team trained mice to perform different tasks, letting some of them fall asleep afterwards. They then used microscopes and sensors to monitor activity in the mice’s motor cortex (see diagram above). The difference between sleep-deprived and sleep-saturated mice was clear.

neuronHere’s a diagram of a neuron cell. A dendrite has tiny ‘spines’ that connect to the axon endings of other neurons, forming millions of connections and potential signal pathways. When you learn, new pathways are formed, and repetition reinforces these pathways so that they become memories or skills or associations.

The mice developed new dendritic spines in their sleep, along different pathways for different tasks. The neurons activated during the new task kept on firing. Cool! The brain ‘practised’ as it slept.

So sleep promotes new dendritic spine growth, and new connections!  Learning isn’t more important than sleep; sleep IS learning. Commenting on his results, Professor Gan says: “One of the implications is for kids studying; if you want to remember something for long periods you need these connections. So it is probably better to study and have good sleep rather than keep studying.”

There, the professor said it. Don’t take more notes; take more naps. Get the recommended 7-9 hours shut-eye. And best of luck in all your studies, wannabe-med-students.

Sources: BBC article and New Scientist article about Gan’s study

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How epigenetics makes sexual reproduction possible in intricate ways you cannot imagine – part 2

Click here for part 1. Part 2 isn’t much fun without it.

Our Azim Surani has had more adventures in the labs. The following experiment not only proves that the world of imprinting exists, but also presents a conundrum not so distant from part 1’s closing question:

Half my DNA is imprinted with “From mummy!” and half with “From daddy!” The assortment of these in each of my eggs is completely random. If one of my eggs should fuse with a sperm, how will the DNA ‘know’ every single time that my contribution comes ‘from mummy’?

Professor Azim Surani, smiling at us

Professor Azim Surani, smiling at us

Grab a hot drink and get cosy with this conundrum. Kettle boiled? Let’s go.

Surani took seven groups of those genetically identical mice and inserted an extra chunk of easy-to-track DNA into their genomes. Each group had this foreign DNA at a different location. Selected mice received methylated DNA; others got it plain and unmethylated. Time passed; offspring were produced. In six of the seven groups, the foreign DNA was reprogrammed, as expected, and little methylation was inherited.

But in one group, the foreign DNA was still methylated in offspring who had inherited it from the mother. It had bypassed the reprogramming. Fathers never passed on the methylations on the foreign DNA, but remarkably, their daughters did. Two things: the epigenetic modifications hopped over a generation, and it was sex-specific. Do you smell a conundrum?

By chance, the foreign DNA in that last group must have been inserted in an imprinted region. Smack-bang in a “From mummy!” label. The methyl groups were thus inherited from mummies, whereas they were erased from daddies’ DNA right after fusion. But it’s the generation hop that’s weird.

In every cell in your body, your DNA is imprinted. Except in your sex cells. At some point in your embryonic development (remember those good old days?), while your cells were specialising and methyl and acetyl groups were being hammered into place all over, a line of cells diverged. Your primordial germ cells.

From these cells, all methylation markers are removed. Not even imprinted modifications are left, making this a full-scale erasure, not just reprogramming. Then, in a cascade of chemistry, new methyl groups are added, so that the germ cells specialise into sperm or eggs. At the same time, the DNA is imprinted from scratch according to the embryo’s sex. Thus, my eggs – unique amongst all my cells for many reasons – are the only cells in my body without any DNA marked by paternal imprints.

  1. The DNA of sperm and egg are highly methylated because they are specialised cells.
  2. Immediately after fusion of sperm and egg, all epigenetic modification is removed, except from the imprinted regions.
  3. As the embryo develops and cells specialise, epigenetic modifications are added.
  4. Germ cells then have all methylation removed from the DNA, including from the imprinted regions.
  5. Germ cells’ DNA is methylated to cause it to become a sperm or an egg, and to stamp it “From daddy!” or “From mummy!”

And why has our human body developed such a complicated epigenetic sequence? Well, step 2 enables specialised cells to become totipotent. It also balances out the competing male and female genomes by leaving the imprints, as explained in part 1. And finally, it prevents dodgy epigenetic modifications from being inherited.

So intricate in ways you couldn’t have imagined! Breathe. Sip your hot drink. There is so much more to know, but you won’t hear it from me. I’m nearly done. Just let me entice you a little.

Dolly and her first lamb, Bonny

Dolly and her first lamb

You might want to know that the egg juice, which does a perfect job of epigenetic reprogramming, cannot perform its job so perfectly when it’s dealing with an adult nucleus, as in cloning – explaining why Dolly the sheep had poor health. Her offspring, however, did not, because of step 4 – which is not caused by egg juice, but by chemistry later on in embryonic development.

You might want to know about the array of syndromes that can arise from mutations in imprinted regions. Totally sex-specific in inheritance, these syndromes demonstrate how finely-tuned the system really is. Stick a pair of these in a search engine if you fancy: Prada-Willi syndrome and Angelman’s syndrome, or Beckwith-Wiedemann syndrome and Silver-Russel syndrome.

You might want to know about region Dlk1-Dio3 on mouse chromosome 12. It’s not a catchy name, but it’s better than calling it ‘The Key Gene That Prevented Sperm-sperm Or Egg-egg Combos In Surani’s Experiment From Part 1‘.

You might want to know that all mammalian females carry a huge feat of epigenetic repression in every cell in their bodies: the inactivation of an entire X-chromosome. It’s worth another three posts, delving into that kettle of fish. It’s seriously beautiful stuff.

It’s all beautiful. I hope you’ve finished your hot drink, because I’ve finished whizzing you through three chapters of The Epigenetics Revolution – the source of my sudden fascination, and indeed all the knowledge I have in this area. If you too are inspired, I recommend you buy the book yourself; it explains all those ‘you might want to know’s, and more. I’ll end with the author Nessa Carey’s words as she opens the chapter on reproduction and inheritance.

“Occasionally, when someone stands up and asks, “How does that happen?”, we all realise that a phenomenom that seems to obvious to mention, is actually a complete mystery.”

Epigenetics Revolution.jpg.opt770x1169o0,0s770x1169

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How epigenetics makes sexual reproduction possible in intricate ways you cannot imagine – part 1

Have you ever wondered why everyone you know has one biological mother and one biological father? I don’t mean the whole egg and sperm thing – all of us here know how babies are made, I hope.

ACXYPW_ivf_342x198-jpg

A photo image of IVF in action. Source: nhs.uk

Perhaps you don’t know that Azim Surani had a go at making a mouse baby with same-sex biological parents. Using techniques from in vitro fertilisation, he took the nuclei from two sperm and put them in an empty egg to fuse. He did the same with two egg nuclei. In both cases, they fused, divided, specialised into placental and embryonic tissues – but then stopped and failed. Meanwhile, classic sperm-egg combos developed into live mice. And all nuclei used were genetically identical. So why were the results so dramatically un-identical?

It’s probably no surprise that this is part of my passionate fling with epigenetics. You may need a bit of epigenetic vocab before you read the good stuff in the following paragraphs, and – oh, how convenient – that’s exactly what my previous mind-blowing post covers.

Ready? Chew on this: sperm cells and egg cells are as specialised as a cell can get, right? But when they fuse, they become totipotent – able to become any other cell type. What a transformation!

All the methylation that kept sex cells so specialised gets stripped off immediately after sperm-egg fusion. It’s like waxing your legs, if legs are the genome and hairs are the epigenetic modifications. Brilliantly, it reduces the opportunity for dodgy modifications to be inherited. Call it reprogramming. Default settings. Nothing repressed.

Meh, almost. Remember, Surani’s genetically identical embryos somehow gave varying results. The difference in maternal and paternal DNA must therefore be epigenetic. (Gasp! Didn’t see that coming.) It’s as if the DNA has a name-badge spelt out in methyl groups. “From mummy!” “From daddy!” Science-speak for this is ‘imprinted DNA’. “So what?” you might wonder. Isn’t this labelling system just an unnecessary chemical complication?

The answer is amongst Surani’s laboratory shenanigans. Sperm-sperm and egg-egg embryos failed, but before they did, he observed that their brief development contrasted. Egg-egg embryos were small, with utterly rubbish placentas. Sperm-sperm embryos were even smaller, with somewhat better placentas. It’s as if paternal DNA favours the placenta (which nourishes the embryo – i.e. it results in a bigger baby), while maternal DNA favours the embryo. We could zoom out for a panoramic evolutionary view and hypothesise the implications of this –

But I’d rather spend words on the microscopic molecular view. To my GREAT excitement, actual molecular examples of this male-versus-female balance have been found. For example: the mouse gene Igf2 codes for insulin-like growth factor 2, which promotes embryo growth. This gene is identical in both maternal and paternal pronuclei – except it is epigenetically repressed on maternal DNA. Meanwhile, the mouse gene Igf2r codes an enzyme that breaks down Igf2 molecules and has the opposite effect on embryo growth. Guess what? It is repressed on paternal DNA.

It’s a beautiful kind of symmetry, don’t you think? Maternal and paternal imprinted DNA complement each other, and therefore both are necessary. There’s your answer to the opening question of this post. As to why mammalian DNA bothers with this complicated imprinting system at all – well, from that panoramic evolutionary viewpoint that we didn’t visit, it is a system that balances out the competing objectives of the male and female genomes.

With Surani’s help, we’ve learned that everyone you know must have one biological mother and one biological father – mother-mother or father-father combos are genetically impossible because maternal DNA and paternal DNA are imprinted complementarily. One encourages big babies, the other does not, and both are necessary to create a balance.

Imprinted DNA has even more marvellous stories to reveal. Hold on to your hats for part 2. In the meantime, mull this over:

Half my DNA is imprinted with “From mummy!” and half with “From daddy!” The assortment of these in each of my eggs is completely random. If one of my eggs should fuse with a sperm, how will the DNA ‘know’ that my contribution is maternal?

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My mind is blown by my own blog post

We learned that DNA is the blueprint for the body. Somehow, all following the same blueprint, one cell grows a tail and a head of enzymes, while another squeezes itself into a bowl shape and ejects its nucleus, and yet another sprouts light-sensitive membranes.* Whaaat?

Epigenetics blows my mind. If the genome is the supreme blueprint, then the epigenome crosses out and highlights specific instructions for each type of cell. That’s why the nerve cell follows the instruction to be long and spiky, while a skin cell ignores this instruction and sticks to being round-ish. It’s epigenetics that enables each cell to be specialised – and stay specialised after replication.

This topic is intriguing enough from the outside – seeing epigenetics in action, in a schizophrenic person with a neurotypical identical twin, or in mice that determine their offspring’s fur colour by what they eat during pregnancy, or in adults with disrupted hormone patterns directly caused by less-than-pleasant events in the first few years of their lives. But what is it that really grips me by the hair and hauls me into the enchanting realm of epigenetics?

Image from a great 'quick sketch overview' of epigenetics with more lovely diagrams. Take a look. It's worth it.

Part of a great ‘quick sketch overview’ of epigenetics, with more lovely diagrams. Take a look. It’s worth it.

It is the beauty of the molecular details. There are two types of marker: acetyl groups, and methyl groups. Look, I found a really nice diagram that shows how they interact with the genome. As you can see, methyl groups (a simple -CH3, if you’re chemistry-literate) just stick on somewhere, while acetyl groups (-CO-CH3) are on the pink histones, helping the DNA strands to coil up and cuddle them more tightly. To use the words of Hank from the SciShow, methyl groups are like on-off switches, while acetyl groups are more like dimmer switches.

But it’s waa-hayyy more complex than on-off/dim. There’s bits of DNA – previously known as ‘junk DNA’ – that can regulate the expression of adjacent genes. They’re called retrotransposons. I think that’s a really cool robot-like name. Anyway, retrotransposons are super weird because they can actually jump around the genome, in a copy-and-paste way. (Note to self: investigate how on earth this is even possible.)**

Now add in non-coding RNA. This used to be ‘junk’ too. RNA is the perfect transcript of your DNA that gets pruned like hedge before it is translated into proteins. The bits that are snipped off are non-coding RNA, or ncRNA. Previously thought to be good-for-nothing compost waste, it turns out that they are key to gene regulation. There are long ones with a function that is still a bit mysterious to us, and there are short ones (microRNA) that, being perfectly complementary to a section of DNA, can lay right on top of that section and repress it.

So we have methyl groups, acetyl groups, retrotransposons and ncRNA. They all interact in such intricate ways that the metaphor of simple on-off switches seems like wishful thinking. Right, hang on to your hats; I’m going to attempt to show this in an example.

Imagine a mini strip of ncRNA covers a gene like a blanket, repressing it. Imagine that gene usually produces an enzyme (or to be pernickety – produces RNA that codes for a protein that is an essential part of an enzyme) that catalysed the methylation of a retrotransposon. This leaves the adjacent gene ‘switched on’ and it codes for an enzyme that removes acetyl groups from a specific histone. Without these acetyl groups, the coiled DNA strands loosen up and become more accessible for transcription. In other words, they are ‘less dim’.

The chain of events began with epigenetic repression. Yet it finished with the opposite effect, elsewhere. Mind-blowing, right? I told you so. And now, we’re ready. We’ve got the essential vocab for next time: epigenetics and sexual reproduction – a myriad of molecular interactions both intricate and incredible.

*sperm cell, red blood cell, rod or cone cell in the eye – if you were wondering.

**Edit 21/05/14: I found out how.

Source:  The Epigenetics Revolution by Nessa Carey (it’s mint: read an excerpt here)

 

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When Hepburn, famine and DNA appear in the same post, it can only mean one thing

So many suffered because of The Dutch Hunger Winter - even those who were born after.

So many suffered because of The Dutch Hunger Winter – even those who were born after.

Audrey Hepburn would have turned 85 this week. She was on Google, with her slenderness and her iconic features. But did you know that her fragile beauty is the result of famine? Audrey Hepburn was a survivor of The Dutch Hunger Winter during the Second World War, when food was so scarce that people ate tulip bulbs and grass. So many died. Its impact left an important legacy – not just for history, but also for science, written in the very genes of the descendants of survivors.

For decades, epidemiologists followed a group of people who were no more than foetuses during the Hunger Winter. Those malnourished in the last months of pregnancy – the period of most growth – were born underweight, and they stayed small their entire lives, with lower rates of obesity. If malnourishment occurred in the early months of pregnancy, the baby was born at a normal weight, but as a group they suffered from higher rates of obesity as well as a buffet of other chronic health problems. What’s more, the second group tended to give birth to smaller-than-average babies.

Something happened in those first months of existence. The famine affected unborn children in a way that was passed on to the next generation. Somehow, the environment affects DNA expression. Nature and nurture are no longer separate influences. That’s epigenetics, everybody!

Epi – at, on, to, upon, over, or beside – genetics. It is seriously cool. So very very fascinating, which is why you must read Nessa Carey’s “The Epigenetics Revolution: How Modern Biology Is Rewriting Our Understanding of Genetics, Disease, and Inheritance.” It’s been my source for this post so far. Here’s a sweet excerpt. (I promise to follow with a post on the chapter that gripped me most – how epigenetics makes sexual reproduction possible in intricate ways you cannot imagine.)

There’s a reason that I’m bringing this up, other than its obvious magnificence. In this week’s health news, there is the BBC article about the study in a rural Gambian community that supports what was found after The Dutch Hunger Winter. A mother’s diet during early pregnancy – which, in the Gambian community, is entirely dependent on the season, rainy or dry – affects the methylation of the baby’s DNA. Have you heard of the concept of on-off switches for your DNA expression? Methylation is one type of switch. Epigenetics in action.

I’m telling you: next time you procrasinate and you’re just surfing around, you need to read up on this stuff. You can start with hilarity of the SciShow. Epigenetics. Go.

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Do-it-yourself HIV tests

Let’s play a game. Nearly 100,000 people are living with HIV in the UK, but how many are unaware of their infection? Go on, take a guess. Read more about the virus first, if you need to.

Obviously, this life situation is dangerous for the HIV+ individual, as it’s early detection and treatment that give the best chance for more years and better health. But it is also dangerous for the greater population. The virus can continue spreading through those who are unaware that they ought to be extra careful.

As long as we don’t yet have a vaccine or a cure for HIV, preventing infection is the most effective way to fight it. The law has just recognised this. Previously, it was illegal to sell HIV self-testing kits – and fair enough, you can imagine how problematic it would be to have dodgy kits giving out faulty results.

Now, there will be regulations to prevent this. The change in the law will make it possible to order self-testing kits as soon as they’re commercially available. See, they don’t actually exist in the UK yet. It seems quite odd to permit something not existent, but actually it will encourage companies to develop these kits and get them on the market. And if we take on board the information about a halfway home-testing scheme in this BBC article, it’s gonna be hella-popular.

Here’s the answer. There are 25,000 people estimated to be living with HIV without a diagnosis. That’s a quarter of all people with HIV in the UK. Did you guess right? In any case, let’s hope that that figure gets lower with these changes in HIV detection.

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What ‘The Structure of Scientific Revolutions’ was banging on about

Thomas Kuhn essentially wanted to blow the idea of ‘the linear history of science’ out of the water. Textbooks may make it seem like knowledge is a canvas gradually being filled in with newly discovered details of the universe – when in fact, many canvases have existed, and been scrunched up, replaced and forgotten. Each canvas is a paradigm – a ‘backdrop’ of the current widely accepted theory. (I like this canvas metaphor. Let’s roll with it for a bit.)

Eventually the known information doesn’t fit on the canvas anymore, and the mistakes that were once erased are now recognised as anomalies that need to get back in the picture, but they don’t fit. This becomes a crisis. In the end, the canvas must be rejected and replaced in a paradigm shift. Then research can return to what Kuhn named ‘normal science’.

Normal scientific research does not strive for new discoveries – gasp, shock, oh Thomas you old revolutionary you. Rather, it affirms the current favourite theory, aka the paradigm. Facts stemming from the paradigm are confirmed ever more precisely, new applications of the paradigm are explored, and the theories within the paradigm are refined to better describe the applications. Don’t believe it? Kuhn uses chapters to explain it. Accept this definition of normal science and read on.

But even though normal science doesn’t want to find new, strange stuff, it is nonetheless an extremely efficient mode for progress. Many concentrate on a particular set of problems or puzzles, and they go into such detail that anomalies are unearthed, and eventually there is a lot more knowledge and a need for a new paradigm.

Kuhn managed to pinpoint some interesting features of these scientific revolutions. For example, when a crisis arises, scientists begin to argue about the requirements for legitimate research – what counts, what doesn’t. He also discussed the way that perception changes: mistakes become anomalies. The information doesn’t change, but the interpretation is able to change in context of a new paradigm. Kuhn talked about Gestalt psychology – and this was my favourite bit of the book.

Gestalt psychology summed up in one image!

Gestalt psychology summed up in one image!

Take the classic duck/rabbit image. You can only see one at first – just as scientists can only see one interpretation of science, the one that fits the current paradigm – but then something shifts and you are aware of another interpretation that once seen, cannot be unseen. With this image, the trigger may be the word ‘duck’ or ‘rabbit’. In a scientific revolution, the trigger may be a new set of methods and tools acceptable under the new paradigm. Yup, it’s all very metaphorical.

All these words in italics are Kuhn’s special collection of words he effectively defined. They’re easier to understand in context of examples. Kuhn used examples from physics. I say, pick up ‘Great Feuds in Medicine’ or ‘Harvey’s Heart’; they are easier to digest than Kuhn’s ‘Structure’, and more medical too. You may as well read at least one of them, fellow wannabe-med-students. Your life is a CV now, isn’t it?

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What if science is only changing and not progressing…

I bet that if I were to begin a post with the quotation below, you would give up on my blog at the first full stop. Fifty points if you know the source of this freshly-pinched sentence. Twenty if you only need to read it once to ingest its meaning.

“History, if viewed as a repository for more than anecdote or chronology, could produce a decisive transformation in the image of science by which we are now possessed.”

So that’s fifty points to me. Shh, yes, I had to read it twice – don’t judge me. Anyway, I think I’ll award myself a hundred points for double-reading every sentence that followed Thomas Kuhn’s hefty first sentence in his best-known work, ‘The Structure of Scientific Revolutions’. This guy practically invented the phrase ‘paradigm shift’ as we know it. Back in 1962.

It took me three quarters of the book to realise that the reason Kuhn writes in such verbose detail is because he’s convincing his 1962 sciencey peers that paradigms are actually A Thing. Today, we know they’re A Thing. A paradigm, in Google’s words, is a worldview underlying the theories and methodology of a particular scientific subject; in my words, a canvas backdrop of theories to which current research is added. And it can shift, okay? Kuhn’s sciencey peers didn’t have a clue about this philosophy, and they needed a hella-load of convincing. That’s why this book has a low score on the fun scale, and why I only recommend this classic philosophy-of-science text for people who want to say they’ve read it. For example, people who find it on a pre-university reading list.

Why did the put this tome on the list? It isn’t particularly medical – on the contrary, Kuhn mainly uses examples from the history of physics. But it did get me wearing my Theory of Knowledge hat. (Thanks, IB.) When Kuhn started pulling in metaphors threaded around natural selection, he made a disquieting suggestion: that the current paradigm is the one that is best adapted for the times – not necessarily the best of all, ever. A paradigm shift is an evolution, but that is by no means the same as progress.

“We may, to be more precise, have to relinquish the notion, explicit or implicit, that changes of paradigm carry scientists and those who learn from them closer and closer to the truth.” Thanks for that thought, Thomas Kuhn.

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“Envy, malice, hatred, destruction and calumny.”

Claude Bernard, pioneer of experimental science

Claude Bernard, pioneer of experimental science

In the words of Claude Bernard, this was the fate of any scientist who dared to make a new discovery in the 19th century. His words apply just as well to medical research today.

From blood circulation to DNA, the history of controversial discoveries spans the centuries. Hal Hellman explores ten select cases from this history in ‘Great Feuds in Medicine’, one of the tomes from my future uni’s recommended reading list. I know; the title isn’t thrilling. I’m not going to lie, all the titles on the list look textbooky. But I do have some spare time during my gap yah, so I figured I’d better put the effort in. And this book surprised me from beginning to end.

The birth pains of medical research were intense and drawn-out. Blood circulation, animal electricity, hospital hygiene to prevent childbed fever, scientific experimentation to investigate the body – these revolutionary ideas were released into a medical community that still believed illnesses were caused by spirits and vapours. It is no wonder that the pioneers of these ideas were shot down by their peers again and again, with name-calling and catty comebacks to boot. How very stressful.

But before you start feeling thankful that we live in a more enlightened age, have a glance at the later great feuds. Hellman’s final two chapters discuss scientists who are still alive – those involved in the discovery of DNA, and in AIDS research. While the DNA conflict seemed to focus on who should be credited, the AIDS feud is alarmingly vicious. At least, it is alarming to someone who is considering a career in research. It involved court cases, untruths in the media, and international tensions that escalated from research groups to governments. Yep, ‘Great Feuds in Medicine’ is a surprisingly exciting read.

“Envy, malice, hatred, destruction and calumny,” said Bernard, who was the pioneer of experimental science in medicine at a time when doctors preferred guesses and untested theories. There have been so many breakthroughs in medicine since his time, and yet one aspect refuses to advance: human’s general hostility towards revolutionary  ideas.

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