I WAS 15 years old and halfway through a family meal when the blow to my head came out of nowhere. It felt as if someone had clobbered me on the side of the skull with a mallet, the sudden pain making me drop my fork. Then came a second hit. And a third. I remember pleading with my sister to stop her noisy whingeing before running to hide under a duvet until the pain eventually subsided. I had experienced my first migraine.

Twenty years later, my migraine-coping technique remains largely unchanged, except that it is now my toddler whose whining becomes unbearable. Migraine treatments don鈥檛 really work for me. They don鈥檛 really work for a lot of people.

Despite migraine being among the most common neurological conditions, affecting around , we know incredibly little about what causes them, how to avoid them and how best to treat them.

That is partly because migraines are so complex. They impact people differently, can be unpredictable and affect many more women than men. Migraine research has been dismissed, derided and underfunded. But a handful of dedicated scientists have spent decades trying to make progress. For the first time, they have uncovered a mechanism behind migraines in the brain, and with this knowledge have developed treatments not only to relieve them when they strike, but possibly to stop them occurring. Finally, migraine science is having its moment.

For those lucky enough to be unfamiliar with migraines, they can seem far-fetched. Someone can be fine one minute, then suddenly unable to speak or see. The symptoms are varied, and can last from a few hours to days. 鈥淲e talk about migraine collectively, but actually migraine comes in lots of different forms,鈥� says . While many people experience headaches 鈥� often severe 鈥� a migraine is much more than that and can involve other symptoms. 鈥淭he famous saying is that migraine is just a headache, which is a little bit annoying because it isn鈥檛 just a headache 鈥� it鈥檚 a brain disorder,鈥� says . 鈥淗eadache is just one of the features of migraine.鈥�

Premonitions and auras

Migraine attacks can begin with what is known as a premonitory phase, or prodrome, which can involve a range of symptoms, such as mood changes, neck stiffness and yawning. My prodrome is marked by a vague feeling that something bad is going to happen.

The prodrome is usually followed by the migraine attack itself, which is often associated with pain. The pain can be debilitating and might be preceded by an aura. Aura symptoms 鈥� sensory disturbances that might affect a person鈥檚 vision, speech or movement 鈥� can range from mild to unbearable. This can occur independently of any headache. However, the headache tends to be the most debilitating symptom, lasting for minutes, hours or days, depending on the attack and the effectiveness of treatment.

Finally, there is the migraine 鈥渉angover鈥�, or postdrome, in which some people can continue to feel tired or unwell for days.

Migraine is the third most prevalent disorder in the world and the third-highest cause of disability. The annual indirect cost of migraine due to missed work and reduced productivity alone 鈥� and that doesn鈥檛 include the substantial cost of treatment.

Despite all this, headache research . Funding for research on other common chronic conditions, such as asthma and diabetes, received, on average, $153.90 per person experiencing them. The figure for migraine, on the other hand, was a mere 36 cents. People with migraine can be let down at the clinical level, too. Only around . In the UK, a quarter of those with a diagnosis say they had been having attacks for over two years beforehand, according to . Most of those who responded were never referred to a headache specialist, and many struggled to get a prescription for migraine treatments.

At a science conference, I once heard a pain specialist dismiss pain in those who experience migraines as 鈥減sychological鈥�. 鈥淚 don鈥檛 believe this is a one-off experience,鈥� says Hay. 鈥淭he neurologists I speak to in my department are fighting against this all the time.鈥�

Some of this prejudice can be attributed to the fact that pain is such a subjective experience, and so hard to unravel, and because migraine causes such varied symptoms. Added to which, migraine has been derided as an affliction of hysterical women, says Peter Goadsby at King鈥檚 College London. 鈥淭he peak prevalence is at age 40, three women experience it for every male and it manifests around periods,鈥� says Goadsby. 鈥淚t鈥檚 a prejudice born in prejudice heaven.鈥�

Finally, migraine doesn鈥檛 result in the severe damage to the brain that is seen in degenerative conditions such as Alzheimer鈥檚 and Parkinson鈥檚 disease, and in stroke, all of which also affect life expectancy, so understandably attract more funding.

This is something that . He found it almost impossible to get funding for his migraine research in the 1980s and 1990s. In the end, he secured funding to study stroke, which 鈥渒ept me going in science鈥�, he says. His migraine research became something of a side project. But he persevered with it and this paid off. Last year it won him, along with three other migraine researchers including Goadsby, award of 10 million Danish krone (around 拢1.1 million) in recognition of pioneering work in neuroscience. One revolutionary discovery that led to the win was that neurons, as well as blood vessels, play a vital role in migraines.

The idea that blood vessel dilation causes migraine was originally based on the fact that people who have migraines usually experience a throbbing headache, says Gazerani. This hypothesis was supported by research that involved injecting volunteers with drugs to dilate their blood vessels, which tends to cause headaches and can trigger migraines. The success of . These drugs, introduced in the 1990s, were the first designed specifically to treat migraine 鈥� and seemed to work by constricting blood vessels.

But cracks in the dilation theory had been starting to appear well before then, when neuroscientists developed tools to better measure blood flow in the brain. They saw that people experiencing a migraine didn鈥檛 appear to have dilated vessels as expected. Even where there was dilation, it didn鈥檛 seem to trigger the headache, with studies finding it started afterwards and outlasted the pain.

Then, 40 years ago, came the discovery of a chemical called calcitonin gene-related peptide (CGRP) that seemed to influence the function of neurons in the nervous system and the brain, and could also dilate blood vessels. Around the same time, Michael Moskowitz at Harvard Medical School, another of the four 2021 Brain Prize winners, identified the trigeminal nerve 鈥� which connects the brain to the face 鈥� and its associated blood vessels as .

In 1988, Edvinsson teamed up with Goadsby to learn more about what CGRP might be doing. By the mid-1990s, the pair and their colleagues had discovered that CGRP was released from the trigeminal nerve during a migraine attack, pinpointing for the first time a brain chemical that could be triggering migraines. The fourth 2021 prizewinner, Jes Olesen at the University of Copenhagen in Denmark, was part of a team that confirmed this by showing that giving CGRP to people who are prone to migraines caused an attack, and that natural CGRP release could be prevented with sumatriptan, the most often-prescribed triptan drug. Finally, the group had discovered a mechanism for migraine and a possible way to treat it, other than the one type of drug available.

That was desperately needed because triptans come with their own issues. Because they act to constrict blood vessels as well as restrict CGRP, you can鈥檛 take them if you have a history of stroke, for example. And there are side effects, including nausea, fatigue and neck, jaw and chest tightness. What鈥檚 more, they don鈥檛 work for everyone: studies show triptans to be effective in stopping pain within 2 hours in 42 to 76 per cent of people, and even then, they act only on the pain, not the aura.

With CGRP as a target for new treatments, research has now led to new types of drugs for migraine. These block the action of CGRP, but, unlike triptans, don鈥檛 constrict blood vessels, so can be taken by more people. Some of these are monoclonal antibodies, which are injected every few months to help prevent migraines. Erenumab 鈥� one such drug that was found to halve the number of migraine days experienced by volunteers in a clinical trial 鈥� was approved by the US Food and Drug Administration (FDA) in 2018, becoming the first new migraine drug since the 1990s. Others have followed, and still more are under review.

鈥淲hat this tells us, for the first time, is that we can treat migraine acutely and preventatively via the same mechanism,鈥� says Hay. 鈥淚t was always thought it has to be different鈥� This suggests we are targeting a key part of the migraine pathway.鈥�

Goadsby and his colleagues have also been developing new CGRP-targeting drugs, called gepants, that don鈥檛 have to be injected. , and there is evidence that one might also be useful for preventing the onset of attacks.

Getting real

The discovery of the CGRP mechanism and the development of new migraine-specific drugs have gone a long way to highlight the status of migraine as a real neurological condition, too. 鈥淣ow we have mechanisms, and we have specific drugs, and that makes a difference,鈥� says Edvinsson. 鈥淵ou can鈥檛 argue with biology,鈥� says Goadsby.

Despite these breakthroughs, we are still some way from understanding exactly what causes an attack in the first place 鈥� in other words, what fires up the trigeminal nerve. The aura that many people experience offers some clues to the pain side. Brain-imaging studies have shown that, during an aura, there is a wave of changes in brain activity, starting from the occipital lobe at the back of the head. Neurons first switch on, then off again, and this pattern spreads across the brain. This helps to explain some of the common symptoms of aura 鈥� flashing lights are thought to result from the switching on of neurons in the visual cortex, while blind spots are likely to occur when nerves switch off, says Goadsby.

, or that it triggers the trigeminal nerve to release CGRP.

Goadsby, however, thinks that aura and pain are two separate phenomena that both happen to be triggered by something that occurs in the prodrome. 鈥淚t鈥檚 not that aura causes pain, it鈥檚 that something else causes both,鈥� he says.

Other mysteries remain, too. One elephant in the room is the fact that migraine affects so many more women than men. People tend to experience their first migraines around puberty, and the incidence rises throughout adulthood, before declining after menopause. Some people find that their migraines disappear during pregnancy or become more frequent during perimenopause, which precedes the menopause.

All this implicates certain hormones. 鈥淲e have found that trigeminal neurons contain receptors for oestrogen and oxytocin,鈥� says Edvinsson. So the hormones might influence the perception of pain in migraine, he says. Both hormones are known to fluctuate with menstrual cycles and are more stable in men.

At Leiden University in the Netherlands, Gisela Terwindt is part of a team trying to unpack the link through a study looking at levels of several sex hormones in blood samples from female volunteers who experience migraine to see if they fit with the timing or symptoms of migraine attacks. The team is also giving volunteers contraceptive pills containing synthetic oestrogen to see whether this helps with migraine, a commonly touted treatment despite a lack of evidence. 鈥淚t鈥檚 not without side effects, so we need clear proof,鈥� says Terwindt.

Another lingering question is why there is so much variation in symptoms between people who have migraines. My auras usually start with flashing lights. A friend of mine sees light in zigzags during her migraines, and some people develop blind spots or tingling sensations.

鈥淚t might be that we鈥檙e classifying it too broadly, and actually there are multiple individual diseases here that we haven鈥檛 quite got a handle on diagnosing,鈥� says Hay. 鈥淚t could be an individual combination of different genes in a person that鈥檚 creating their unique experience.鈥�

Terwindt has spent much of her career trying to understand the genetic factors. She was part of the team that identified the first gene linked to familial hemiplegic migraine 鈥� a subtype that is thought to have an especially strong genetic component 鈥� in the 1990s.

Heritable headaches

Since then, Terwindt has been looking for genetic factors that might explain more common types of migraine. After all, , there is a 50 to 75 per cent chance that person will experience attacks too. 鈥淲e recently published that ,鈥� she says. 鈥淚t鈥檚 quite complex.鈥�

On top of all that, we still haven鈥檛 answered perhaps the biggest questions: why and how migraines start in the first place.

People who experience migraines often have a list of things that seem to trigger them, and are usually advised to keep a migraine diary, so they can keep track of any changes in their routines, diets or anything else that seems to reliably occur before a migraine.

But how might things like stress, a lack of sleep or a cheese-laden snack lead to an attack? Some researchers believe that the brains of people who get migraines have a lower threshold for responding to stimulation, and that certain stimuli can essentially tip them over the edge, switching on neural activity that leads to the attack. Given the common early signs, such as yawning and tiredness, it might also be that some sort of change in the brain鈥檚 hypothalamus, which is linked to things like this, is triggering the attack (see 鈥�How does a migraine start?鈥�). And some apparent triggers, such as food cravings or bright lights, might simply be a result of the attack already being under way. 鈥淚f you think chocolate gives you headache, but actually the craving starts during the premonitory phase, then avoiding chocolate doesn鈥檛 make [any] difference,鈥� says Goadsby. 鈥淧unishing yourself for things doesn鈥檛 make any sense.鈥�

What is clear is that, given the huge variation in migraine, what works for one person won鈥檛 necessarily work for another. Some trials in which people take a high daily dose of vitamin B2 have found that some, but not all, of them experience fewer migraines. One man made headlines in November for . That doesn鈥檛 mean that others should start swapping triptans for kale.

It is also clear that more treatments are desperately needed. No single drug so far works for everyone. And many of those who do benefit still experience migraine attacks, even if they are reduced in number or severity. 鈥淭hat tells us we haven鈥檛 quite figured out that system properly, or that there are more factors involved,鈥� says Hay.

鈥淢igraines affect three women for every man. It鈥檚 prejudice heaven鈥�

Until we discover what those factors are, there are things that doctors, employers and all of us can do to make life better for people who get migraines. One step is to improve knowledge among doctors. 鈥淭he amount of training healthcare professionals receive is abysmally small,鈥� says Hay. She is also a proponent of changing the language used for migraines, to bring it in line with the way we describe other neurological conditions. 鈥淵ou don鈥檛 have a migraine, you live with migraine, and sometimes you have an attack,鈥� she says.

I鈥檓 one of the lucky ones 鈥� my migraines have decreased in frequency and severity since I entered my 30s, perhaps due to the hormonal changes of pregnancy. Given the propensity for migraine to run in families, I hope that the new buzz around migraine research will mean my whingeing toddler won鈥檛 have to hide under her own duvet a decade or so from now.

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Patricia Brennan has forged a controversial career in studying the twist and turns of the evolution of animal genitalia. A biologist based at Mount Holyoke College in South Hadley, Massachusetts, her latest research suggests that bottlenose dolphins have clitorises that have evolved for pleasure 鈥� something she says makes sense given the amount of sex the animals have. Brennan tells New 女生小视频 about her latest discovery and why it鈥檚 so important to study female genitalia.

Jessica Hamzelou: Why study dolphin clitorises?

Patricia Brennan: I have been collaborating with a researcher who was studying vaginas in dolphins. Dolphins have very complicated vaginas, which contain many folds. The hypothesis was that these folds were there to exclude salt water during copulation, because it is supposed to be lethal to mammalian sperm. But nobody had actually ever really studied these folds or tried to test the idea.

We haven鈥檛 been able to pinpoint exactly why they are that way. But when we dissected the vaginas, I would look at these clitorises and be just amazed. I was like: 鈥淥h my gosh, these are pretty big, well-developed clitorises.鈥� And I thought that might be something interesting to look at.

We know that dolphins have sex all the time. They have sex for social reasons, not just for reproduction. It makes sense that the clitoris would be functional [and give pleasure when stimulated].

Are dolphins really having sex all the time? Are they more sexually active than other animals?

We don鈥檛 really know if they are having more sex than other marine mammals. It鈥檚 really hard to study sexual behaviour in cetaceans because they鈥檙e out there [in the ocean]. But bottlenose dolphins live close to the shore, where scientists can go out on their boats and study them. They see them having sex year-round, even when the females are not receptive, so not ready to get pregnant and have babies.

And not only do they have sex all the time, they have a lot of homosexual sex as well. The females will rub each other鈥檚 clitorises with their snouts and their flippers really often. It鈥檚 not like every once in a blue moon you鈥檒l see females stimulating each other, it鈥檚 actually pretty common. Females also masturbate.

If they鈥檙e out there seeking all these sexual experiences, it鈥檚 likely that it鈥檚 probably feeling good.

Do you see these behaviours in males too?

The males, for sure, have lots of homosexual sex. The males will have anal sex, they鈥檒l insert their penises into each other鈥檚 blowholes. Bottlenose dolphins are really hypersexual animals.

How did you go about studying dolphin clitorises?

They came from dolphins that have died from natural causes, mostly from strandings [when a marine mammal is found on shore]. It has taken years to get a sample size that is good enough for a study because it鈥檚 rare that an animal becomes stranded and that a scientist finds it before it has decayed too much.

We get a frozen package that has been sent overnight in the mail. They come from all over the US. When they arrive in our lab, we begin thawing the tissues, doing a lot of measurements and performing the dissections.

And for the clitoris in particular, we cut around the entire clitoris structure as much as we can, and then do a couple of different things. We stain some of the tissue so that we can examine it in a micro CT scanner to see the soft tissue. Other samples are dissected, and some undergo histology [detailed analysis under a microscope].

What are you looking for specifically?

We were particularly interested in looking at the erectile tissue. Does it have spaces within it that could fill up with blood? And does it have a blood supply that indicates blood would rush into these spaces on arousal and engorge them? This is what happens in humans.

We also look for the tunica albuginea, a thick band of collagen and elastin that surrounds the erectile tissue. The presence of this tissue suggests that it allows the erectile tissue to distend, but prevents it from bulging out.

We look at the nerves, too. We were able to see that they have very large nerves. Some of these nerves are up to half a millimetre in diameter, which is pretty large. There aren鈥檛 many measurements that we could compare them to, we were just shocked by how big they were.

From there, we were also able to see these free nerve endings that are right underneath the skin. These are known to increase sensitivity. We have these in great abundance in our fingertips, and of course in the clitoris and in the human glans penis.

And then we found that the skin itself in the clitoris is about the third of the thickness of the adjacent skin in the genitals. Once we put all of those things together, we were pretty certain that this is functioning in pleasure, just like in humans.

Does this tell us anything new about dolphins or how they form social bonds?

No. I think it makes perfect sense. Dolphins have a lot of sex, females have a lot of sex with each other. Their clitoris is very well developed and it looks like it provides pleasure. It just makes sense. It鈥檚 basically providing the morphological evidence that we need to close that case and say, yes, this is what a functional clitoris looks like.

Is this controversial?

There is this hypothesis out there that, because penises and clitorises share the same developmental pathway, the clitoris is just a mini penis. It鈥檚 not really designed for anything and it doesn鈥檛 necessarily have a function. It鈥檚 just there because males have a penis.

There is debate whether even human female orgasms are functional or just a byproduct. It鈥檚 one of those things that just refuses to die.

Obviously, as a female scientist who studies sex and sexual reproduction, I have a problem with that idea that there would be no function for a structure because it鈥檚 developmentally homologous with the penis.

We can show that this is more than a mini penis; this is actually a fully functional organ that鈥檚 serving some kind of purpose. It鈥檚 probably evolutionarily a good idea because it makes you seek out sex more often.

Where does the research go from here?

Now we have this set of criteria, we can start looking at other species that normally you wouldn鈥檛 keep in a lab and start asking the same questions. We know bonobos have sex all the time, and we know that their clitoris looks very much like a human clitoris. It鈥檚 much easier for people to imagine that, of course, if a bonobo is grimacing and vocalising when it鈥檚 having sex, it looks like they鈥檙e having a pleasurable response, kind of like ours.

Dolphins are very different animals from primates. Now, we鈥檙e starting to look at the alpaca clitoris and look for the same kinds of morphological features. We鈥檝e got a whole bunch of vertebrates. In my lab, we work with sharks, snakes, alpacas, dolphins, ducks 鈥� just a diverse group of species. And we always find something interesting.

What about male genitalia?

We also have collected plenty of penises and we are interested in looking at their morphology and how they function.

In general, I study genital coevolution. I鈥檓 interested in looking at males and females and how they co-evolved together. When it comes to genitalia, you have to look at both sides of the equation to figure out how they work, because mechanically they have to fit together.

The job of genitalia is to facilitate male and female gametes getting together, and you could have a tube going into a cylinder that would achieve that basic goal. But genitalia are not like that. They have all sorts of weird elaborations and other features that are going on. They have spines, bumps, turns, pockets and spirals. We鈥檙e trying to understand the evolutionary processes that are influencing their morphology and their function.

We do study both, but what I keep finding is that because people have tended to study the male more than the female, there is a lot about the female that we don鈥檛 know. We鈥檙e kind of catching up with all the female stuff.

Critics have questioned the importance of your research in the past. What is your response to people who say this kind of work is irrelevant?

It is basic science. It鈥檚 not designed to solve a particular problem. When people ask why we study it, they [want to know if] it is going to make any money or heal some disease. The answer is: maybe, we don鈥檛 know. We鈥檙e trying to describe natural phenomena and understand how they work.

Your question touches on something else. There are people who are uncomfortable with studies of sexual behaviour in general, whether in humans or other animals. That doesn鈥檛 mean that sex is unimportant or that we shouldn鈥檛 be studying it.

I could be looking at stomach morphology, and that probably wouldn鈥檛 bother people. Part of the reason people are bothered is because it鈥檚 sex and sexual reproduction. That鈥檚 understandable, but I鈥檓 a scientist. I ask questions where I think there are interesting questions to be asked.

This interview has been edited for length and clarity.

Losing weight won鈥檛 necessarily help you live longer, and the best predictors of a long and healthy life are mobility, strength and balance.

That鈥檚 what at the Children鈥檚 Hospital at Montefiore in New York and her colleagues found when they looked at the outcomes of older women who had participated in a long-running study.

鈥淚 have a lot of family members who are on the elderly side, and they talk a lot about losing weight,鈥� says Underland. 鈥淭here鈥檚 a lot of talk in the media, in our society and in medical circles about weight loss.鈥�

To get a better picture of the link between weight loss and mortality, Underland and her colleagues looked at data from the Women鈥檚 Health Initiative, a series of studies involving more than 161,000 volunteers in the US that has been running since 1992.

The team looked at 5039 women who were over 65 in 2012, with an average age of 79. Around this time, each woman took a series of tests to determine their physical strength, balance and mobility, which included measuring their grip strength and their ability to stand up from sitting in a chair, for example.

Underland and her colleagues also looked at how much weight the women had gained or lost since they first enrolled in the study, 14 to 18 years prior to the tests. They then noted how many of the women were still alive around five years after they took the tests.

The team found that women who lost weight were much more likely to die within the follow-up period than those that didn鈥檛. Those who had lost 5 per cent of their body weight in previous years were 61 per cent more likely to die within the following five years.

The weight loss is unlikely to have been caused by illness, as women with cancer were excluded from the study, and the team controlled for other conditions that might affect weight.

People who performed well in physical tests appeared to have the best survival odds. Women who scored in the top quartile for strength, balance and mobility were 71 per cent more likely to be alive five years later than those whose scores were in the bottom quartile.

Weight gain, on the other hand, had no effect on mortality. 鈥淭his information doesn鈥檛 tell everybody to go out and buy a bunch of Cheetos,鈥� says Underland. 鈥淜eep moving, eat a healthy diet 鈥� focus on that.鈥�

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A strain of the antibiotic-resistant bacterium MRSA seems to have evolved in hedgehogs in the early 1800s 鈥� long before the introduction of antibiotics. The finding demonstrates how antibiotic resistance can occur in nature 鈥� and underlines the need for cautious use of antibiotics.

Staphylococcus aureus is a bacterium that can live harmlessly on our skin and up our noses. But it can sometimes cause infections of the skin and gut.

Methicillin-resistant Staphylococcus aureus (MRSA) is a type of these bacteria that can鈥檛 be killed with antibiotics like methicillin. As a result, it can cause infections that can be difficult to treat. Most cases are picked up in hospitals, and some are fatal.

Over the past decade or so, researchers have begun to find a type of MRSA known as mecC-MRSA in all sorts of wildlife, including boars, storks, snakes and hedgehogs.

While mecC-MRSA seems to be relatively uncommon in most of these species, researchers have found it in plenty of hedgehogs. To find out why, Ewan Harrison at the University of Cambridge and his colleagues studied swab samples from 276 European hedgehogs (Erinaceus europaeus) from 10 European countries and New Zealand.

Hedgehogs from Greece, Romania, France, Italy and Spain didn鈥檛 seem to have any mecC-MRSA on their skin. But others did 鈥� 66 per cent of hedgehogs from England and Wales tested positive for the bacteria, for example.

These animals also had a fungus called 罢谤颈肠丑辞辫丑测迟辞苍听别谤颈苍补肠别颈 living on their skin. This fungus is known to produce chemicals that can kill bacteria.

In experiments, the team found that T. erinacei made an antibiotic called KPN that could kill mecC-MRSA only when the bacterium鈥檚 genes for antibiotic resistance were removed. This suggests that the antibiotic resistance genes are key for the bacteria to survive alongside the fungus on the hedgehog鈥檚 skin.

鈥淭his kind of MRSA likely emerged as a result of a co-evolutionary battle on the skin of hedgehogs,鈥� says Harrison.

By comparing the number of mutations in strains of the bacterium, the team estimate that the mecC-MRSA arose in hedgehogs around 1800 鈥� long before the introduction of methicillin in 1959.

MecC-MRSA can cause infections in people, but these are rare. It is unlikely that humans will pick up MRSA from hedgehogs, because we don鈥檛 often interact with them. But mecC-MRSA can pass from hedgehogs to livestock, which are more likely to pass an infection to people.

The findings should underline the need to use antibiotics carefully 鈥� even new drugs that might seem to kill many types of bacteria, says Harrison. 鈥淩esistance is out there,鈥� he says. 鈥淛ust because we haven鈥檛 seen it in humans, doesn鈥檛 mean it doesn鈥檛 exist somewhere and can鈥檛 end up in humans.鈥�

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Book

Stuck: How vaccine rumors start 鈥� and why they don鈥檛 go away

Heidi Larson

Oxford University Press

RHETT KRAWITT was just 7 years old when he petitioned local law-makers in California to tighten restrictions on who could avoid vaccinating their children. Rhett had been through years of chemotherapy for leukaemia, so wasn鈥檛 able to receive the MMR vaccine, which protects against measles, mumps and rubella. This left him, and others like him, vulnerable to these diseases.

But many of the parents of healthy children in the state were turning down the MMR vaccine, using the 鈥減ersonal belief exemption鈥�. Such refusal is thought to have contributed to a measles outbreak tied to a Disneyland theme park, which was linked to 147 measles cases across seven states.

The story is one of many that demonstrates how emotions, as well as misinformation and culture, come into play in debates surrounding vaccination. As anthropologist Heidi Larson demonstrates in her new book, Stuck, such debates aren鈥檛 new and crop up continually around the world, and the fact that they are so persistent suggests we need a new approach to them.

The book, largely written before the covid-19 pandemic, is a guide to many of the problems faced by vaccination campaigns. Larson, based at the London School of Hygiene & Tropical Medicine, and who founded the Vaccine Confidence Project to better understand how people feel about vaccines, points out that rumours have always played a role in the misinformation and fear around vaccines. This has been the case since the first vaccines were introduced for smallpox.

If the thoroughly debunked belief that 5G phone masts were responsible for the covid-19 outbreak sounded familiar, that might be because similar ideas linked 3G to the SARS outbreak of 2002-2003, and 4G to swine flu.

Rumours and misinformation may be nothing new, but they can still have devastating effects. And the rising use of the internet and social media has only contributed to their spread, says Larson.

鈥淓motions, culture and misinformation come into play when debates surrounding vaccination come up鈥�

In extreme cases, people administering vaccines have been killed. We have also seen, most recently with measles, how a drop in vaccination can lead to the loss of herd immunity, and the resurgence of diseases that claim lives.

So how do we tackle them? Larson points out that simply countering misinformation with facts isn鈥檛 enough. She quotes epidemiologist Stephen Ledeer, who wrote that 鈥渇acts are not rejected because they are seen as being wrong, but because they are seen as being irrelevant鈥�. Larson herself describes this as 鈥渁 near reversal of the Age of Enlightenment鈥�.

Instead, it is important to understand the emotions that drive these rumours. A common problem is people feeling that vaccination of their children is something that is out of their control, for example. And it is important to acknowledge that vaccines do have risks, even if the risks of side effects are minimal, says Larson.

In the book, Larson draws on the need for open dialogue to share information, and the importance of including those who oppose vaccination for whatever reason, and treating them with empathy and kindness. Frustratingly, given her obvious expertise, there is no direct call to action, or clear suggestion for a solution to the problem.

Having highlighted the fatal consequences of vaccine misinformation and avoidance, Larson says 鈥渢he global vaccine enterprise needs to reboot鈥� and that the scientific community is pondering how to manage people鈥檚 relationship with information, and misinformation, surrounding vaccines. Larson concludes by writing that she is a 鈥減atient optimist鈥�, but given what鈥檚 at stake, this doesn鈥檛 seem quite enough.