The science of brain freeze

Everyone loves summer with its long days, blazing sun and ice-cold drinks – all too often accompanied with the head-splitting pains associated with so-called ‘brain freeze’. The culprits range from ice-creams and milkshakes to chilled drinks, all having the same effect of leaving you feeling like you’ve been poked in the brain by a large sharp object. Suffering from brain freeze is not uncommon so you’re not alone. In fact approximately 40-80% of the population experience brain-freeze at some point in their life.

The scientific name for this is Sphenopalatine ganglioneuralgia which literally means nerve pain of the sphenopalatine ganglion, the nerve found at the roof of your mouth.

Brain freeze is characterised by sharp stabbing pains in the head, particularly across the forehead and temples, associated with the quick consumption of cold food or drinks. Although the sensation can be extremely painful, the pain normally fades quickly. So what causes this mysterious and painful phenomenon?

Although it is certainly not caused by our brains actually freezing, some scientists have suggested that the pain may indeed be linked to a decrease in brain temperature. One particular study from Japan found that during bouts of brain freeze, brought about by consuming a large volume of ice, the temperature of patients heads (taken from the ear) actually dropped in accordance with the cold stimuli, suggesting that brain temperature also decreased.

So what aspect of brain ‘cooling’ causes the pain associated with brain freeze? A pioneering study carried out by Jorge Serrador at Harvard Medical School may have found the answer. The study monitored blood flow to the brain in 13 volunteers as they sipped ice cold water (directed, with a straw, at the roof of their mouths). When brain freeze was induced volunteers were asked to raise their hands as a signal, then raising them again once the pain subsided.

It was found that one of the brains major suppliers of oxygenated blood, the anterior cerebral artery, dilated (increased in size) whilst drinking the iced water. This lead to an increase in blood flow to the brain and was regularly followed by pain. Interestingly, as the cerebral artery shrunk back to its original size, restoring regular blood flow, the symptoms associated with brain freeze subsided. Serrador concluded that the increase in blood flow and therefore size of the cerebral artery was responsible for the pain associated with brain freeze. Specifically, he speculated that the pain may be brought about by an increase in cranial pressure caused by the increased blood flow.

The brain is one of our most delicate and sensitive organs; extremely sensitive to changes in temperature. It is possible that brain-freeze may be a defence mechanism, protecting our brains from large fluctuations in temperature. If the ganglion, in the roof of the mouth, detects extreme cold it causes an increase in blood flow to the brain, which is important to keep it warm. As more blood flows into the brain, the pressure inside the skull increases causing pain. The blood vessel then constricts again to reduce the pressure.

It’s also interesting to note that migraine sufferers are actually more likely to experience brain-freeze than those who don’t suffer from migraines. Indicating that the two may share a common mechanism.

So, that’s a quick run-through of the science behind what is actually happening to your body during brain freeze. So next time you’re in the pub and someone tells you they have brain freeze, you can astound them with your knowledge of the science behind it!

Post by: Sam Lawrence

Is your brain wired for facebook?

I ‘like’ Facebook as much as the next person, or rather any of the other 950+ million users. The fact that people can stay in touch so easily in a metaphorically shrinking world without having to use a pen, paper, stamp or pigeon carrier is brilliant. However, what really amazes me about Facebook, Twitter, Tumblr, LinkedIn or any other social media is the phenomenon of ‘socialness’ itself.

In order to find the ‘social’ or ‘friend’ centre of the brain, scientists measured the size of different brain structures associated with making and maintaining friendships. In two different studies, they found that the size of an individual’s amygdala (the emotional centre of the brain) and their orbital prefrontal cortex (oPFC) were proportional to the number of real friends and social groups they had. In other words either having a larger amygdala or oPFC means you are more likely to be friendlier, or the more friends you ‘add’ to your social network, the larger those parts of the brain become. In fact, it’s probably a mix of both situations.

Robert Dunbar, a British anthropologist interested in the evolution of society, also attempted to define how the structure of the brain linked to the size of an individual’s social group: the equivalent to the average Facebook friend count. His early work focused on the brains of various species of monkey. From this work he found that he could predict the size of the animal’s social group from the size of their neocortex compared to the rest of their brain. He discovered that primate species which have a larger neocortex relative to the rest of the brain hang out in larger social groups, whereas those with a smaller neocortex have fewer ‘friends’. These monkeys’ brains have either evolved or changed to maintain friendships with a certain average number of other monkeys. From this Dunbar was able to predict that, if humans are like monkeys (which we are), our neocortex:brain ratio predicts that we should be cliquing into social groups of around 147.8 (with an upper limit of 300). What’s interesting is that this is essentially the case in real life: 150 is the average size of a tribal village, the optimum size in the Roman army’s military unit and the average number of friends on Facebook is actually creepily close too.

One question raised by Dunbar’s research is how or why the neocortex developed in the first place? The “Social Brain Hypothesis” suggests that primates evolved a larger neocortex and bigger social networks when they started eating fruit instead of leaves. Fruits contain way more calories than leaves, but are also harder to obtain and have a much shorter ‘shelf life’, meaning they pose more problems for a hungry monkey. Therefore if a monkey is to maintain a fruit-rich diet it is important for it to learn where to find fruit and how to tell whether or not it is ripe or safe to eat. It is thought that being part of a bigger social group allows all individuals to benefit from the group’s collective knowledge and thus from the extra energy found in fruit. Since the brain uses up so much energy to develop, it may be that this extra food source is partially responsible for the increase in neocortex size in these primate species.

Whether or not we realise it, most of us are hard-wired to seek out friendship. Our brains are social and we have evolved to cooperate and share – that’s why Facebook is such a massive phenomenon. But what does the size of our ‘friends’ section say about us? In a very modern experiment, psychologists asked people to rate another person’s attractiveness based on a fictional Facebook profile. These profiles were identical other than one factor: for each profile the experimenters altered the number of friends these fictional people had, either 103, 303, 503 or 703. These experiments found that 303 seemed to be the magic number, with participants rating profiles with this number of friends as being most ‘attractive’. Perhaps this could be a reflection of the upper limit of Dunbar’s number. Interestingly, both profiles with lower and higher friend counts were rated as being less attractive. Perhaps fewer friends is taken as an indication that a person is less sociable, whilst having too many friends may be seen as ‘trying too hard’. So when honing your online persona it’s more than just the pictures of that dodgy night out you have to worry about.

So why is Facebook in particular so popular so, dare I say it…addictive? There have been countless studies which show that going onto your Facebook account makes the pleasure centres of the brain, the same ones which activate when eating chocolate or having sex, ‘light up’. It seems that thinking and talking about ourselves is something we all enjoy. Psychologists found that participants in a study were happy to receive very little payment to talk about themselves whereas if they were required to chat about someone else they generally expected at least double the amount. The participants, on average, found talking about themselves so much more enjoyable that they would actually give up money in order to avoid talking about another person instead. Maybe that will help explain why people insist on posting mundane statuses online. (It doesn’t, however, give any excuses for those who use hashtags on Facebook…#wrongsocialmedia.)

But there are many more important benefits from having a strong, optimally-sized social group. Researchers in Kenya watched wild baboons to see how long higher socially ranking males and lower socially ranking males took to heal or recover from naturally occurring injuries and illnesses. Despite the highest and lowest ranked baboons experiencing a similar amount of biological stress, the lower-ranked baboons took an average of six days longer to heal or recover than alpha males. The researchers think this could be due to the positive impact that close friendships have on the immune and repair systems.

I’m definitely not saying that everyone should use Facebook in order to avoid getting ill, or that we should all frantically cull or add friends until our account reaches the magic ‘Dunbar’ number. But next time you log on to your account and scroll aimlessly through the trivial happenings recorded in your newsfeed or indulge in a little chat with an old friend, don’t blame yourself. Our brains are wired up to be social.

Post by: Natasha Bray

Right to Die: Is it ever justified? – one scientist’s perspective

For this post I’m going to break from my normal light-hearted blogging to talk about a topic which is very serious and close to my heart – the “Right to Die”.

The “right to die” is the ethical entitlement of someone who is suffering from a debilitating and permanent illness and who has no quality of life to choose to end their life on their own terms often through either suicide or, if necessary, assisted suicide. This is a subject which crops up in the news on a regular basis and there is, understandably, a great deal of controversy surrounding this question.

Recently the “right to die” issue has surfaced surrounding the case of Tony Nicklinson, a 58-year old man who suffered from a condition known as locked-in syndrome. His condition meant he was unable to move or speak, communicating solely through eye movements. Mr Nicklinson went to court in an attempt to make it possible for a doctor to end his life without fear of prosecution. He argued that he was suffering a miserable and undignified life and wanted to end it on his terms. However, his appeal was unsuccessful. The court ruled that it was unable to “usurp the function of parliament” and did not have the power to grant his request. His devastation was clear to see and harrowing to watch. Sadly or fortunately, however you want to look at it, Mr Nicklinson died peacefully of ‘natural causes’ at home just 6 days after the court date, after refusing to eat and finally contracting pneumonia

I believe that the UK government urgently needs to review its policies on the right to die and voluntary euthanasia. This is partly so people, such as Mr Nicklinson, don’t have to suffer needlessly. However science also foresees a bigger problem society may soon have to face, one which is set to cause huge economic and ethical problems: the dementia time-bomb.

I have a personal interest in wishing that the law for euthanasia be changed, specifically with regard to dementia. I have seen two of my grandparents suffer from this devastating disorder – my paternal grandfather and maternal grandmother. In my grandfather’s case, he suffered from a low-level form of dementia for many years, before suddenly and rapidly going downhill. However, just a few months after his sudden deterioration, he died of an infection. When I heard about his death I was relieved: at least he didn’t have to suffer the indignity of full blown dementia for many years. However, this was the sad fate which befell my grandmother.

In 1999 my grandmother was diagnosed with suspected Alzheimer’s disease (the most common form of dementia). Our whole family, including her husband of nearly 60 years, watched her turn from a happy, chatty, busy woman into one who forgot who or where she was. She became violent and confused. She had a long, slow, painful descent into being completely helpless – unable to remember who she was or basic things like how to dress herself. After several years my mother made the heartbreaking decision to move her to a care home, since the burden of caring for her was too much for my 82-year old grandfather, who had been diagnosed with cancer. During her time in care she continued to deteriorate, a process we believe was accelerated by bad practice within the care home (we know she often went without sufficient food since no one ensured she ate her dinner – another simple necessity she had long forgotten the need for). As she descended, she slowly forgot who her grandchildren were, then her children. I still remember the moment she forgot who my grandfather was, when there was no recognition of the man she had married in 1948. This devastated my grandfather; he never really got over it, and began to give up his fight against his cancer, succumbing to the disease in 2010.

My grandmother eventually plateaued, but only after she’d forgotten how to walk, speak, go to the bathroom or do anything other than sit in a chair, constantly grinding her teeth and very occasionally mumbling a nonsensical sentence. Even those things stopped eventually and she essentially became a corpse whose heart happened to be beating … this was in no way a dignified way to live. She finally died in June 2012, after 13 long, painful years. My whole family was relieved when she passed away – she wasn’t suffering any more.

Syringe by bocian - It is this experience which has strengthened my view on euthanasia. I strongly believe that it should be legal for people who are suffering enormously and have no quality of life to be able to end their life on their own terms.

Of course I’m aware of the problems surrounding legalising euthanasia. There’s a huge difference between the case of Tony Nicklinson and my grandmother. Tony Nicklinson was mentally sound but trapped in his non-functioning body, my grandmother was OK physically but mentally there was nothing left. These two cases would have to be treated very differently. The main difference being that, in one case the person is able to state for themselves that they wish to die whilst in the other, they are no longer in sound mind therefore unable to make that decision.

One of the main objections to the legalising of euthanasia is that it may put vulnerable people in harm’s way. Take for example people who are disabled and believe they are a burden on their relatives and carers, or a family who might just ship off their mad old grandma and be done with it, no matter what she may have wanted. These are all very real concerns which need to be addressed, however, I think that the vulnerable can be protected by implementing very strict controls around the process. These controls must ensure that euthanasia is only allowed in extreme cases, such as those mentioned above and that each separate case is subject to an extensive and thorough review. I also believe that interviews and psychiatric assessments are necessary for both the patient and their chosen representative (in cases where another person will ultimately have to make the decision) and that no action should be taken unless two or more doctors agree that euthanasia is the best option. Of course in the case of dementia it will be necessary for the patient to express their wishes whilst still in sound mind, perhaps relying on an advocate/representative to ultimately decide when euthanasia should be performed. It is also important to take into account the wishes of the doctor(s) involved in the process – no doctor should be forced to perform an act of euthanasia against their wishes, much like they cannot be forced to perform an abortion. But what’s wrong with introducing a legally-binding document, such as an advanced directive, stating that “if I get to a stage where my life has become devoid of any quality or dignity due to a debilitating and permanent illness, then I trust a designated person/people to decide when my life can be ended (subject to legal red tape and psychiatric evaluations).

My feelings on this matter don’t just come from my own personal experiences, but have also been formed through my research on Alzheimer’s disease. However, I must stress that I have had many debates with friends and colleagues (including those doing Alzheimer’s research) on the matter and that not all scientists agree with my views. The bioethics behind euthanasia are tricky – most people would only want their lives to end if they knew there was no possibility of a cure. As far as dementia goes, there is a huge amount of research being undertaken into a possible prevention or cure for the disease. A definitive prevention and/or cure is the ideal and if this ever occurs then there will be no need for euthanasia laws to exist. However, dementia is an extremely complicated condition, believed to be caused by a multitude of genetic and environmental factors. A cure still seems a very, very long way off. Clinical trials for drugs take many years from conception to being available on the market, so even if a breakthrough does occur at the research level, it may take ten years before any drugs are freely available. This also isn’t taking into account that dementia takes many forms – Alzheimer’s disease is the most common, but there are many other versions of dementia, including vascular dementia, dementia with Lewy bodies and Fronto-temporal dementia, which all have their own causes.

In cases such as locked in syndrome, the outlook may be even bleaker. A quick search for “locked in syndrome” on the journal website Pubmed doesn’t produce many papers (8124) and few seem to be about treatment. This is a big contrast to papers published on Alzheimer’s (85847) or lung cancer (211982). There is no cure for the syndrome; research is mostly concentrating on helping sufferers communicate. The best hope scientifically would be to prevent the syndrome by preventing strokes, which cause many cases of locked-in syndrome. Although there are a few isolated cases where people have recovered from the disease these cases seem to be rare.

Time is something which is not on our side when it comes to dealing with dementia. According to the Alzheimer’s Society, there are 800,000 people suffering from dementia in the UK at the moment. By 2021, only 9 years away, they estimate that this number will rise to over a million. The cost of dementia to the UK is predicted to be £23 billion in 2012, minus £8 billion a year which is saved by people caring for relatives with dementia themselves. Worldwide, there is expected to be 36 million people suffering from dementia, with that number expected to rise to 115 million by 2050(source).

I find those numbers utterly staggering, to me it seems like politicians are metaphorically sticking their fingers in their ears and singing loudly rather than confronting the issue, which is just getting bigger and bigger. Like it or not, in 9 years’ time, 1 million people are going to be suffering from dementia, most requiring round the clock care. This doesn’t even take into account the pressure and emotional stress put on the families of those 1 million people. Maybe a cure will be forthcoming sometime soon, but something needs to be done to combat this rising crisis – through increasing funding for Alzheimer’s research, improving the quality of care (for example, reclassifying from “social” care to “medical” care) and for helping people who are suffering to end their lives with dignity, and on their own terms.

Of course, I’m not saying that the minute someone gets diagnosed with dementia that we should ship them off to dignitas or some future UK based equivalent. This has to be a choice made by the individual when they are of sound mind, stated clearly by them in a legally binding document with assurances that it is not decided under pressure from anyone else. I just think that the opportunity should be there if it comes down to it – I know anyone in my family would prefer to end their lives rather than enduring the indignity my grandmother had to go through. It’s time for the government to at least seriously assess the possibility and consequences of making euthanasia legal. In my opinion, the option of euthanasia should be available to those who require it, but it should not be made easy. So my take home message would be – Make it hard, but make it possible.

Post by: Louise Walker

The Science of a Hangover

I have a love hate relationship with wine – I love it and it hates me. That’s at least the way it seems the morning after we’ve been in close proximity. But why does alcohol make you feel so rotten the morning after and can the dreaded hangover be avoided? I decided to look into the science behind a hangover and see whether I can enjoy a glass of pinot without wanting to spend the next day in bed eating my own body weight in carbs.

Cause number 1: Dehydration

Most people are aware of the fact alcohol is diuretic, which means it makes you wee more. The result is that the next morning you run the risk of dehydration along with a dry mouth and headache. Lovely stuff.

Prevention: Try to drink water between alcoholic drinks and/or drink water before you go to bed.

If you’ve ever tried the approach of downing a pint of water before you go to bed after a heavy night on le booze you’ll be aware of the fact that, although it may help, it doesn’t mean you get away hangover free. So there must be more to a hangover than just the dehydration… In fact, it turns out alcohol is pretty poisonous and not just in the “what’s your poison?” sense, more in a surprisingly toxic way.

Cause number 2: Acetaldehyde

When we drink alcohol it is absorbed into our blood stream and works its way around our body. When it reaches the brain it makes you feel relaxed an uninhibited, which is the part we all enjoy, however this is not the only place alcohol leaves its mark. In the liver alcohol is metabolised (broken down) into different compounds which can then be removed from the body as waste. This process requires several steps before the final non-toxic products of water and carbon dioxide are made.

The first step is to turn the alcohol into acetaldehyde using an enzyme called alcohol dehydrogenase. The side effects of having acetaldehyde in your system include nausea, headaches and vomiting – sound familiar?

: There is none. I know – rubbish. You just have to wait for your body to metabolise the acetaldehyde into its less harmful by-products. So unfortunately if you spend the morning having an unwanted date hugging the toilet you just have to wait it out. As acetaldehyde is even more toxic than alcohol moderation is probably the key.

Cause number 3: NAD+ depletion

The metabolism of alcohol and acetaldehyde use a compound called NAD+. This NAD+ is also vital for the day to day health of your cells. It helps converts water, oxygen and a compound called pyruvate into energy. If the NAD+ has been used up metabolising alcohol, your cells need to make more. The cells convert pyruvate into lactate and this reaction produces more NAD+. Unfortunately  long term build up of lactate is also linked to kidney damage. The more I read about alcohol the more I realise it’s pretty nasty stuff! The second consequence is that when pyruvate is converted to lactate, your liver becomes less efficient at regulating your blood sugar levels and blood sugar can become very low. Ever had the desire to eat the entire contents of your cupboards post pinot? That’ll be the low blood sugar.

Prevention; There’s not a lot you can do about the depleted NAD+ other than wait for your liver to do its magic (otherwise known as metabolism) and restore the natural balance. As for the low blood sugar, based on the assumption you’re not still hugging the potty, it’s a good idea to make sure you eat. That’s a free pass for a one way ticket to pasta-ville in my eyes.

Cause number 4: Reactive oxygen species and cell damage: 

I’ve grouped these together because I don’t think it’s fair to say they cause a hangover  however for regular drinkers they probably represent the biggest danger since they can cause longer lasting damage.

The acetaldehyde that is made during alcohol metabolism is a bit of a renegade and can attach itself to things in the cell that it shouldn’t, including a protein called glutathione. When attached to acetaldehyde, glutathione is prevented from doing other important jobs inside the cell which, when experienced regularly can lead to cell damage . More worryingly acetaldehyde can also bind to DNA and damage it, which can increase the risk of developing cancer.

There is a separate chemical pathway that your liver cells can use to metabolise alcohol. Instead of using alcohol dehydrogenase it uses an enzyme called cytochrome p450. This method of alcohol breakdown still produces acetaldehyde but has the added bonus of churning out reactive oxygen species. These little nasties are, as the name suggests, incredibly reactive. They can cause a lot of damage to your cells by reacting with proteins and DNA. This method of breaking down alcohol is used far less by your cells than the alcohol dehydrogenase method so the less you drink the less likely you are to produce the reactive oxygen species.

Prevention: Eat food rich in cysteine post alcohol which includes eggs, chicken and oats. Cysteine is an important building block of glutathione, so making sure you get more into your body gives your cells a fighting chance at making more glutathione. Have a glass of vitamin C rich orange juice. Vitamin C is powerful anti-oxidant, meaning it can interact with the reactive oxygen species, preventing them from reacting with protein and DNA in your cells.

I’m sorry to say the best prevention for a hangover and damaging your health long term is avoiding alcohol in the first place. Regular exposure to alcohol and the damage caused to cells is linked to an increased chance of developing cancer. To me this is a far more important reason to avoid drinking than a fuzzy head the morning after and is a very good argument in favour of moderation.  If you feel drunk that means there’s too much alcohol in your body for your liver to metabolise and you’re getting a backlog of alcohol related nasties in your system – so moderation really is key. On that note, if someone can recommend a low alcohol wine that doesn’t taste like a mix of sugar water and ass, please do let me know.

Post by: Liz Granger

Twitter: @Bio_Fluff


Bullock, C. (1990), The biochemistry of alcohol metabolism — A brief review. Biochemical Education, 18: 62–66. doi: 10.1016/0307-4412(90)90174-M.

Wu, D. and Cederbaum, A. I. (2003) Alcohol, Oxidative Stress, and Free Radical Damage.

HK Seitz, P Becker  (2007) -Alcohol Metabolism and Cancer Risk. Alcohol Research and Health Vol. 30, No.1: 38-47.