The Health Benefits of Kissing

Pucker up, because it seems kissing has a number of important health benefits ranging Kissing1from improving mood and stress levels, to actually enhancing our bodies natural immunity to illness.

Mouth to mouth kissing is a behaviour seen in almost 90% of all human cultures, and used as a non-verbal communication of intimacy, affection and love. For centuries scientists have been pondering the origins of this primitive behaviour and whether it has a functional purpose in our lives.

So where did kissing come from? Apparently, the earliest record of kissing dates back to 1500 BC where references to  ‘drinking moisture from the lips’ were mentioned in Northern Indian Vedic texts. What’s more is that the Kamusutra, which details over 30 different types of kissing, dates as far back as the 6th century AD. According to Philematologists (scientists that study kissing!), it is hypothesized that kissing evolved from an early primitive behaviour known as the ’maternal permastication of food’, which quite literally involved the mouth to mouth contact between a mother and child in the exchange of food during infancy. Despite kissing not being a necessary requirement for successful reproduction, it is hypothesized that sexual kissing may have evolved from this display of care and affection, to eventually promote pair bonding and to facilitate in assessing mate suitability. While mouth to mouth contact is seen in numerous animals as part of courtship rituals, sexual kissing appears to be unique to our species, and may explain why our inverted shaped lips appear to differ from all other animals, almost as if they were shaped for such a purpose!

Despite the seemingly unhygienic nature of kissing, and the fact that it does expose us to the risk of oral infection, this primitive affectionate behaviour represents an evolutionary benefit in conferring protection from diseases that may impose more serious consequences. Mouth to mouth contact essentially exposes each person to the diseases of the other, which while not sounding particularly clean, can actually enhance our own immunological control of exposure to infection. Kissing2According to research by the journal ‘Medical Hypotheses’, kissing represents an evolutionary conserved biological behaviour that boosts our immunity to the Human Cytomegalovirus (HCMV). HCMV is a particularly nasty type of the Herpes virus that can carry a significant teratogenic risk for women i.e. it can have a severe impact on the their unborn children during development, if primary infection occurs during pregnancy. The risks to infected neotates include a number of serious development abnormalities such as enlargement of the liver and spleen, as well as a number of neurodevelopmental disorders including abnormal brain growth, seizures, cerebral palsy and mental retardation. For 30% of infected fetuses the disease is lethal, and as a result, numerous pregnancies are terminated if infection is detected. HCMV is transmitted in saliva, urine and semen. As the disease is only symptomatic during the active phase, it is not an easy virus to readily detect and thus avoid, especially when trying to conceive. In order to avoid infection of the HCMV during pregnancy,  researchers have hypothesized that kissing has evolved to allow women to control the time of inoculation, and that transmission of small amounts of the virus at this point through the saliva will confer immunity to the condition and prevent the presentation of symptoms.

It is now understood that affectionate behaviour has a number of stress-relieving effects. As stress, mainly via the ‘stress hormone’ cortisol, has a number of detrimental influences on our endocrine, nervous and immune systems, kissing may in fact confer significant health benefits by reducing these effects. Interestingly, not only does kissing improve our mood and thus reduce stress levels, it may actually act to reduce a number of parameters that are exacerbated by stress. Stress can elevate blood cholesterol levels, in one manner through stimulating the release of cortisol. Chronic elevation of cholesterol can lead to the build up of plaques and the clogging of arteries that may eventually trigger the development of coronary heart disease. It was identified that an increase in kissing behaviour between marital couples during a 6-week trial period lead to a decrease in blood cholesterol levels, and thus an improvement of blood lipid composition and reduced risk of cardiovascular complications.

Surprisingly, kissing may also enhance your dental health! While it wouldn’t be recommended as a replacement for brushing your teeth in the morning, the extra saliva generated during a kiss washes bacteria off your teeth, and as a result encourages the break down of oral plaque. Kissing also burns calories and raises your metabolism too. According to the research, a vigorous kiss burns up to two calories a minute and can almost double your metabolic rate (the rate at which you can process food). And it makes sense, as kissing involves the coordinated contraction of more than 30 facial muscles, the constant exercise improves muscular tone in the face.  One in particular, known as the orbicularis oris muscle, is used to pucker the lips and has been informally termed the kissing muscle. It has been suggested that the regular contraction of these muscles during a passionate kiss enhances muscle strength and tone and may actually contribute to maintaining a youthful complexion. So a passionate kiss may be the perfect non-surgical remedy for keeping your face young!

Kissing3On what is seemingly quite an obvious level, kissing enhances the release of endorphins in the brain and has a number of other emotional health boosting benefits that improve mood and mental well-being, reduces depression and stress, and most importantly promotes intimacy and pair bonding. So not that we need an excuse, but it seems that appreciating the importance of a good kiss will benefit your health and mental well-being in more ways than one, and if not for anything else, then use it as a happiness boost!

For more information see;

Hendrie CA and Brewer G (2010): Kissing as an Evolutionary Adaptation to Protect Against Human Cytomegalovirus-like teratogenesis. Medical Hypotheses 74: 222-224.

Floyd K, Boren JP, Hannawa AF, Hesse C, McEwan B and Veksler AE (2009): Kissing in Marital and Cohabiting Relationships: Effects on Blood Lipids, Stress, and Relationship Satisfaction. Western Journal of Communication 73: 113-133.

Posted in Isabelle Abbey-Vital | 5 Comments

Diving narcosis and laughing gas

Photo by Derek Keats

I watched a programme the other day about a deep sea mystery. A strangely high number of experienced deep sea divers had been lost on diving trips in a particular bay, and no one seemed to know why. The presenter, being a decent diver himself, went for a dive in the bay and noticed that he could make out the sunlight shining through the water at the other end of an underwater tunnel. His conclusion was that the now deceased divers saw this light and thought they could swim through the tunnel to the other side. What wasn’t obvious to the divers was that this light was deceptively far away and they would have to swim very fast for a long time to make it to the other end of the tunnel before running out of oxygen. But what could cause these supposedly experienced divers to make such a rash, fatal decision?

Nitrogen narcosis can give you tunnel vision, making it harder to read diving instruments. Image by RexxS

Above sea level, nitrogen is a pretty boring gas – it makes up about 80% of the air around us and doesn’t normally do us any harm. However, a problem arises when we breathe it in under high pressure – such as when diving. Several gases, including nitrogen, carbon dioxide, and oxygen are normally dissolved in our bloodstream. When you dive deep underwater, the increase in pressure exerted on your body by the surrounding water causes more of these gases to dissolve into your blood through your lungs when you breathe from the gas tank (because going deep-sea diving without a gas tank would be an even less recommendable thing to do). In fact, for every 10m a diver descends, their blood holds an extra 1.5 litres of dissolved nitrogen.

All that extra nitrogen rushing round in the bloodstream has weird, wonderful, and incompletely understood effects on the brain, collectively known as nitrogen narcosis.

Nitrogen narcosis is experienced by all divers – to varying degrees – and feels essentially like being drunk. Because of this similarity, nitrogen narcosis is often referred to as the ‘Martini effect’. Divers liken every 10m below sea level as the equivalent of having one martini – meaning they feel increasingly intoxicated the deeper they get. Even at comparatively shallow depths (10-30m below the surface), a diver will become less co-ordinated and a bit giddy – 20m lower they’ll start making mistakes and bad decisions and may start laughing for no reason. At 50-70 metres, they may start experiencing hallucinations, sleepiness, terror, poor concentration and confusion, and at 90m they risk losing consciousness or even dying.

So, the worse symptoms of nitrogen narcosis aren’t exactly like getting drunk, because even a huge amount of alcohol doesn’t give people hallucinations (though some alcoholics experience hallucinations when withdrawing from alcohol). Actually, the closest similarity to nitrogen narcosis you can find on dry land is from breathing laughing gas, or nitrous oxide.

A pretty sexist cartoon from ages ago showing some ‘scolding wives’ being prescribed laughing gas. I wonder why they were usually so unhappy with their husbands.

Nitrous oxide has been used by doctors to relax patients since 1794 and it is still used today as a form of pain relief for women during childbirth. It has been in the press a lot recently, dubbed ‘hippie crack’, as it’s often used recreationally (though usually not legally) for its mild hallucinogenic and euphoric ‘feel good’ effects, which have often been likened to nitrogen narcosis. So how does nitrous oxide affect the brain?

Although nitrous oxide is hugely understudied, there are several theories about how it can affect the brain. Because gases like nitrous oxide and nitrogen are really fat-soluble, they may interfere with cell membranes (which are made from fatty molecules) disrupting their normal function. In the case of brain cells, this may alter the way they communicate with one another. In addition, the dissolved gas molecules may directly bind to the receptors on the surface of brain and nerve cells. Nitrous oxide is used as a mild anaesthetic because it has been shown to block NMDA receptors – which normally ‘excite’ the brain – and because it activates potassium channels, which further suppress brain cell excitation. All this means is that brain activity is generally depressed and so users are more prone to making bad decisions or losing concentration.

As I mentioned before, nitrous oxide is also good for pain-relief, as it’s believed to activate opioid centres in the brain. When activated, the opioid system – the same one stimulated by drugs like heroin and morphine – then disinhibits certain adrenergic cells in the spinal cord, which dampen down any feelings of pain.

While there have been reports that nitrogen narcosis also decreases the perception of pain, it’s obviously difficult, and, well, not very practical to test the potential of high pressure deep sea diving on pain relief. Instead, what should be studied more are the effects of nitrous oxide on the nervous system. We’ve used the stuff for more than 200 years and yet the biology behind its uses and its dangers is still not fully understood. What’s more, the fact that people use nitrous oxide recreationally (and probably will continue to do so in spite of its non-legal status in many countries) means we really ought to know what its short and long term effects on the brain are. Unlike the mystery of the missing deep sea divers, the full extent of the ways in which nitrous oxide works remains unsolved.

Post by Natasha Bray

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Night Nurse: The problem of night-time noise in hospitals

hospitalPicture the scene: It’s been a long day, you’ve been violently ill and feel like every ounce of strength has been drained from your body. Finally, after being poked and prodded, interrogated and tested, you find yourself in a warm bed with a soft pillow behind your head. Drained and slightly disoriented, you manage to overcome the nagging nausea and discomfort and eventually your eyelids grow heavy and the days trials begin to wash away as you drift into a gentle sleep… AAARRGGHH, you’re suddenly jolted awake as a distressed cry pierces the air. Confused and groggy you turn to see an elderly woman moaning and sobbing in a bed to your left, alarm bells ring and soon a young nurse is by her side cooing gently and diffusing her confused rage. Flustered, you turn your head away and close your eyes, trying to blank out the unfolding scene. You must have fallen asleep again, since the next time you awake the drama is over, but now you notice a small frail woman standing at the foot of you bed tugging your sheet. “Excuse me” she mutters politely, “I don’t know where I am and I need to get home, can you help?”. After trying in earnest to console her, you drag yourself out of bed and fetch a nurse to help settle her back into bed. Soon after this you are awoken a third time, now by a pair of nurses loudly chatting a few meters from your bed. Exasperated, you notice that their conversation isn’t even about their patients and instead centres around some dodgy sounding shenanigans that occurred on a staff ‘night out’.

Unfortunately this story is not fictional, this is an actual account of a night I recently spent in hospital whilst receiving treatment for a kidney infection. Further to this, I don’t believe my experience was isolated. Over the past two years I have been unfortunate enough to experience both first and second hand the nocturnal practices of four separate NHS hospitals. One, as described above, was my own personal experience, while the remaining three have been accounted to me by both my late grandma and my fiancé’s nan. Each account has shared a common thread specifically, sleep deprivation blamed on excessive night time noise – usually from both fellow patients and staff.

loudThe World Health Organisation recommends that hospital patients are not exposed to noise over 35-40 decibels, the equivalent of a loud whisper. However, a range of studies have found that noise levels in hospital wards often significantly exceed 60 decibels, even during the night (60 decibels being equivalent to a regular conversation). Noise levels in this range are expected to cause sleep disturbances and have been highlighted in patient surveys as being responsible for increased stress and lack of sleep.

Sleep is an essential biological function and lack of it has been associated with a range of adverse outcomes including; altered immune function, metabolic dysfunctions and psychological disturbances including depression, stress and anxiety. Although most studies of sleep disruption are performed on healthy volunteers, it makes sense that those recovering from illness will also benefit from a good night’s sleep; a fact which was recognised over 100 years ago by Florence Nightingale in her ‘Notes on Nursing’, where she writes: “Unnecessary noise then is the most cruel absence of care, which can be inflicted either on sick or well…. A nurse who rustles (I am speaking of nurses professional and unprofessional) is the horror of a patient, though perhaps he does not know why. The fidget of silk and of crinoline, the rattling of keys and of shoes, will do a patient more harm than all the medicines in the world will do him good.”

Noise levels undoubtedly affects some patents to a greater extent than others and studies are yet to conclusively link hospital noise levels with sleep disturbances or negative patient outcomes. However, it has been suggested that disrupted sleep can cause additional stress to acutely ill or injured patients and may potentially impede successful recovery. Anecdotally, I often wonder whether the hospital environment played a significant role in my grandma’s passing. She was a kind, quiet woman who loved her own home comforts. I still remember the distress in her voice when she explained to me how she couldn’t sleep because her fellow patients and the nursing staff were always so loud, even at night. She was a sensitive soul and it was painfully obvious that the hospital environment caused her distress. The cause of her passing was officially registered as ‘frailty of age’. However, I wonder whether the degeneration of her condition and her ultimate decision to refuse food was linked to distress caused by her surroundings, and whether things would have been different had she been cared for at home?

bedI have no doubt that nurses and doctors perform the best job they are capable of, given the structures in which they are expected to work. However, I also think it’s time that hospitals dedicate more time and resources to optimising patient comfort and ensuring that they achieve adequate recovery sleep while under hospital care. Ironically, much of the noise present in the hospital environment is created by measures put in place to improve patient health and safety. This includes: loud machinery, a high density of staff working to care for patients and uncarpeted floors, which reduce the risk of infection but can be loud underfoot or under the wheels of rolling equipment. Noise sources such as these must be assessed and noise reduction measures brought into place. Indeed, some hospitals are already addressing these issues by training staff about noise reduction and by providing patients with ear plugs and eye masks (to reduce the effect of continuous light in hospital wards). It is promising to note that such interventions, alongside structural alterations designed to reduce noise, appear to have a positive effect on reported patient satisfaction and recorded levels of noise on hospital wards. Therefore, I believe that practical noise reduction measures are a must for the future of all public hospitals. A good review of hospital noise and practical solution to these problems can be found here.

Note: I have no intention of revealing the names of hospitals mentioned in this report since, I believe this is a wide-spread problem involving hospital structure and not specifically the fault of any individual establishment.

Post by: Sarah Fox

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A tale of anxiety and reward – the role of stress and pleasure in addiction relapse

At the start of February we heard the horrible news that Philip Seymour Hoffman, a wonderful Academy Award winning actor, had died from a drug overdose. This followed news from last year of the death of Glee star Cory Monteith from a heroin and alcohol overdose. Perhaps the most shocking thing about these deaths was that no-one saw them coming.

Worryingly, the reality is that drug relapses such as these are all too common, but often go unnoticed. Our understanding of the science behind these relapses has come on leaps and bounds in recent years. We have moved from understanding how a drug makes us feel pleasure, to understanding how a drug may cause addiction and subsequent relapse.

Classically, scientists have explained addiction by focusing on how a drug affects the reward systems of the brain. Drugs have the ability to make us feel good due to their actions on this pathway. The reward system of the brain is a circuit that uses the chemical dopamine to stimulate feelings of elation and euphoria. This system has a motivational role and normally encourages survival behaviours such as obtaining food, water and sex. Drugs of addiction can hijack this system to induce euphoric feelings of their own.

Cocaine, for example, is a highly addictive drug that blocks reuptake transporters of dopamine. These transporters normally soak up excess dopamine and ensure that the reward system is not overactive. Cocaine stimulates euphoria by preventing dopamine from being retrieved and increases stimulation of the reward system. Another addictive drug, nicotine directly stimulates the reward system to produce more dopamine.

These classical views work well when considering the motivation to start taking drugs and to continue taking drugs in the initial stages. The drug stimulates feelings of euphoria, ‘rewarding’ the taker. The taker learns to associate taking the drug with these feelings of euphoria and therefore the taker wants to do it more.

This theory can also explain some aspects of withdrawal. Just as activation of the reward system has a physiological role, so does shutting it down. It appears there is such a thing as ‘too much fun’. If we spent all of our time copulating and over-eating we’d be prime targets for predators. Due to this, the body has its own off-switches in our reward pathways that try to limit the amount of pleasure we feel. These normally work by desensitising the brain to dopamine, so that dopamine isn’t able to produce the effects it once could.

Addiction

During drug use, when dopamine levels and subsequent pleasurable feelings are sky-high, the brain works to limit the effects of this overload of dopamine. When the drug wears off, dopamine levels fall but the desensitisation to dopamine persists. This causes withdrawal, whereby when there are no drugs to boost dopamine, one fails to gain pleasure from previous pleasurable day-to-day activities. The dopamine released when one has a nice meal for example, is no longer sufficient to cause enough activity in the reward pathways and no satisfaction is felt.

Scientists believed for a while that the reward system could tell us all we need to know about addiction and how it manifests itself throughout the brain. However, tolerance builds and the euphoric responses to these drugs begin to wane. Some users start feeling dysphoria, a horrible sombre feeling, and don’t know why they continue using these drugs as they are no longer experiencing euphoria – the reason why they took the drug in the first place.

On top of that, when doctors and therapists talk to drug addicts who relapse, the addicts often do not talk about wanting to feel pleasure, wanting to feel elation again. They talk of stress building up inside them, the release from this stress they want to feel.

When asked about why they relapsed, previously clean addicts often talk of stressful events leading to their relapse – they lost their job or they broke up with their partner. First-hand accounts suggest this stress seems to be the driver of a relapse, the driver to continued addiction.

This is depicted clearly back in the 19th century by the eccentric American author and poet Edgar Allan Poe:

“I have absolutely no pleasure in the stimulants in which I sometimes so madly indulge. It has not been in the pursuit of pleasure that I have periled life and reputation and reason. It has been the desperate attempt to escape from torturing memories, from a sense of insupportable loneliness and a dread of some strange impending doom.” 

Intrigued by this, scientists have now found many threads of evidence to suggest that stress pathways within the brain play a key role in addiction and relapse. For example, work into this so-called ‘anti-reward system’, has led to proof that stress can instigate drug-seeking behaviours in animal studies.

Our stress pathways are built around a hormone system known as the HPA axis – the hypothalamic-pituitary-adrenal axis. This axis is responsible for regulation of many biological processes but plays a crucial role in stress.

The HPA axis is the stress hormone system of the body.
CRF = corticotrophin releasing factor; ACTH = adrenocorticotropic hormone

Much like other drugs of addiction, drinking alcohol feels good due to its actions on the reward system. In line with addicts of other drugs, alcoholics commonly talk about the release of stress they want to feel. Evidence is building to suggest that alcoholics have increased activity through the HPA axis.

A hormone called cortisol is the final chemical involved in the HPA axis, released from the adrenal glands during times of stress. Compared to occasional drinkers, alcoholics have higher basal levels of cortisol and a higher basal heart rate – two common measures of HPA activity. This pattern has also been seen in other addictions. For example, in previously clean cocaine addicts, higher basal HPA axis activity correlates with an earlier relapse and higher levels of stress hormones (e.g. cortisol) can predict a higher usage of cocaine in the future.

A puzzling scenario surrounding addiction is how most users can enjoy occasional usage but for some, this can spiral uncontrollably into an addiction? The likelihood of different individuals having a higher propensity to addiction could well be explained by differences in how different people respond to stress.

So what begins as a behaviour driven by the reward pathways appears to have now escalated into a behaviour dominated by stress pathways. It seems it is the stress that drives the craving and relapse, not the longing for a ‘reward’.

Armed with this knowledge, work into how we can design medicines to alleviate cravings and prevent relapse has shown early potential. Blocking the first stage of the HPA axis has been able to prevent alcohol addiction in rats. Blocking a suspected link between the stress pathways and the reward pathways has shown to be able to prevent stress-induced cocaine seeking behaviour.

These compounds have yet to be tested in humans but the early promise is there. It is an intriguing theory that the susceptibility to stress of different individuals may explain the varying susceptibility to addiction. This idea provides a basis for further work to try to understand why some individuals can only occasionally use, whilst others become addicted. Relapse is a horribly common situation amongst drug addicts and with the stigma attached giving addicts substantial additional stress, it is well-worth the research to prevent more unnecessary deaths. Unfortunately, this will be too late for those we have already lost, but the future is bright with continued progress in understanding these horrible ordeals.

By Oliver Freeman @ojfreeman

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A smoking revolution – What’s in a cigarette?

CigaretteTravel back in time to the forties and fifties. Smoking was seen by some as a fashion statement. This was before we were clued-up on the abundant chemicals and the massive impact it could have on our health.  As research into cigarettes snow-balled, smoking became less fashionable. Even so, there are still many people around the world who smoke.

This week has seen a drastic change in UK laws regarding smoking.

The UK Government has decided to ban smoking in cars when children are passengers. This change has come after shed-loads of research over the last couple of decades has highlighted health risks associated with smoking that far outweigh the benefits.

But is smoking really as harmful as the Government drums into us on a daily basis?

The statistics seem to speak for themselves; almost 80,000 deaths occurred in the UK in 2011 as a direct result of smoking. What’s more, around 11,000 people die from passive smoking each year (according to Cancer Research UK), and around 9,500 children are admitted to hospital with smoking-related problems from passive inhalation.

So what exactly is in cigarettes that make them so addictive and what produces these toxic effects?

Nicotine-  a plant-derived chemical in cigarettes that is responsible for the addictive nature of smoking. The chemical enters the blood stream by inhalation and absorption through the air sacs in the lungs. It is then carried by the blood into our brains, where it binds to cholinergic receptors.  Usual functioning of these receptors helps to maintain some of our normal bodily processes, but  when nicotine is inhaled  it changes the number of these receptors and also alters their sensitivity to nicotine.  This is the mechanism responsible for smoking addiction- nicotine needs to be used regularly to keep the brain ticking over.

Tar- the gunky stuff in cigarettes that is deposited mainly in the gas exchange region of the lung, and carries all the nasty chemicals that are toxic to our bodies. Apparently there are almost 4,000 of these chemicals in each cigarette smoked, many of which can cause cancer.  Not surprisingly, tar can affect the proper functioning of the lungs. It also ‘clogs’ the cilia that trap bacteria and dirt, so that dangerous substances can enter our lungs.

Carbon monoxide- the chemical in cigarettes that significantly reduces the oxygen-carrying ability of our red blood cells, as it is 200 times more attractive to our blood than oxygen. As the lungs are no longer able to supply our bodies with enough oxygen, we start to have issues with our breathing as we try to take in more oxygen, and also put our heart under immense strain as it tries to supply us our organs and muscles with enough oxygen (amongst many other things!).

Cigarette 2

Arsenic- a carcinogen that affects how the body repairs DNA.

Benzene- a solvent and carcinogen used in petrol

Formaldehyde- a chemical and carcinogen most commonly used to preserve dead bodies.

Polonium – a radioactive substance

Hydrogen cyanide- poisonous gas that damages the heart and blood vessels

Yet despite these major health risks, large numbers of us are still regularly lighting up.

In 2012 approximately 20% of the UK population smoked cigarettes on a regular basis. Astonishing statistics also showed that 10% of school pupils aged 15 were regular smokers. Not only this, but the average number of cigarettes smoked per day was 12.  Despite these figures, many smokers say that they wanted to give up smoking.

Based on all the frankly quite frightening research that hasn’t been brought to our attention, reducing smoking and passive inhalation is something that the Government is beginning to take seriously. Some of the changes that have already been introduced are;

  • Government bans smoking in public buildings and enclosed places in 2007. Having just been old enough to go to clubs and pubs before the smoking ban came into place, I really reaped the benefits when smoking was banned in public places. I was able to enjoy a night out with my friends, without coming home smelling of an ash tray. I wouldn’t have minded so much if I actually smoked myself!
  • Stopping promotion of tobacco products- Advertising of cigarettes is banned (2003), and supermarkets are permitted to hide tobacco displays (2012).
  • Tobacco tax- Tax rates on cigarettes are high, apparently with the aim to put people off smoking, and nothing to do with the revenue it makes them!
  • Anti-smoking campaigns- These campaigns aim to get people to quit smoking by making them aware of the health risks, dissuading young people from taking up smoking and trying to educate people on the risks of passive smoking.
  • E-cigarettes- These electronic imitation of cigarettes are currently a massive craze in the UK. In theory these are a great alternate to smoking; they retain all the ‘good parts’ of smoking, without all the added health risks. As these are relatively new they are not well regulated, so more research is needed to evaluate their health impact.

We know for certain that smoking is damaging to the body and has serious health implications. I have provided a (somewhat biased) summary of the health-related impact that smoking can have, from a non-smokers perspective. Another thing is also clear; the Government are taking smoking seriously. They are tackling this issue in a number of vital ways from trying to stop the ‘glamorisation’ of smoking by banning advertisements, reducing the impact on non-smokers, research and regulation into ‘better’ alternatives and in my opinion the best way possible; educating the public on the harmful effects of smoking. Next time you reach for a cigarette just cast a thought to some of the chemicals and toxins that you are putting into your body, and be aware of how this may be affecting yours, or someone else’s health.

 

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What is a headache?

We all know the feeling after a long stressful day, when the tensions of the past few 415px-Tension-headachehours begin to amass in your temples, perhaps starting as a dull throb before advancing in waves to a deep pounding ache. The headache is a common malady, but what mechanisms lay behind these debilitating pains and which aspects of your life may be triggering them?

The question of why and how we experience headaches is significantly harder to answer than you might imagine. Particularly since the term ‘headache’ is in itself non-specific, being a broad term used to describe a range of common head pains, each of which may stem from a different underlying cause. Interestingly, however, one thing we do know is that the pain you experience during a headache does not originate from the brain itself. Indeed, the brain lacks pain receptors (nociceptors), therefore does not have the capacity to feel pain.

543px-Gray507But then where does the pain of a headache come from? The pain we experience during an everyday headache originates in pain-sensitive structures surrounding the skull. These include; the extracranial arteries, veins, cranial and spinal nerves, neck and pericranial muscles – all of which express pain receptors and are therefore susceptible to these sensations.

It is possible to pin down a number of simple lifestyle factors which commonly contribute to the development of headaches. These include; emotional disturbances, stress and mental tension, certain types of food, alcohol, cigarette smoke, exercise and even the way you wear your hair – hair-dos (including the tight ponytail, braids, headbands and even tight hats) can strain the connective tissue that lies across the scalp and cause headaches. So simply letting your hair down can relieve this pressure and thus the pain of the headache.

A number of the factors which lead to headaches (including certain foods, cigarette smoke and alcohol) involve the blood vessels which lie around the brain. For example, inhaling nicotine from cigarette smoke causes narrowing of blood vessels around the skull. Narrowing of these vessels can often induce extremely painful headaches. Changes in blood pressure also explain hangover and exercise headaches and why, for some people, certain foods can act as headache triggers.

6708719835_b2f15fc2e3The episodic tension headache (the type you may get after a long day at work) is the most commonly occurring type of headache. However despite the extensive research into the cause of migraines, this common type of headache remains one of the least investigated. As relief can normally be sought through over-the counter painkillers, most sufferers will not consult a doctor. The mechanisms underlying what specifically causes these headaches remains elusive, however, a number of theories regarding their pathophysiology have been proposed:

It appears that the occurrence of headaches are commonly linked to general problems of the musculoskeletal system. Skeletal muscle constitutes the largest muscle mass of the body, controlling movement, breathing, facial expressions and numerous other normal physiological functions. Each individual skeletal muscle is composed of hundreds of cells, arranged in muscle fibres. Each muscle fibre is connected to the nervous system via interactions with a single branch (an axon) of a nerve cell.

Each fibre of a muscle can relax or contract in response to signals sent from the brain via these nerves. These muscle fibres also contain sensory receptors which can feedback the health of the muscle to the brain. This helps tell you when the muscle is tired or overstretched for example. Abnormal activity in these nerves, perhaps as a consequence of injury, stress or poor posture, can therefore result in the relay of pain signals to the brain. For example, bad posture places abnormal pressure on the muscles of the neck which can result in heightened tension and the subsequent development of ‘tension headaches’.

Interestingly, tension headaches can also be induced by activation of so-called ‘trigger points’. A trigger point is defined as ‘a hypersensitive area of the body, associated with taut bands within a skeletal muscle’. Pressure or compression on these localized trigger points can cause the referral of pain along linked nerves to a nearby area. So, the presence of active trigger points in your head, neck and shoulder muscles can refer pain that will be subsequently experienced as a headache.

A number of studies have confirmed this, identifying an increased number of trigger points in the muscles of the head in patients prone to headaches, compared with patients who do not regularly experience headaches. What causes these trigger points to develop in the first place still remains unclear, however, some have speculated that they may be associated with past muscular injuries, fatigue, diet and even as a result of chronic repetitive strain, such as persistent typing.

5621720708_3e3b9c45c1Infrequent headaches, while menacing, are nothing compared to their chronic cousins. Infrequent headaches can become chronic as a result of changes that originate in the brain and spinal cord. This involves so called ‘second-order’ nerve cells which act as connectors between peripheral organs (e.g. the skin and muscles) and nerve cells in the spinal cord and brain.

A number of studies have proposed that chronic tension headaches may be triggered by changes in the sensitivity of these second order nerves, particularly those in the spinal cord and an area of the brain known as the trigeminal nucleus. This process is known as ‘central sensitization’ and can alter pain thresholds and trigger nerve cell activity. It is hypothesized that, in the presence of persistent stress or pain signals from peripheral muscles (such as that brought about through regular bad posture), nerve cells can grow forming new connections and effective contacts to low-threshold nerves that do not normally signal for pain. Furthermore, increased sensitivity can be caused by the enhanced release of chemicals that facilitate nerve cell communication. This increase in the number of pain signalling nerves and their sensitivity to strain and tension results in enhanced pain sensitivity, lower pain thresholds and the development of chronic pain states.

Chronic pain states, may be a result of prolonged stress and musculoskeletal tension, alongside central changes in the brain and spinal cord. So, if regular headaches are wearing you down you might benefit from trying to reducing your stress levels, being aware of dietary triggers, improving your posture and trying exercises to relax your muscles.

Post by: Isabelle Abbey-Vital

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Michael Schumacher’s traumatic brain injury explained

Photo by Mark McArdle

Seven times Formula 1 World Champion and holder of a huge number of driving records, Michael Schumacher is thought of as the greatest F1 driver of all time, a champion among champions. On 29th December last year on a ski slope in the French Alps, Schumacher fell and hit his head on a jagged rock. Witness reports claim that he lost consciousness for about a minute, but that ten minutes later, when the emergency helicopter arrived, he was conscious and alert. Over the next two hours, however, Schumacher’s condition deteriorated and since that day, he has had two head operations and has remained in intensive care under a medically-induced coma.

An epidural haemotoma caused by a fracture in the skull (indicated by the arrow). Image by Hellerhoff.

Traumatic brain injury, or TBI, is quite a vague medical term and simply describes any injury to the brain sustained by a trauma – that is, a serious whack to the head. TBI is the most common brain disorder in young people: while older people are at higher risk from degenerative diseases, young people are more likely to find themselves in car crashes, fights or…ski accidents.

The specific type of TBI that Schumacher is believed to have suffered is an epidural haemotoma (click here for a seriously gory video of a haemotoma clot removal – you have been warned). Between the brain and the skull are a number of protective layers; these are membranes which encapsulate the brain and spinal cord, all of which swim around in cerebrospinal fluid. An epidural haemotoma is a bleed between the tough outermost membrane, called the dura mater, and the skull. Technically this sort of bleed isn’t in the brain itself, but this injury seriously affects the brain due to one important factor: pressure.

Six ways a brain squeezed by a bleed can go. Coning (indicated by number 6) is a last resort but compresses respiratory centres and can be fatal. Image by Rupert Millard.

Since the skull is an almost totally enclosed space, a bleed that grows too big in size could end up pushing, not just on the inside of the skull, but on the brain itself – squeezing it into an ever-decreasing volume. When put under pressure the only way the brain can physically go is down towards the spinal cord, but if this happens, the brainstem at the base of the brain may become compressed. This horrible scenario, known as ‘coning’, has a really high fatality rate, as the brainstem is needed to keep our heart pumping and lungs breathing. So keeping intracranial (in-skull) pressure low after TBI is key.

Doctors have reported that, as well as a haemotoma, Schumacher suffered contusion and oedema. Cerebral contusion is essentially bruising, as you might expect in other parts of the body: tiny blood vessels bleed when they have suffered a serious hit – in this case either from the rock itself, or from the other side of Schumacher’s skull in a ‘rebound’ type impact. Oedema, or swelling, may come as a result of the contusion – like when a bruised knee swells – and again would need to be curbed in order to prevent the pressure inside the skull from rising dangerously.

Illustration by Max Andrews.

So what have the doctors done to treat Michael Schumacher’s condition? Well, firstly, the surgeon Prof. Stephan Chabardes has reportedly performed two operations to remove blood clots from the haemotoma, as well as a craniectomy – removal of part of the skull – in order to relieve the intracranial pressure and prevent coning. Craniectomy has been used for some time to treat both TBI and stroke, but remains somewhat controversial, mainly because of the risks of further bleeds, infections, or herniation of brain tissue through the surgically-made hole in the skull.

The second main strategy in treating Michael Schumacher has been to keep him under an artificial or medically-induced coma. This involves sedating him with strong anaesthetic agents. Propofol, which quietens brain activity by boosting inhibitory GABAA (‘off’) receptor activity and by blocking sodium (‘on’) ion channels in neurons, or barbiturates, which also enhance GABAA receptors, but block excitatory glutamate (‘on’) channels could be used to keep him sedated and to ‘slow’ his brain down. Slowing is achieved through a net reduction in excitatory activity within the brain. Thus, the medically-induced coma not only stops the patient being conscious, through what no doubt would be a painful experience, but also limits the amount of activity-related blood flow, curbs swelling and prevents what’s known as excitotoxicity.

Risk of post-trauma seizures after TBI by the severity of the initial injury. Graph by Delldot (wiki).

Excitotoxicity can occur after TBI, stroke or in patients with epilepsy. It is a term used to describe what happens when brain cells run out of energy or become overloaded with excitatory inputs. In this state cells become overexcited and die, either immediately, or after a delay. Seizures, which can cause excitotoxic cell death, are fairly common after severe TBI and are thought to drive brain damage after the original injury. Seizures after TBI can be worsened by swelling and higher temperatures, so it is likely that Schumacher has been kept a few degrees cooler than his normal body temperature to limit this risk.

Data as interpreted from Laureys S, Owen AM, Schiff ND (2004). “Brain function in coma, vegetative state, and related disorders”. The Lancet Neurology 3 (9): 537–546. Graph by Shin Andy Chung.

If he is still in a medically-induced coma, or is gradually being weaned off the anaesthetic agents, Schumacher may be undergoing physical therapy to move his limbs and joints to prevent muscle wastage, or contracture, which is irreversible muscle shortening. If his condition improves and he is able to move, his limbs will need re-strengthening.

Some conflicting reports suggest that doctors treating Michael Schumacher may have started removing him from his coma. If they are doing this, the full extent of their patient’s rehabilitation needs won’t become clear for some time. While I obviously hope the driving legend makes a full and speedy recovery, it is hugely unlikely that his brain will completely recover all its previous functions. The brain is such a delicate organ and Schumacher’s tragic case only highlights its fragility.

Hugo Lloris in 2012. Photo by Stanislav Vedmid.

Schumacher’s injuries also raise the debate on the guidelines of treating head injuries in sports. Last November, Tottenham’s Hugo Lloris lost consciousness after a hit to his head during a football match, but after waking up was allowed to return to the pitch to finish the game. Lucid intervals, such as the one reported shortly after Schumacher’s fall, can be deceptive and players of contact sports should always be given immediate medical attention after losing consciousness. It’s no news that the cumulative effects on the brain of losing consciousness multiple times – as many boxers do on a regular basis – are to be avoided at all costs.

Every year in the USA, 1.7 million TBIs – more than double the number of heart attacks – contribute to almost a third of all accidental deaths as well as varying levels of lasting disability. While we hold our fingers crossed for Michael Schumacher’s successful rehabilitation, we must also think of the other thousands of people, and their families dealing with the long-term aftermath of serious brain injuries around the world.

 Post by Natasha Bray

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