It’s well into the spooky season and Halloween just round the corner. With many of us indulging in a few scares and horror movies. I felt now was a thematic time to talk about fear. That primal emotion that causes goose-bumps, butterflies in our stomachs and sweat to drip down our necks. What is fear and how do we develop it?

At its base fear is a survival instinct. All things that cause us to be afraid, can in our minds lead us to death. That is the base of all fears we experience, the body’s natural need to survive and prevent anything that would do us harm, potentially leading to our demise.

The Amygdala

This region of the brain is responsible for controlling our response to the things that scare us. It receives vast amounts of sensory information, from our vision, hearing and sense of touch. The amygdala shares a close connection to another region of the brain known as the hippocampus (our memory centre), allowing the processing of past experiences or information to determine the threat level and therefore the strength of fear produced. It learns from experience, measuring the dangers of the world, and acts to trigger the fight or flight response. Allowing us to defend ourselves against imminent danger or to run like hell to get away from it. During the fight or flight response there is a huge release of adrenaline, causing increases in heart rate drawing blood to the muscles ready to act. Blood is also redirected away from less important processes to focus on the muscles. It is this diversion of blood that causes the feeling of butterflies, as your digestive system has a reduced supply.

Becoming Afraid

There are several innate fears we as humans possess. Scientists can categorise these into 6-8 distinct groups. We are born with two innate fears these are a fear of falling and loud noises. New-born babies surprisingly feel comfortable in the dark, as it reminds them of being in the womb. As we develop we gain other fears that all link to the pinnacle fear of death. These fears include:

• Falling
• Pain
• Unknown – the abnormal, creepy faces or the dark.
• Sudden Movement/Noise
• Disease
• Isolation – being alone or rejected. Linked to the fear of public speaking.
• Suffocation

Many of the common fears people experience can be linked back to these base fears. Such as a fear of spiders can be connected to the sudden movements they exhibit or the potential chance of being bitten, hence pain aversion. Many fears are learned or inherited through one’s own experience or the stories from others. Fear can also be obtained vicariously, seeing another afraid can instil that same fear onto you. Understanding how fears develop was first shown in the real life horror story of the Little Albert Experiment.

A psychological study on fear was published in 1920. This was called the Little Albert Experiment. It set out to determine whether you could condition a phobia into an emotionally stable child. A nine-month old referred to as “Albert” was exposed to several different stimuli. They were introduced to a rat, a rabbit, a monkey and other furry things including cotton wool. As expected the baby showed no sign of fear to these things. The true experiment started at age 11 months. The child was placed upon a bed with a white rat and allowed to play with it. Though, each time Albert made contact with the rat the experimenters hit a metal bar with a hammer. This unpleasant loud noise being a natural fear to children was repeated each time Albert tried to play with the rat. Albert showed the signs of fear along with crying in response to this noise. Eventually Albert would recoil and retreat whenever the rat was brought close. The level of distress was then observed upon Albert seeing a rabbit and a dog, even a Santa Claus mask with a furry beard triggered fear in the child. Scientifically this was the first true demonstration of fear conditioning. However this experiment was morally wrong, the lead scientist John B Watson did not have the time to desensitise the child again and it is believed that the phobia continue post experiment. Modern fear studies are not conducted in this manner and work is performed to prevent any lasting harm.

The Woman with No Fear

The next story I shall cover is patient S.M, a woman from the USA whose identity is kept private for her own protection. S.M is incredibly unique, as at a young age she suffered with a condition called Urbach-Weithe disease which left her amygdala destroyed. She was later dubbed by the media the “woman with no fear.” S.M went through several studies proving that she was unable to experience being scared. Haunted attractions, scary movies, snakes, spiders were all met with curiosity or excitement rather than terror. She has been the victim of muggings at knife point to which she showed no behaviour response associated with panic or desperation. She has experienced an extraordinarily high number of life threating events, which is believed to be due to her inability to determine the danger of specific situations. Situations that could have been avoided. S.M is unable to truly recognise threatening behaviour from people and an inability to interpret aggressive facial expressions. Interestingly, there is something that scares even S.M. The brain is an incredible thing and doesn’t need to amygdala to know that something is terribly wrong causing panic to set in. S.M was given a ventilation mask and the amount of CO2 was increased generating the sensation of suffocation. Her reaction was immediate and extreme, for the first time in her life S.M was afraid. Something very crucial was learnt from this experiment on S.M. Another role of the amygdala in suppressing fear. Her reaction was very extreme, when other participants with functioning amygdala were tested they showed fear, but deep down knew that this experiment wasn’t going to kill them. They believed they were safe, S.M was unable to make this connection in her brain.

Getting Over Fear

Many of these irrational fears we as humans possess can be dealt with through therapy. Two major techniques have seen success in treating phobias. The first and most gentle method is through systematic desensitisation. Take for example the fear of spiders. Early on in therapy you may be asked simply to read a book about spiders, then move on to looking at pictures of them. You are fully aware that these images and words can’t harm you. This helps to unravel the connections you have made in your mind between spiders and death that your amygdala has set up. The next step would be to be in a room with a spider in a tank. The spider can’t get you it’s just there. Finally you would likely be asked to handle a spider. Over time this trains your brain that spiders don’t control your fear, and you can overcome it. The second therapy method is through flooding. This usually involves putting the fear front and centre. Day one placing a spider straight in your hands for example. An extreme method, but apparently quite effective.

Obviously medical therapeutics are also an option. Anti-anxiety drugs are effective for reducing the panic associated with fears. Drugs including diazepam or alprazolam (probably better known as Valium and Xanax respectively). However only tend to be prescribed in cases where the fears are irregular and unavoidable. Such as a fear of the dentist, flying or surgical procedures. Beta-blockers can also be used. These act to prevent the action of adrenaline, therefore avoiding the blood flow changes, heart rate increases and sweating.

Joy in Fear

Fear is a fascinating part of our brain. It aims to prevent us from death. However the world is so messy and memories impact how we perceive normally innocuous things. There are many of us that get enjoyment from being scared. Particularly when sharing it with others. Interestingly the state we enter during fear is not dissimilar to that of excitement. The major difference between these two states is the context through which we are experiencing them. Fear is triggered by danger and excitement through fun. There are many things that we deem fun that trigger fear and it is the knowledge that we are safe that turns that fear into joy. Fear can work as a natural high. The falling feeling and speed of rollercoasters can make the amygdala think we are in danger, but we know better so that rush of adrenaline is put to better use. This is the origin of the adrenaline junky. The seeking of scary situations for pleasure. So however you spend your Halloween, being scared isn’t all that bad.

Reading Sources

• The Biology of Fear, Ralph Adolphs, 2014.
• Retrieving fear memories, as time goes by…, Do Monte et al., 2017.
• Mechanisms of Fear Learning and Extinction: Synaptic Plasticity – Fear Memory Connection. Luchkina & Bolshakov, 2020.
• Fear and panic in humans with bilateral amygdala damage, Feinstein et al. 2013.
• Impaired recognition of emotion in facial expressions following bilateral damage to the human amygdala. Adolphs et al. 2016.

During this time of lock-down and social distancing many people are now trapped at home without regular social interaction, or a stable income. This sudden change in life style can be extremely stressful, and in turn detrimental to your mental health. It is important that people try to maintain a level of safe social interaction and aid in a healthy mind.

Depression during such extreme changes is a potential threat. So I wanted to take this time to talk a little about depression and the theories behind it. It is important to note that depression is a very complicated area of medical science and it is not fully understood to this day. There are many factors and ideas to take into consideration. So take this post as a small introduction to these ideas.

What is Depression?

Depression is to put it simply an illness that affects the brain. Depression is categorised by several different symptoms; the sensation of being down, persistent sadness, a feeling of worthlessness, loss of appetite, exhaustion, loss of sleep etc. Usually consisting of 3-5 of these symptoms combined together. Depression is an umbrella term that encompasses several different conditions, such as bipolar disorder, persistent depressive disorder, major depression, seasonal affective disorder, postpartum depression etc. Each needs to be treated differently through therapy, lifestyle changes or medication. I feel it is very important to know that people who suffer with depression are unable to control how they feel, there is no easy out, “cheer up” option. Their brains are functioning in a completely different manner to non-sufferers.

This post will be discussing depression in general and some of the theories behind it. Along with the methods and drug interventions medical professionals can prescribe to help alleviate this condition. It is impossible for everything to be covered in the breadth of a short article.

The Cause

The causes for depression are numerous and the underlying internal changes we see in the brain are still being studied. Many will have heard that depression is caused by a chemical imbalance within the brain. Now this is not wrong to say however it is not known as to whether the changes we see are due to the depression or the cause of it.

There are two major neurotransmitters (chemicals released to communicate with nerves) in the brain that are linked to depression. These are dopamine and serotonin. Dopamine i have mentioned in the past as it has an important role in reward and the sensation of pleasure. Serotonin often termed the “happiness chemical” has a role in positive emotional states like joy. It is important to note that these are not the sole roles of these neurotransmitters, they are produced in numerous areas of the brain each with distinct functions. For example serotonin has roles in blood pressure and heart rate, and dopamine in muscle control. With regards to depression I will only be discussing their effects on emotional states.

One of the main theories is called the monoamine hypothesis of depression. This states that in people who are depressed there is a reduction or depletion of specific neurotransmitters in the brain leading to a negative emotional state. The problem scientists have is that we are unable to measure the levels of these neurotransmitters in the brain of living patients. Studies were done looking at the levels of neurotransmitter in the spinal fluid however results were inconsistent and therefore inconclusive. There are 3 main neurotransmitters that have an involvement in depression.

Neurotransmitters

Serotonin

Serotonin (often referred to as 5-HT in scientific publications) has a number of crucial roles in our daily function and emotional mood. There are specific receptors within the body (5-HT receptors) that detect and respond to the presence of serotonin. Located throughout the our system they have functions in the sleep/wake cycle (serotonin is used to make melatonin see sleep post), appetite and sexual arousal (it has been shown that licking, biting and grooming triggers serotonin activity in the brain), one or all of which tend to be irregular in those suffering from depression. Serotonin is as mentioned also involved in blood pressure control along with pain sensation and digestion.

In regards to mood and emotion the role of serotonin is still being studied, attempting to put numbers to emotion is difficult. What we do know is that depleting the stores of serotonin within the brain causes depressive symptoms. For years we have known that the use of the drugs called SSRIs (selective serotonin re-uptake inhibitors, which I will cover later) reverse this depressive state as well as being the gold standard go to drug for sufferers of depression.

Dopamine

One common symptom of major depression is anhedonia, this is the loss of pleasure or reward from previously enjoyable activities or experiences. There have been imaging studies looking at brain activity within some depressed individuals. These have shown a dysfunction in the areas of the brain that are responsible for generation the sensation of reward. Further work has shown that it is the loss of dopamine signalling that causes anhedonia in depressed patients.

Noradrenaline

Noradrenaline has roles in the limbic system which is responsible for mood and emotional cognition within the brain. Studies working with noradrenaline receptors have shown that by increasing noradrenaline within the brain can prevent stress induced depressive symptoms. Which is corroborated by depleting noradrenaline leading to the return of depressive activity.

In depressed people, the monoamine theory states that there is an irregularity in the way their nerves behaviour. This dysfunction is likely located at the junctions between nerves called synapses.

Genetics and Immunity

Your genetics can play a major role in whether a person develops depression or not. It has been found that depression can be hereditary, if a member of your immediate family has or has had depression then the chances you could be susceptible are increased. Genetic dysfunctions within transporters of serotonin on synapses can increase the probably that someone could develop depression.

There is also evidence of the immune system causing symptoms of depression. Depressed patients have higher levels of cytokines. These are small proteins that aid in the fighting of an illness however also produce symptoms such as exhaustion and loss of appetite. Experiencing high levels of stress can cause an increase in the production of cytokines leading to a worsening of depressive symptoms.

Cognitive Theory

This idea is linked to the concept that negativity in one’s life can trigger and feedback loop that leads to depression. Loss of a loved one, or getting fired from a job can lead to a person pulling back from life and things they previously enjoyed. Along with this comes the likelihood that the only positivity that person receives is from the sympathy of others. Reinforcing negative behaviours like weeping and complaining.

There is an idea back from the 1960s (Beck’s Theory) that referred a negativity triangle:
1. Negative view of self
2. Negative view of the future
3. Negative view of the world

Each impacts on the other and drives a person into a downward spiral eventually leading to depression.

Depressed Brains Look Different

Finally we come to the actual structure of the brain. Everyone’s brain is made up of white matter and grey matter. Grey matter is where all the processing your brain does occurs, it contains the cell bodies of nerves as well as synapses. It has been found through imaging brains, that those with depression have smaller amounts of grey matter in regions important in the processing of emotion and memory. This means that depression can actually change the shape and size of areas of our brains making it harder to control our emotional states.

Another crucial process that occurs in the brain is called neuroplasticity. This is the process by which the brain will make changes to connections from different stimuli for example how we make and store memories. Chronic stress has been show to inhibit neuroplasticity within the brain potentially interfering with how depressed people can adapt to new stimuli.

Treatment

The go to treatment for general depression is by using antidepressants. These come in many forms, but the most common are the SSRIs (serotonin-selective reuptake inhibitors). These work by increasing the amount of serotonin within the brain with the aim of improving mood. Antidepressants take a while to work usually 4-6 weeks after starting treatment. This is because their function is to effectively re-balance the amount of serotonin in the brain, some patients might feel stressed due to not seeing an immediate effect.

Another group of drugs are the MAOIs (monoamine oxidase inhibitors). This is a structure in synapses that breaks down excess neurotransmitter like noradrenaline and serotonin. These drugs prevent this from occurring increasing the amount of neurotransmitter available for use.

Not every drug works for every patient and treatment needs to be tailored to each individual. Therapy can be a viable and helpful method in treating depression. One in three patients have been found to respond positively to guidance and psychiatric help. Techniques are now being developed to use brain imaging to predict the effectiveness of using antidepressants.

Conclusion

Depression is an incredibly complex area of medicine and I haven’t been able to cover half of the theories and ideas. It is important to bring attention to this condition as there are still people out there who pass it off as a phase or a moment of sadness. The world health organisation predict that by 2030 depression will be the number 1 condition affecting individuals. The better we understand the condition and learning how to recognise when someone you know might be suffering from depression. Will lead us to treating it early and effectively.

Reading Sources

• World Health Organisation Statistics
• Genetics Factors in Major Depression Disease, 2018, Shadrina et al.
• Dysfunctional Attitudes and 5-HT₂ Receptors During Depression and Self Harm, 2003, Meyer et al.
• Depression and Hypersomnia: A Complex Association, 2017, Lopez et al.
• The Association of Cigarette Smoking with Depression and Anxiety: A Systematic Review, 2016, Fluharty et al.
• The Role of 5-HT Receptors in Depression, 2017, Yohn et al.
• Neuroimaging Advances in Depression, 2017, Dunlop et al.
• Dopamine System Dysregulation in Major Depressive Disorders, 2017, Belujon et al.
• Basic Neurochemistry: Molecular, Cellular and Medical Aspects. 6th Edition.
• Functional Selectivity and Antidepressant Activity of Serotonin 1A Receptor Ligands, 2015, Chilmonczyk et al.
• What has serotonin to do with depression? 2015, Cowen et al.
• An Electroencephalographic Signature Predicts Antidepressant Response in Major Depression, 2020, Wu et al.
• Depression: The Case for a Monoamine Deficiency. 2000, Delgado.
• The importance of norepinephrine in depression, 2011, Moret et al.
• Photo by Justin Silva.

During this time of people isolating themselves at home to prevent the spread of COVID-19. There are pharmaceutical researchers working on treatment methods, and importantly the development of a potential vaccine. This seemed like an appropriate time to cover a little of the history of vaccine and the theory behind how they work.

History

It is always fascinating how we as humans come up with these ideas and methods to fight disease. Using the chemicals in nature to produce drugs that relieve pain, or in the case of vaccine; using pathogens to fight off pathogens. Many will have heard the story of Edward Jenner the founder of vaccination in 1796, but the story begins quite a bit earlier than that. In fact a method called variolation was being used centuries before Jenner in China, the Middle East and parts of Africa. Variolation follows a similar process to vaccination but is a little less refined. Used to prevent small pox, people would take the scabs of sufferers dry them out and grind them into a powder. This powder was then inhaled into the nose. This would cause a mild version of the viral infection that effectively provided immunity from a future infection. This technique eventually made its way to Europe.

In 1768 John Fewster an English physician made a key observation. He noted that people who had been infected with cow pox appeared to having an immunity to small pox. Many replicated this, famously Benjamin Jesty used cow pox to immunise his family from small pox in the early 1770s. Jesty wasn’t a doctor so didn’t end up publishing his findings, meaning we would have to wait another 20 years before Jenner conducted his work.

Jenner put together a study taking the pus from a milkmaid, called Sarah Nelmes who had caught cowpox from a cow named Blossom. Blossom’s hide hangs in the library of St George’s medical school in London today. The pus was administered into both arms of 8 year old James Phipps. The boy experienced a mild fever and symptoms of cowpox, but recovered unharmed. Jenner then injected Phipps with variolous material for small pox. He showed no sign of infection. Follow up injections also yielded no signs of small pox. This confirmed to the scientific community that the boy had developed an immunity. This was a landmark in medical science as Jenner had proven that the method of vaccination (named from vacca meaning cow) could provide people immunity from small pox. A commercial vaccine was generated in 1798 and since its wide spread use small pox has been completely eliminated from the human population.

With advances in medical technology, along with out understanding of microbiology scientists were able to develop a whole host of vaccines for problematic pathogens. Including rabies, influenza, measles, rubella, polio, tetanus the list goes on and on.

Vaccine Theory

We know that the aim of a vaccine is to generate immunity in the recipient to a specific viral or bacterial infection. Simply put vaccination follows the idea of “know your enemy” training your immune system in case it encounters the infection. I have discussed the immune system in previous posts, but I will do a small recap. We divide the immune system into two parts, which we call the innate and adaptive responses. Our innate immune system will do its best a front line defence force. Identifying foreign pathogens and eradicating them as quickly as possible. Sometimes that is not enough, some viruses and bacteria replicate too quickly or have ways to avoid detection long enough for them to cause damage. This is where the adaptive immune system comes in. These specialised cells change their tactics depending on what exactly they are fighting against.

Our adaptive immunity is constantly learning and it is this ability to learn that is utilised when administering a vaccine. The cells of the adaptive system produce structures called antibodies. These are Y shaped proteins that can be customised to suit their purpose in targeting one specific virus or bacteria. The antibodies once produced can neutralise foreign pathogens in a number of ways. They can mark them out for other cells to target and kill, disable their ability to invade other cells, or cause their death directly. However it takes time for the adaptive immune system to obtain the required information to produce these antibodies. In most cases the virus or bacteria needs to be caught and digested for valid weaknesses to be identified. We call these targets antigens, and antibodies bind to antigens. Some viruses or bacteria are able to avoid being broken down and suitable antigens targeted. This means that the adaptive immune system cannot work effectively and the infection is free to spread through the body. Viruses such as the one for HIV chooses to target immune cells directly killing them before they can kill it. Problems like evasive pathogens and the delay between infection and the production of antibodies can lead to a huge escalation in the infection leaving the body in a state it can fight back from.

One of the most crucial cells of the adaptive immune system are the memory cells. These as their name suggests will remember previous attacks and the types of antibody used then immediately produce the required antibodies in response. This allows the body to quickly react to an infection it has experienced before without the need to produce new antibodies.

The concept of vaccination is to therefore introduce the immune system to a pathogen in a safe manner so that it can prepare antibodies in case it encounters the real live version in the future. The way we introduce the immune system to these viruses or bacteria is through one of 4 methods.

1. Live Attenuated: this is a weakened version of the pathogen it is unable to cause infection in healthy individuals, but will cause a very rapid immune response.
2. Killed Whole Organism: a dead version of the pathogen.
3. Purified Proteins or Polysaccharides: the antigens of the pathogen extracted and purified no injection of the original pathogen.
4. Genetically Engineered: we can use genetic techniques to make the antigen without the need for the original pathogen. These can be injected safely triggering a smaller immune response.

By studying individual viruses or bacteria we can identify suitable antigen targets than can be used in vaccines for future immunisation within the human population. Vaccination has prevented innumerate deaths from diseases we no longer have to worry about. I will caution this with the worrying movement of parents not vaccinating their children. The United States last year saw large outbreaks of measles with the disease making a resurgence due to a failure to vaccinate. Through fear and misinformation people are being put at risk. The work being done today to develop a vaccine for COVID-19,which will hopefully prevent the lock-down many of us are under now from occurring again. We are living through the impact, an uncontrolled virus can have on our species. It is vaccination that has prevented that from happening with many other potentially worse pathogens. It is important to note that a vaccine takes years to fully develop with the pharmaceutics trials required before it is safe for usage with the general population. Vaccines have proven themselves to save lives time and time again. Understanding their benefit is crucial to our future.

Reading Sources

• History of vaccination, Stanley Plotkin 2014
• Functions of Antibodies, Donald N. Forthal 2014
• CDC US Statistics for Measles 2019

The Wuhan virus has gripped the media for the past month since its outbreak in December 2019. Officials in China announced that 27 residents, mainly market stall owners of Huan seafood market had become sick with an unknown virus. Over the next month the virus has been spreading throughout Wuhan and neighbouring countries. With recent cases in both the USA and France.

Timeline of the Spread of the Wuhan Virus

• Dec 31st 2019: Wuhan officials announce the outbreak within Wuhan, China. 27 residents of Wuhan with 7 in critical condition.
• Jan 3rd 2020: There are now 44 confirmed patients and another 5 in Hong Kong. Scientists rule out that this is influenza or avian flu.
• Jan 5th 2020: 59 confirmed cases and now 21 in Hong Kong. The possibility of the resurgence of SARS is dismissed.
• Jan 9th 2020: The world health organisation (WHO) confirm a novel coronavirus isolated from a hospitalised patient.
• Jan 10th 2020: The virus claims its first victim; a man in Wuhan.
• Jan 13th 2020: First case in Thailand.
• Jan 16th 2020: Chinese national hospitalised in Japan confirmed to be the same virus after the individual was likely in contact with an affect person.
• Jan 21st-23rd 2020: First cases in the USA in Washington and Chicago.
• Jan 22nd 2020: China suspends all travel from Wuhan placing the city under quarantine.
• Jan 24th 2020: First confirmed case in France.
• Jan 26th 2020: Two more cases of the virus in California and one in Arizona.
• Jan 30th 2020: First confirmed case in Tibet. With cases now confirmed in all 21 provinces of mainland China.

Introduction to Viruses

The reason I want to talk about this outbreak is to explain how these viruses work and what is the best way for us to help prevent its spread. Viruses are unique, they are in the most simplistic way a living organism. Although they possess no cellular structure or need to gain sustenance. They do contain genetic material that allows them to reproduce and evolve.

Viruses are defined in many ways (for more information search for the Baltimore Classification), but here I will mention only DNA and RNA containing viruses. In the situations I will discuss their functions are identical. DNA and RNA are both genetic instructions, that hold information for the creation of more virus.

Viruses are unable to self-replicate or undergo sexual reproduction. They instead require a host cell to conduct this for them. Once a virus enters the body it will infect the hosts cells injecting within them the DNA or RNA that they are carrying. The internal machinery of our cells will read this foreign genetic material and use it to make more of the virus. Our cells are relatively simple in this regard. Provide them information and they will make it no questions asked. So our cells unwittingly go about their normal function leading to the production of more viruses. This eventually leads the cell to die allowing the new born viruses to escape to infect further cells down the line.

Treating Viruses

This life-cycle makes viruses a tricky area to treat medically. The common cold has no cure and treatments for HIV have taken years to be developed. The reason for this is that the virus spends a large amount of its time within the host’s cells. This effectively hides them from the drugs that could target them. We struggle to make drugs that are able to differentiate between what is normal and infected. The same obstacle cancer treatments have. Therefore in many situations involving viruses we rely on the immune system to handle the problem. Conditions such as chicken pox or colds are are left up to the individual to suffer through. Only using methods to stem the symptoms such as creams for chicken pox and anti-inflammatory drugs for colds.

That’s not to say there aren’t antiviral drugs. These target the life cycle of the virus in question working to prevent their reproduction. They are however specifically designed for the virus in question with treatments existing for HIV and hepatitis.

Coronavirus

That brings us to the topic of the month coronaviruses. This is actually the name of a family of viruses. From the common cold to influenza to SARS (server acute respiratory syndrome) and the recent novel coronavirus 2019 (nCoV) of Wuhan. It is important to note that there is not much known of this new virus. Therefore things are subject to change, any numbers or statistics posted are accurate from today, but will change in the coming months.

The origin of the virus is believed to have been a jump from animal to human with the suspects being either bats or snakes. It may have been contracted through being in close proximity to these animals carrying the virus or consumption of its meat. There are several factors to take into account when looking at a new virus. These are its method of transmission and the incubation period. With regards to the nCoV it is air-born infecting others through bodily fluids, coughing and sneezing. Inhaling the infected air will allow the virus into the lungs where it will begin replicating. The incubation period is the time it takes for symptoms of the virus to become noticed. Once the virus is in your system it will not immediately cause fever and coughing only once it had spread enough throughout the lungs will these begin to show. For the nCoV this period is currently estimated at 7-14 days, this is the reason why those escaping Wuhan and mainland China are being kept in quarantine for a minimum of two weeks.

Thus far we know the virus causes similar symptoms to that of flu; fever, coughing and in extreme circumstances pneumonia. There is currently no cure to the nCoV with hospitals only able to offer supportive care to those in need. Providing medication for the symptoms, fluids to those undergoing a fever and in some cases respiratory support for patients struggling to breathe. There is now ongoing work to develop a vaccine for the nCoV in the USA. The national institute of health announced their work on January 28th.

It is important not to panic, the WHO have not yet classed this outbreak as a global pandemic. This means it is crucial that people remain vigilant and alert without becoming overly anxious about this subject. This outbreak is not a crisis that requires mass worry. If you are concerned, the WHO and the centres for disease control and prevention (CDC) have provided a list of recommended actions to prevent the transmission and spread of this virus.

1. Wash your hands often with soap and water for a minimum of 20 secs. Or using alcohol based sanitizer with a least 60% alcohol.
2. Avoid touching your face with unwashed hands when outside. Viruses can enter the body through the nose, mouth and eyes.
3. Avoiding contact with those who are already sick. As well as remaining home when you yourself are sick.
4. Make sure to cover your mouth with a tissue should you cough or sneeze and dispose of the tissue into the rubbish. With regard to masks; they will help to prevent people who are already sick spreading their virus too easily. However their effectiveness at preventing the inhalation of infected air is relatively minimal.
5. Avoid unnecessary travel to infected countries. Placing yourself in a higher risk area will increase chances of contracting the virus.
6. If you are concerned you may have the nCoV contact your local medical professional over the phone. They will then be able to prepare correctly to deal with your condition. However it is unlikely you have the nCoV unless you have been in direct contact with someone who has recently travelled from China.

As of January 29th 2020 there have been 7815 confirmed cases of the nCoV with 170 deaths (only within mainland China). Compared to the SARS outbreak of 2002-03 with 8098 cases and 774 deaths, the nCoV does not appear to have the same lethality however it is still within all recommendations to avoid its spread any further.

Reading Sources

• The Centre for Disease Control and Prevention
• The World Health Organisation
• Molecular mechanisms of severe acute respiratory syndrome (SARS) David A Groneberg et al.
• Emerging viruses without borders: the Wuhan coronavirus. Liu SL and Saif L.

A new year, a new you. As December passes into January and we once again have to remember to put 2020 instead of 2019 on paperwork. We often decide to make a change in our lives, one for the better. One of these more common resolutions is to quit smoking. Now I don’t need to tell you that inhaling high temperature toxic gas causes damage, but instead talk about how the brain becomes addicted to these bad habits.

Sorry I lied, I can’t not give a general warning. Smoking causes cancer, damages the lungs and trachea as well as leading to discolouration of the skin and rapid ageing. Not a good habit best we get rid of it. Vaping won’t be left to its own devices either. Dosages of nicotine alone is also no better for you.

This post will aim to focus on addiction. Using nicotine as the example, this chemical is the reason people becoming hooked on smoking and more recently vaping. We will delve into how the brain is able to develop a dependence on toxic chemicals.

Nicotine

The addictive component of conventional and electronic cigarettes. Nicotine is able to enter the brain and cause all manner of issues throughout your system. There are many natural chemical signals within the brain that all conduct specific functions; from the control of your emotions, the processing of pain and the integration of your muscles. One of these chemical signals is the neurotransmitter acetylcholine. Nicotine happens to be able to conduct the same function as acetylcholine activating different areas of the brain outside of your control. In fact nicotine is so good at this that scientists named a group of acetylcholine receptors (detectors of acetylcholine) as nicotinic. Nicotine is able to turn on these receptors without acetylcholine being present.

Nicotine has some minor benefits in the form of improved short term memory and increased focus. However these benefits do not outweigh the increased chances of cancer, increased blood pressure, along with other cardiovascular complications, and eventually dependence.

Reward

The reward pathway is found within the brain and acts to promote actions that improve our health and keep us going. Things such as eating, sex and social interactions all work toward your basic instincts to survive and procreate. Whenever you engage in these activities the brain rewards you with feelings of pleasure. The areas of the brain responsible of this are, the ventral tegmental area (VTA) and the nucleus accumbens (NA), together they make up this “reward” pathway. When activated they will release dopamine which generates the feelings of euphoria. This in turn promotes you to repeat those actions reinforcing it into your memory.

Mechanisms that Drive Dependence

Abusive drugs take advantage of this system tapping into the potential of reward to develop addiction. Along with all the negatives; they provide that one positive people crave, pleasure! Nicotine being our example of the day, is able to activate the reward pathway by binding to acetylcholine receptors within the VTA. Carrying out the function that internal acetylcholine would have conducted. This leads to the NA releasing dopamine effectively rewarding you for something that is causing you harm. This is what leads to the development of addiction.

By repeatedly engaging in the drug activity, such as smoking the inhaled nicotine continues to promote dopamine release. The brain eventually becomes accustomed to the constantly higher level of dopamine, therefore more of the drug is required to achieve the same levels of pleasure. Through the usage of the drug the addict has reprogrammed their brain into thinking these high levels of dopamine are normal. This means that the act of quitting is even more difficult.

Quitting Addiction

As simple as it may seem to an outsider, quitting is not an easy undertaking. To remove the new programming your brain has developed over the usage of the drug is extremely taxing. There is now an innate imbalance, in the chemicals within the brain. It is therefore advised in most cases to use medicinal help, to slowly reduce cravings and help with withdrawal. Going “cold turkey” can cause all manner of issues both mentally and physically, some may have experienced these effects when failing to get their morning coffee. Headaches and irritability are just a few of the potential withdrawal symptoms one might experience when quitting an addiction. Medicinal help for nicotine dependence consists of using nicotine patches or alternative nicotine replacement. Then to eventually reduce the dose over time, allowing you to correct the chemical imbalance without too much of the craving or withdrawal. This takes time, the brain has completely changed how it responds acts of pleasure. It needs to slowly repair the damage the drug has caused to its internal circuits. The best method to quit any drug is to seek medical consultation and to develop a regime works best for you.

Summary

Good luck to those who are trying to make a positive change in their life, I shall leave you with a quote and a clip from Dr Robert Lustig. These drugs and substances provide pleasure not contentment or happiness in your life. “Pleasure is short lived and happiness is long lived.” Seek happiness for a better state of mind and a Happy New Year!

Reading Sources

• Molecular and Cellular Aspects of Nicotine Abuse, John Dani and Steve Heinemann.
• Drug addiction: the yin and yang of hedonic homeostasis, Koob GF.
• Neurobiological mechanisms of addiction: Focus on corticotropin releasing factor, George Koob and Eric Zorrilla.
• Effect of nicotine on brain activation during performance of a working memory task, Ernst et al.
• Reward, Addiction, Withdrawal to Nicotine, Mariella de Biasi and John A. Dani.