The Chemical Quest for Love by Sophie Ball

With Valentine’s day just passing, everyone’s emotions have been tested; whether that means you were one of the lucky bunch that had the romantic company of your significant other or you were someone who shared brunch with their ‘galantines’ to make themselves feel a bit better. So what actually is the chemistry behind that fuzzy feeling?

In history, there have been many suggestions to how and why we fall in love. One scientist from Germany even suggested that relationships are affinity reactions and can be measured through browsing tables. More recently, although not completely understood, different chemicals within the body are thought to control the feelings of love.

When you bump into someone that takes your fancy, you tend to find your palms go sweaty, you stutter and your heart feeling likes it’s physically pumping out of your chest, so no wonder love was thought to come from the heart. However, *spoiler alert* love isn’t actually found in the blood-pumping organ but rather is just the brain (how unromantic!) making the rest of your body go a bit mad.

This feeling of lust is driven by the sex hormones, testosterone and oestrogen, from our evolutionary need to reproduce. Both hormones increase in both men and women when you see features that you desire – a symmetrical face and/or proportional body dimensions. This properly explains why the majority of people say they believe in love at first sight.

Next, follows attraction – being ‘star struck’. Once the initial butterflies have settled, the ‘reward pathway’ kicks in. When doing things that feel good such as spending time with your partner or having sexy time (whitwooo), dopamine and norepinephrine neurotransmitters are released. This initiates the feelings of excitement and making you feel giddy when thinking about that special someone. Wow, doesn’t that play on your heart strings (wait sorry, *chemical reactions).

Attraction can also cause a decrease in serotonin hormones, involved in the response for appetite and mood. Scientists have found a similar pattern in those who have OCD suggesting this is what causes the brain to constantly fixate on your love and nothing else.

Finally, to keep out of that annoying friend zone, attachment is the final contributor in falling in love. Attachment is also involved in friendships, mother-baby bonding and other relationships but the addition of lust and attraction factors separate relationships from these other intimacies (well those who don’t have their own problems to deal with).

Oxytocin, known as the ‘cuddle hormone’, is released to make us feel this attraction and want to be close to our other half. It is stimulated by touch and trust – from feeling supported to an orgasm. This increase in oxytocin over time builds a cycle of social trust.

Given these oxytocin attachments’ powerful nature, they are hard to break causing severe heartbreak when losing a loved one. This is why falling in love is seen to follow similar behaviour to drug addictions (although much healthier than recreational drugs, of course). Similarly, endorphin is stimulated by physical pain to reduce its effect and trigger a positive feeling. If it’s a loved one that stimulates this hormone, the brain can learn to associate the pain with a better feeling, allowing people to tolerate painful relationships.

So although there is no particular ‘formula’ for love, it’s understanding is being improved. Love can be one of the best things and worst things that happens to you but everyone is capable of it – it’s just a bit of hormone fluctuation!

Hopefully, you will find that chemistry soon if you haven’t already, happy belated Valentine’s!

 

References

https://www.psychologytoday.com/gb/blog/your-neurochemical-self/201802/the-neurochemistry-love

http://www.eoht.info/m/page/Love+the+chemical+reaction

http://sitn.hms.harvard.edu/flash/2017/love-actually-science-behind-lust-attraction-companionship/

Dorothy Crowfoot Hodgkin by Fatima Sheriff

For this year’s International Women’s Day, I introduce Dorothy Crowfoot Hodgkin. She was the first British woman to win the Nobel Prize for Chemistry (1964) for “determination by x-ray techniques of the structures of important biochemical structures” and the second woman to win the Order of Merit after Florence Nightingale.

She elucidated the structure of penicillin in 1946, proposing a model containing a beta-lactam ring. This was so contrary to the belief that nitrogen would be too unstable, chemist John Cornforth stated “If that’s the formula… I’ll give up chemistry and grow mushrooms”. (Though wrong, he didn’t make good on his promise, probably for the best as he later won the 1975 Nobel Prize.)

In 1956, Hodgkin cracked the structure of vitamin B12. As the most complex vitamin, this discovery was said to be as significant as “breaking the sound barrier” according to Lawrence Bragg. 35 years from her first attempt, she also discovered the structure of insulin in 1969. She was proactive in raising awareness of the hormone and was critical in educating doctors as to what it meant for the treatment of diabetes.

Working closely with John Bernal, she was part of the emerging community of crystallographers in the 1930s, a new field made more accessible to women due to outbreak of the Second World War. Notably amongst her pupils was Margaret Roberts (later Thatcher) who gave her a tremendous amount of respect, putting up a portrait of her in Downing Street, though they were polar opposites politically.

Hodgkin was the longest running president of Pugwash, a high-profile socialist committee formed to reduce dangers raised by new scientific research. For 13 years, she oversaw campaigns mainly concerning prevention of nuclear war. Her husband was a communist, so she was banned from the US and in 1987 she was awarded the Lenin Peace Prize for her anti-nuclear efforts.

She truly let nothing get in her way; she once nonchalantly presented a paper to The Royal Society when she was 8 months pregnant and was the first woman to get paid maternity leave from the University of Oxford. Despite a diagnosis of early onset rheumatoid arthritis at 24, she remained scientifically active for most of her life, though wheelchair bound later in her career. “[my doctor] thinks I should take a month off work but of course I’m not going to do that”. She even attended a conference of the International Union of Crystallography at 83, a year before she passed away.

Dorothy seemed like an empathetic character, one who fought for a safer world and helped encourage many women within her field – Clara Shoemaker, Rita Cornforth, Barbara Low and Cecily Darwin Littleton to name a few. In 2010, she was the only woman commemorated in a series of stamps for the 350th anniversary of the Royal Society, in the honourable company of Edward Jenner, Joseph Lister and other scientific pioneers. Though dubbed merely as ‘the Oxford housewife’ by newspapers at the time of her achievements, her legacy is illustrious and incredible.

Sources:

http://www.rsc.org/diversity/175-faces/all-faces/dorothy-hodgkin-om-frs/

https://en.wikipedia.org/wiki/Dorothy_Hodgkin

https://www.telegraph.co.uk/only-in-britain/who-was-biochemist-dorothy-hodgkin/

https://www.theguardian.com/science/political-science/2014/aug/13/margaret-thatchers-surprising-relationship-with-dorothy-hodgkin

https://www.independent.co.uk/news/people/obituary-professor-dorothy-hodgkin-1373624.html

https://www.theguardian.com/science/occams-corner/2014/jan/14/dorothy-hodgkin-year-of-crystallography

The Hidden Water Contamination Scandal – Fiona McBride

Scientists have discovered that over 90% of the world’s water supplies are contaminated by a deadly chemical known as dihydrogen monoxide. It is estimated that every human on earth has come into contact with some of this deadly substance during their lifetime – every minute, a newborn baby dies as a direct result of dihydrogen monoxide!

 This chemical is a sneaky killer: large quantities of it cause suffocation, while smaller amounts lead to poisoning. Low levels of it have been found inside the corpses of those who starved – it is thought that dihydrogen monoxide may reduce some people’s ability to take nutrition from food. The substance is also a very common occurrence in all types of tumours, and is almost always found in the brains of stroke patients and the blood of those who have suffered from heart attacks.

 And, to make matters even worse, dihydrogen monoxide is absolutely everywhere. It’s present in the atmosphere in such high levels that it falls to earth with the rain, it’s in the stuff that flows out of your taps, it’s almost certainly in the coffee you drank this morning. Even if we could avoid all of the ways in which it contaminates the liquid water we use every day, it’s still unavoidable: dihydrogen monoxide makes up around 4% of the air we breathe. That might not sound like a lot, but it adds up to three million litres of the chemical entering your lungs every year. No wonder it’s found in almost all corpses.

 But, fear not, the very same scientists who discovered dihydrogen monoxide and revealed just how widespread it is are working on a cure for its effects! It turns out that a processed form of the deadly chemical – known as dehydrated dihydrogen monoxide – can reverse some of the issues caused. For example, if someone is at risk of suffocating as a result of dihydrogen monoxide, the very presence of the dehydrated form will reduce the amount of the dangerous chemical to the point that the person is no longer at risk. However, this solution is not yet perfect: although dehydrated dihydrogen monoxide can greatly reduce the amount of dihydrogen monoxide present in the body, it can also have some nasty side effects. These include weakness, dizziness and headaches, heart palpitations, fainting, and, in the case of overdose, death. A way to safely reduce these symptoms is currently the focus of significant research.

 A bigger question, though, and perhaps the key to solving our dihydrogen monoxide related issues once and for all, is where does it come from? The answer: scientists aren’t sure yet. Some chemical reactions such as those used to make plastics produce it, however dihydrogen monoxide has been present on earth for centuries, and we don’t make nearly enough plastic for it to be as widespread as it is. And that definitely doesn’t account for the evidence of dihydrogen monoxide found on the moon! There is a theory that it could have arrived on earth during an alien landing, however we haven’t met any aliens yet so that theory remains unconfirmed.

 For the moment, though, until we discover the source of the dihydrogen monoxide on earth and develop a reliable sure for its effects, perhaps the best way to stay safe is to avoid water wherever possible. You never know if it’s going to be contaminated!

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 Happy 1^st April! Dihydrogen monoxide is actually the longhand name for the chemical formula H₂O – the scientific name for water.

 The first three paragraphs of this article are pretty much true. For instance, every minute a newborn baby does die due to lack of access to clean water. Paragraph five is also fairly accurate; if humanity ever does make contact with aliens, presence of water on their home planet is probably pretty high on the list of topics to discuss.

 Paragraph four is a little less true. “dehydrated” literally means “water has been removed”, so dehydrated dihydrogen monoxide does not exist! However, if it did, then it probably would react with water to make it disappear as is described here. The side effects described for dehydrated dihydrogen monoxide are actually symptoms of dehydration; this is what would happen if a proportion of the water in your body disappeared.

**DISCLAIMER: This was an article written for April Fool’s Day, 2018. The above article was intended for entertainment purposes only and may include completely fabricated facts.**

 

New Glasses Let Wearer See Dead People – Charlie Delilkan

Do you remember one of those old icebreaker questions that asked which five people either living or dead you would take to dinner? Well it could be possible in a few years for this dinner to become a reality! Kind of…

 Turns out, Samsung have discovered a way to detect a new type of particle called fizons, which only exist in an alternate universe where deceased people go. It’s basically a purgatory – we still don’t know anything about a proper afterlife, unfortunately. However, they also predominantly constitute the “people” there so when we visualise these particles, we can see people who have passed on! Cool or creepy? You decide.

With Fizoptic glasses, we would be able to do this! However, we wouldn’t be able to interact with anyone, as they wouldn’t be able to see us since they’re still in another universe, remember. But wouldn’t it be fascinating to see what Stephen Hawking does in his spare time now that he’s left us? Or see whether Adolf Hitler is being consumed by his own guilt or if he’s at peace? Or if you’re a lonely widower, you may be able to put on Fizoptics and see that your deceased partner is actually sat right next to you, watching the same television show!

The glasses have a tiny transmitter in them which broadcasts a beam of extremely high frequency waves (out of reach for human detection). They are so small that they are picked up by fizons in the alternate dimension. When fizons detect these waves, they get highly excited and start to vibrate. After a few milliseconds, they relax again, which transmits energy back to the glasses to allow us to visualise the particles.

Think of it like that old Doctor Who episode (spoiler alert) where everyone was interacting with ghosts only to find out they were really Cybermen and then Rose died and the world ended. Minus the last part.

Now, I understand that there aren’t many advantages to having these glasses other than maybe curing some loneliness or quenching some curiosity, but these glasses are still in their early stages of testing so it may not even make it to the market. But perhaps given time, the deceased people on the other side will also create these glasses too, and maybe one day we’ll be able to communicate! The possibilities are endless. Besides, the other side has Stephen Hawking AND David Bowie, so it’s probably a lot better over there, anyway.

So, get your dinner tables ready, because in a few short years, your imaginary dinner parties may just become a reality.

**DISCLAIMER: This was an article written for April Fool’s Day, 2018. The above article was intended for entertainment purposes only and may include completely fabricated facts.**

Sugar Certified as MORE ADDICTIVE Than Crack Cocaine – Vanessa Kam

In a brave, valiant study against the sugar-loving food conglomerates dominating our kitchen cupboards, Dr Dia Beatez¹ of the University of Duncee has proven that sugar is more addictive than crack cocaine.

Using state-of-the-art facilities in Yu Chun, China, Dr Beatez attached pedometers to adult pandas² and fed them regularly with sugar water for three weeks.  Upon withdrawing the sugar solution in place of GMO low-sugar bamboo shoots, the pedometers recorded a staggering 401% increase in the pandas’ physical activity, with the youngest subject Benben even exhibiting tree-climbing activity in search of sugar water, much to the surprise of the team.

The experiment was repeated using 1tsp crack cocaine³ in solution, but failed to elicit the same effects as the everyday commodity—sugar.

Commenting on her findings, Dr Beatez says the evidence is clear cut.

“Pandas share 68% of their DNA with us.  Accounting for the small difference in genetic makeup, our pedometer results are still significant.  Sugar is more addictive than crack cocaine.  It’s a fact.”

The research has yet to be published, but Beatez is driven to enlighten the masses before reporting her results in the likes of Nature and the BMJ, acting in the interest of the public.

“Just as craving ice cream will make the couch potato stand up, walk 10m to the kitchen, open the freezer and dig in to a tub of cookie dough ice cream, the panda too will quadruple its physical activity in search of sugar.”

Other experts echo these findings.  An article published last year in the British Journal of Sports Medicine demonstrated that sugar is more addictive than opioid drugs in rats, causing behavioural problems and depression on withdrawal, due to dopamine-related changes in the brain.

“Cocaine?  It’s as irrelevant to pandas as it is to most of us in our daily lives,” Beatez added.

These findings come in light of the Soft Drinks Levy sweeping England, which charges manufacturers per litre sugar-loaded beverage produced.

However Dr Beatez insists the government is not doing enough, neglecting the heavy consumption of sugary snacks.  “I have had patients come in because they simply cannot just eat two squares of Cadbury’s Dairy Milk—they must finish the pack, all 200g of it.”

Speaking on account of anonymity,  a student at the University of Duncee confesses to daily binge-eating of Dairy Milk.

“I used to beeline to Sainsbury’s right after lectures to pick up a bar of that milky sweet stuff, demolishing it before even reaching the library.  …  Thanks to Dia’s help, I have been taking DIAgram© twice daily and it is a true miracle!  I walk down the vegetable aisle now!”

When asked to compare sugar to crack, the student was unable to testify, having never been on the drug.

“I am convinced that sugar is more addictive than any Class A drug, just because Dia says so.”

Inspired by her patients’ success, Dr Beatez has founded the Group for Large Unhealthy Companies’ imprisOnment & Sentencing (GLUCOSE), fighting for the incarceration of “global sugar daddies” and the criminalisation of “sugar-dealing”.

The sugar war, is one to match the war on drugs.

Footnotes:

1. Dr Dia Beatez is a registered dietician, with a Masters in Nutritional Science from the Universidad de Noticias Falsas.  Beatez is not a medical doctor, but prefers the title “Dr” and is a recognised expert in the field.
2. Beatez’ research on pandas was conducted in accordance with the Good Laboratory Pandas and approved by the Medical Religious Church.
3. Beatez declined to comment on the procurement of crack cocaine for the experiment, but assures it was ethically-sourced from organic, Fairtrade croppers just south of North America.

 

**DISCLAIMER: This was an article written for April Fool’s Day, 2018. The above article was intended for entertainment purposes only and may include completely fabricated facts.**

Author’s notes

• Dr Dia Beatez – Diabetes
• University of Duncee – Dunce
• Yu Chun, Benben – Chinese words for stupid, dumb
• 401% for April Fool’s
• British Journal of Sports Medicine study real, and was criticised in the following article https://amp.theguardian.com/society/2017/aug/25/is-sugar-really-as-addictive-as-cocaine-scientists-row-over-effect-on-body-and-brain
• DIAgram© – Mirroring how “experts” who give nutritional advice on the internet often sell their own health products as well
• La Universidad de noticias falsas – “The University of Fake News” in Spanish
• GLP – Play on “Good Laboratory Practice”
• MRC – Play on “Medical Research Council”

 

 

Why is HIIT so effective? Keerthana Balamurugan

HIIT, or High intensity interval training, has become increasingly popular over the last couple of years among casual gym goers and professional athletes alike. It is the concept of being able to achieve faster and consistently better results in a shorter period of time rather than spending an hour on the treadmill that attracts the populace. We know that HIIT works, but what is the reason behind it? And why are we only figuring this out now?

High intensity interval training essentially consists of performing a variety of vigorous exercises for around minute each in order to increase your heart rate and push your body to its limit, with short breaks in between. You repeat the cycle until your body eventually tires out. This workout technique has caught the interest of many as intense bursts of exercises seem to be having positive results.

The increasing popularity of HIIT has piqued curiosities of many researchers around the globe. A professor of physiology and pharmacology at the Karolinska Institute in Sweden conducted a study in search of the scientific reason behind the success of this type of workout. The study consisted of two groups of volunteers: one group rode a stationary exercise bike as fast as they could for thirty seconds, taking three-minute breaks in between, the other performed the same exercise but for a much longer period at a maintainable pace. Blood and muscle samples were taken from the two groups before and after the exercise. The results showed a much higher concentration of calcium ions being released for the group that had performed the intense exercise. (released from where? To where?)

During exercise, calcium ion channels open in the muscle cells, allowing calcium ions to pour into the cellular fluid. This increase in calcium ions signals molecular machinery in the muscle cell to contract, causing the entire muscle to flex. Tests showed that after a HIIT workout these calcium ion channels were fragmented. The break down of these receptors meant that calcium ions were able to leak into the cell continuously. This causes stress to the cell, but only a little bit, as the calcium ions are only released in small amounts. Cells react to this stress by increasing their endurance, making them better equipped to withstand more intense sessions of HIIT. Subsequently, there comes a point where after years of doing HIIT that the body is adapted fully to the rigorous exercises. The muscles no longer react dramatically to the intense exercise. In conclusion, this form of exercise is great for fast results but there will come a point where the body will slowly stop showing quick results due to adaptability. Another amazing conclusion that scientists discovered was that even after 24 hours of performing HIIT, the muscles are still breaking down fat in your body.

For those who do not have the time to commit to an hour’s worth of exercise, high intensity interval training is perfect. Results also show that people who do HIIT manage to stick with it and incorporate it into their daily or weekly regime for longer compared to those who do traditional forms of exercise such as cycling or running on the treadmill. Not only does this form of exercise burn more calories, but it also increases your metabolism and builds up your muscles. The convenience of minimal equipment and ability to do it in the comfort of your own home is also a big plus.

Click the link below if you are inspired to try out a session of HIIT.

https://www.fitnessblender.com/videos/body-firming-hiit-workout-for-beginners-beginner-hiit-home-workout-routine

The Science of The Flash – Naomi Brown

Barry Allen, aka The Flash is a crime scene investigator who developed superhuman abilities allowing him to travel extraordinarily fast, dodge bullets and save the world.  Whilst watching the first series, I wondered: ‘Could the flash actually exist?’  Of course, we would have to choose to ignore some of the physics-bending facts such as that nothing can move faster than the speed of light but just say for a minute someone did have these powers.  How feasible would it be? What forces would this superhuman be subjected to?  What other powers would he need to have?

 Firstly, it is worth considering how The Flash got his powers in the first place. In the original comic book, his powers were gained when he inhaled the fumes of ‘hard water’. Well, it doesn’t sound like the most likely story! However, the reason in the current TV show is a little bit more plausible: Barry Allen is working in a forensic science lab with a particle accelerator when lightening strikes.

 Next, we need to consider what other traits The Flash would need to travel superfast.  Firstly, to travel very fast requires superstrength. This is because you need a large amount of force to create great acceleration (you might remember from physics class that force = mass x acceleration).   Therefore, if the flash were to throw a punch at you, it would be fatal!

 The Flash travels at such fast speed that he would need some other upgrades to his anatomy. For example, his eyesight would need to be highly superior in order to see, and avoid, any items coming towards him. He would also require an adapted brain in order to process sensory information quickly to allow him to react at the same speed as his movement. 

 The Flash has superhealing powers.  It is essential that he have this ability as he can accelerate and decelerate almost instantaneously from up to 200 mph speeds.  This would cause such a huge force that his bones and organs would be crushed every time.  

 Intriguingly, at superspeed The Flash would turn into a magnet! The friction created between the ground and his feet whilst running would cause a static charge to the extent that a magnetic field around his body would be created. This field would mean anything magnetic in the surrounding area would be attracted to him; can you imagine the destruction that would cause?

 We also should consider the suit that the Flash wears: presumably spandex and/or latex. These materials would need to be very heat resistant, as the movement of the Flash’s limbs would generate lots of friction leading to blistering heat.

 Maybe the moral to this story is to sit back and enjoy the entertainment provided by these superhero stories. I imagine any comic book hero that was scientifically accurate would be very boring to watch!

 

 

Does alcohol cause cancer? Beth Firmin

Worrying news: alcohol is a carcinogen. But what does this actually mean? Should you be concerned about that couple of drinks you enjoy with your friends every so often?

What is a carcinogen?

A carcinogen is anything that has the potential to cause cancer, a disease caused by DNA mutations that lead to uncontrolled cell division. Different carcinogens can act in different ways – while some may directly act on DNA, others may cause cells to divide at a faster rate than normal, which could increase the chances of mutation.

You should note that carcinogens don’t cause cancer in every single case of exposure – being exposed doesn’t automatically mean a person will definitely develop cancer. Different carcinogens may have different levels of cancer-causing potential, with some that may only cause cancer after prolonged, high levels of exposure have occurred. In addition, there are a range of factors that affect whether someone exposed to a carcinogen will actually develop cancer – these may include how they are exposed, the length and intensity of the exposure, other environmental factors and the person’s genetic makeup.

There are different groups used to classify carcinogens:

• Group 1: Carcinogenic to humans
• Group 2A: Probably carcinogenic to humans
• Group 2B: Possibly carcinogenic to humans
• Group 3: Unclassifiable as to carcinogenicity in humans
• Group 4: Probably not carcinogenic to humans

Sadly, alcohol is in group 1. That means alcohol definitely can cause cancer.

What types of cancer does alcohol cause?

It is estimated that 5.5% of new cancer cases worldwide can be traced back to drinking.

Consumption of alcohol has been conclusively shown to be the direct cause of seven types of cancer: oropharynx, larynx, oesophagus, liver, colon, rectum, and breast. In addition, there is growing evidence to implicate alcohol consumption in the development of skin, prostate, and pancreatic cancer.

How much alcohol increases the risk?

Sadly, research suggests no amount of alcohol is safe, as even modest alcohol consumption may increase risk of some cancers. A meta-analysis found that drinking one drink or fewer per day is associated with some increased risk for squamous cell carcinoma of the oesophagus, oropharyngeal cancer, and breast cancer.

However, the greatest risks occur with heavy, long-term use. The most common type of excessive drinking is binge drinking (consuming four or more drinks during a single occasion for women, or five or more for men), whereas heavy drinking is defined as eight or more drinks per week/three or more drinks per day for women fifteen or more drinks per week/four or more drinks per day men. Moderate drinking is defined as up to one drink per day for women and up to two drinks per day for men.

The more a person drinks and the longer period of time they drink for, the greater their risk of developing cancer – especially head and neck cancers.

Evidence overall supports a positive dose-response relationship for alcohol and liver cancer.

One review found that people consuming four or more drinks (one drink defined as around 1.5 units of alcohol) per day have about five times the risk of mouth and pharynx cancers, compared with people who never drank or only drank occasionally. Even light drinkers (no more than one drink a day) had a 20% higher risk.

The specific type of alcohol consumed does not affect risk.

However, there can be difficulties in investigating dose-response relationships due to differences in what is defined as a ‘drink’ in different countries and self-reports being used to measure alcohol consumption. Many people are not aware of how many units they are consuming, and people may lie about their alcohol consumption – this could lead to ‘light’ or ‘moderate’ drinking being wrongly associated with increased. cancer risk

How does alcohol cause cancer?

There are a few different mechanisms by which alcohol could cause cancer.

When you drink alcohol (C₂H₆O), this needs to be processed. This is carried out sequentially, catalysed by two enzymes – alcohol dehydrogenase converts alcohol into acetaldehyde (C₂H₄O), and then aldehyde dehydrogenase converts that into acetate (C₂H₃O₂). While ethanol itself is not mutagenic, acetaldehyde is – acetaldehyde binds to DNA and proteins, which can lead to them being damaged. DNA damage can lead to mutations, which could cause cancer. In research carried out on mice and rats, the animals were a lot more likely to develop tumours if they drank water with ethanol or acetaldehyde.

Another way alcohol may cause cancer is by generating what are called reactive oxygen species (ROS). ROS are chemically reactive, toxic molecules containing oxygen, which can damage DNA, proteins and fats in the body. This is done by the reaction of oxidation.

Also, alcohol can impair the ability of the body to absorb and use some nutrients associated with cancer risk, including, vitamins A, the B complex vitamins such as folate, vitamin C, vitamin D, vitamin E, and carotenoids.

Alcohol raises oestrogen levels. Oestrogen is a sex hormone that is linked to a higher risk of breast cancer.

There are some ways in which alcohol may interact with other carcinogens to produce a larger combined risk. Alcohol may change the activity of detoxifying enzymes, which could interfere with the body’s ability to deal with carcinogens. Also, alcohol is a solvent, which can lead to enhanced penetration for carcinogens.

A key factor for a type of liver cancer, hepatocellular carcinoma, a type of liver cancer, is cirrhosis – 90-95% of sufferers have underlying cirrhosis. Cirrhosis is scarring of the liver as a result of previous damage, which can often by caused by chronic alcohol consumption. Therefore, alcohol consumption increases the risk of liver cirrhosis, which in turn predisposes someone to liver cancer.

How do genetics affect this?

The enzymes responsible for processing alcohol are coded for by two different genes. Genes can have multiple forms, called alleles. Certain alleles may increase the mutagenic effects of consuming alcohol.

For the gene encoding aldehyde dehydrogenase 2, there is an allele encoding a catalytically inactive protein. That means, when alcohol is consumed, there is an excessive accumulation of acetaldehyde. As acetaldehyde is a carcinogen, people with this defective gene are expected to be more susceptible to alcohol-induced cancer. Studies carried out in East Asian populations, who have the highest prevalence of the defective allele, show that drinking alcohol is more strongly associated with cancers of the upper aerodigestive tract in people with the defective allele.

In addition, some people have an allele of the gene coding for alcohol dehydrogenase, which leads to enhanced production of acetaldehyde in the liver. Studies of high alcohol intake found that this allele is significantly associated with increased risk for liver cancer and some other cancers.

Massive Insects in the Carboniferous – Alex Marks

Travel back in time, 300 million years, and you will most likely be surrounded by massive swamp forests that stretch beyond the horizon, with the ground covered in mosses and weird looking trees resembling massive ferns. This is the Carboniferous period.

 A bird is flying towards you, but as it gets closer, you realise that it is actually an enormous dragonfly. This massive insect is called Meganeuropsis permiana and belongs to a family of estimated insects called griffinflies, a cousin to today’s dragonflies. From wing tip to wing tip it was a gigantic 71 centimetres (about the size of a pigeon). Today the largest dragonfly measures a mere 17 centimetres from wing to wing – four times smaller than the Meganeuropsis.

 In the Carboniferous period arthropods were extremely common and much larger than their descendants today. There were no mammals and no birds. Insects and other arthropods ruled the skies, seas and the ground. Millipedes that were up to 2 meters long and 50 centimetres wide could come crawling along towards you.

Drawing of the Carboniferous Period (Source: https://commons.wikimedia.org/wiki/File:Our_Native_Ferns_-_Carboniferous_Pteridophyta.jpg)

 The largest fossilized millipede is called Aurthoplaura and was probably the biggest arthropod that ever lived. There were mammoth cockroaches and massive scorpions. The largest fossil of a scorpion belongs to the Jaekelopterus rhenaniae, which was bigger than a tall man with claws up to 46 centimetres – not something you would like to meet while taking a quick dip!

 Fossils show us that these massive creatures flourished, but where are they now? To understand why they could exist then and not now we need to look at oxygen concentration in the air.

 The oxygen content of the atmosphere was 14% higher than today (35% compared to today’s 21%). The concentration of oxygen made a difference in the size of these insects due to their respiration system.

 A respiration system is how an animal takes in oxygen. For humans, we breathe air into our lungs, and the oxygen enters our blood, which brings it to every single cell in our body.

 Insects, on the other hand, do not have lungs or blood. Instead, they have openings on the outside of their bodies that allow air to enter. These opening are called spiracles, and they get smaller and smaller and allow oxygen to diffuse into every cell. It is this system that puts a size limit on arthropods. In the Carboniferous period, the oxygen content of the air was high; arthropods could take advantage of this and grow massive.

 In labs, it has been shown that by slowly increasing the concentration of oxygen to a population of insects, each generation gets bigger and bigger. This experiment shows how the size of insects is correlated to the amount of oxygen in the atmosphere and suggests a new theory as to why arthropods got so big.

 Arthropods got so big not because they could but because they needed too. Researchers at Michigan State suggested that arthropods got bigger as small larva could not handle the high oxygen levels as they could not regulate their oxygen intake. Bigger larva could handle the oxygen levels and went on to produce bigger adults, which meant that arthropods evolved to be larger because it was the only way to survive.

 But why was the oxygen level so high in the first place? During this period the land was covered in plants, from mosses to some of the earliest trees. These plants were taking in carbon dioxide from the atmosphere and pumping out oxygen like they do today, but the bacteria that decomposed the plants when they died was not around yet. So the carbon dioxide did not re-enter the atmosphere, and the oxygen level increased, allowing for bird-sized dragonflies and massive millipedes. 

What Causes Alzheimer’s? Emma Pallen

Alzheimer’s disease is a chronic neurodegenerative disorder with a wide range of emotional, behavioural, and cognitive symptoms. It is the most common cause of dementia, causing around 60-70% of dementias and is primarily associated with older age, with around 6% of the global population over 65 being affected and risk increasing with age. This is especially concerning considering our ageing population and, by 2040, it is expected that there will be 81.1 million people suffering with Alzheimer’s worldwide. It is also one of the costliest conditions to society, costing the US $259 billion in 2017.

Symptoms of Alzheimer’s can be grouped into three categories. Perhaps the most recognisable category is cognitive dysfunction, which includes symptoms such as memory loss, difficulties with language, and executive dysfunction. Another category of Alzheimer’s symptoms is known as disruption to activities of daily living (ADLs). Initially this can be difficulty performing complex tasks such as driving and shopping, later developing to needing assistance with basic tasks such as dressing oneself and eating. A third category of AD symptoms are related to emotional and behavioural disturbances. This can range from depression and agitation in earlier stages of the disease to hallucinations and delusions as the disease progresses.

What causes Alzheimer’s Disease?

We know that the symptoms of Alzheimer’s are caused by a gross loss of brain volume, also known as atrophy, in a number of regions that progress as the disease develops. As brain tissue is lost, symptoms associated with the function of the lost area emerge, such as personality changes developing as tissue is lost in the prefrontal cortex.

We also know that this brain atrophy is caused by a loss of neurons and synapses in the brain. However, what we don’t know is exactly why this neuronal loss occurs. One way to attempt to solve this question is to compare the brains of Alzheimer’s patients to normally ageing brains. This has led to the observation that the brains of Alzheimer’s patients have two distinct biochemical markers: amyloid plaques and neurofibrillary tangles, which are both abnormal bundles of proteins. While these features are often present to some degree in normal ageing and are not always observed in Alzheimer’s, they are often more associated with specific brain regions, such as the temporal lobe, in Alzheimer’s than in regular ageing. There are a number of theories as to how these biochemical markers may be linked to neuronal and synaptic loss, however none are fully conclusive.

One such theory is the amyloid cascade hypothesis. This hypothesis suggests that amyloid plaques, which are made up of a protein known as amyloid beta, are the primary cause of the disease and that all other pathological features of Alzheimer’s are as a consequence. This theory suggests that the accumulation of amyloid beta into plaques leads to disrupted calcium homeostasis in the cells, which can lead to excitotoxicity and ultimately cell death. Evidence in support of this theory comes from the fact that Down’s Syndrome, a condition in which almost all sufferers display some degree of Alzheimer’s disease by age 40, is associated with a mutation on chromosome 21 which is also the location for the gene coding for Amyloid Precursor Protein (APP), a precursor protein that leads to the formation of amyloid beta.

However, if the buildup of amyloid plaques are the cause of cell death in Alzheimer’s disease, it stands to reason that the removal of these plaques should at the very least stop the progression of the disease, which has not been found to be the case. Furthermore, whilst APP producing transgenic mice do end up having more amyloid beta and amyloid plaques, this does not lead to other features of the disease such as neurofibrillary tangles and most importantly, no neuronal loss. This suggests that there may be some other cause for the neuronal loss seen in Alzheimer’s.

Another theory about the cause of neuronal loss in Alzheimer’s focuses on hyperphosphorylated tau, a protein that is the main component of neurofibrillary tangles. The tau hypothesis suggests that the hyperphosphorylation of tau leads to the formation of these neurofibrillary tangles which can result in depleted axonal transport, a potential cause of cell death. This idea is supported by the fact that the number of neurofibrillary tangles is linked to the degree of observed cognitive impairment. Additionally the progression of where tangles are found is similar to the known progression of atrophy observed in Alzheimer’s. Dysfunction of tau is also known to be linked to another type of dementia, frontotemporal dementia, so it seems plausible that similar mechanisms may be at work in Alzheimer’s.

Whilst these are the two of the most prominent explanations for neuronal death in Alzheimer’s, there are a multitude of other potential explanations, and it is likely that no single explanation will capture all facets of the disease. Rather, it is more likely that there is a complex interplay of biochemical reactions along multiple pathways that lead to the clinical features we see in Alzheimer’s disease. These are likely affected by many other risk factors, such as genetics, or environmental factors such as smoking or head trauma.