The Science of Sexuality

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Sintija Jurkevica and Jonathan James

The struggle of understanding sexuality begins to muddle even before sexual orientation can be defined. Some sources describe it as a person’s capacity to have erotic experiences and responses. However, in general, sexual orientation or preference, can be defined as “the sex (biological aspects of maleness and femaleness) of those whom one feels romantically and sexually attracted to”, where one’s sexual orientation may be categorised as heterosexual, bisexual, homosexual, queer, pansexual, asexual or among others. However, categorisation of identifiable preferences is more nuanced than it appears; whilst some research may describe orientation as discrete categories, substantial evidence backs up the existence of a sexual continuum or spectrum.

But how does one develop a sexual preference? This riddle is a classic psychological argument of nature versus nurture: do the genes, the environment, or a mixture of them both influence one’s sexual attraction to others? This is obviously an ongoing debate and a matter of significantly more research. A recent September publication, composed by a psychology researcher Michael Bailey and his colleagues in the peer-reviewed journal of Psychological Science in the Public Interest, has been created with the intention of objectively reviewing previous scientific research on sexual orientation to draw impartial conclusions on the topic, without preconceptions of scientific biases and political influences.

Bailey’s review paper concluded that the non-social causes, such as the individual’s genetic make-up, play a larger role than environmental influences in establishment of one’s sexuality. The evidence, supporting such a claim, includes the genetic influences in twin studies and unchanged sexual orientation of infant boys after they are surgically or socially “converted” into girls. Bailey and colleagues also argue against the commonly assumed environmental causes of homosexuality to be weak and distorted in comparison to alternative explanations.

Various genetic hypotheses had been proposed to explain differences in sexuality. In several studies, it was found that a several different genetic markers (i.e. genetic elements) were more likely to be found in gay men in comparison to their straight counterparts. When this news was first published, it caused an outpouring in the media of the discovery of the so called ‘gay gene’, but the media failed to report one significant factor – genetic influences themselves cannot be used to determine predisposition to a trait. In other words, simply having a genetic element doesn’t automatically result in these individual’s sexual orientation. To make matters more complicated, scientists were unable to reproduce these findings in women for same sex attraction, suggesting that sexual orientation is a lot more complex than a few genetic differences.

Other scientists have conducted studies considering the seemingly well establish theory that each additional older brother increases the odds of a male being gay by approximately 33%, with something like 1 in 7 gay males holding their sexual orientation because of having older male siblings. These findings have been controversial, not least because there are several scientific studies that support these proposals, and several that have not found a link.

One attempt to explain this apparent causation is through the maternal immune response. Male fetuses produce H-Y antigens (small proteins) that play a role in sexual development in the womb (i.e. the development of male sex organs). In response to these antigens, the mother will sometimes produce an immune response, which gets stronger with each successive male fetus, resulting in decreased activity of these antigens in later males. One suggestion is that this results in less ‘mascularization’ of the male brain, resulting in the development of same sex attraction. The major flaw with this explanation is simple – the occurrence of the mother’s immune response is significantly lower than the prevalence of homosexuality, suggesting it cannot be the major cause.

The truth of the matter is, despite several attempts to better understand the genetics behind human sexual orientation, scientist know very little about what causes it, or even the true significance of any environmental factors. As Bailey concludes in his paper however, “Sexual orientation is an important human trait, and we should study it without fear, and without political constraint,” Bailey argues. “The more controversial a topic, the more we should invest in acquiring unbiased knowledge and science is the best way to acquire unbiased knowledge.” Therefore, we should look forward to developing a better understanding in the future, in the hope that a better understanding of ourselves, results in a better understanding of each other.

 

 

Sally Ride’s Space Legacy

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Sally Ride was an American physicist and astronaut, most famous for being the first American woman in space, in 1983, and the third woman in space behind Russian Cosmonauts Valentina Tereshkova and Svetlana Sativskaya. As well as being the youngest American to have travelled to space, at just 32, she is less well known for being the first known LGBT astronaut, a fact not revealed until after her death in 2012. Whilst having been married to fellow astronaut Steve Hawley from 1982 – 1987, her partner for the next 27 years would be Tam O’Shaughnessy, who she met when both were aspiring tennis players years earlier.

Ride joined NASA in 1978, having answered an advertisement in a newspaper for people to join the space programme. Prior to her first flight in 1983, she worked as a communicator for the second and third space shuttle flights and worked to develop the ‘Canadarm’ robot arm, used by space shuttles to deploy and recover deliveries. The flight in 1983 subjected her to a lot of media attention, mostly because of her gender. During one press conference, she was asked a series of extremely sexist question by the media, including whether she would cry if things went wrong, and whether the flight would damage her reproductive organs. Despite everything, Ride simply insisted she was an astronaut.

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The Challenger shuttle, moments before the horrific disaster.

On June 18, 1983, Ride because the first American woman in space as a crew member on the space shuttle Challenger. The crew deployed two communication satellites and carried out many drug experiments in space. Ride was the first woman to use a robotic arm in space. A year later, in 1984, Ride embarked on her second mission on the Challenger (sadly to be her last, following the Challenger disaster of 1986, which took place months before she was due to go to space again for a third time.) In total, Ride spent over two weeks in space.

Following the Challenger disaster, Ride moved from space flight to the political sphere, working on the Rogers Commission to investigate the reasons behind the disaster. Later, she would go on to found NASA’s Office of Exploration, which continues to lay the groundwork for much of NASA’s future exploration. She would also work with schools to encourage students to pursue careers in the space industry, contributing to seven short stories aimed at children, and spent some time as a professor of physics at the University of California, San Diego.

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Then US President Barack Obama, awarding Sally Rides posthumous Presidential Medal of Freedom to her partner, Tam O’Shaughnessy.

Sally Ride’s legacy continues to this day – she has received several accolades both during her lifetime and posthumously. In 2013, she was awarded the Presidential Medal of Freedom by then President Barack Obama. A year later, in 2014, she was induced into the Legacy Walk, an outdoor public display that celebrates LGBT history and people.

The Life of Leonardo Da Vinci

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Jonathan James

Leonardo da Vinci is the archetypal renaissance man, a master of painting, sculptor, architecture, invention, and engineering. His work, which spanned multiple disciplines, informed not just art and design, but also contributed greatly to our understanding of zoology, botany, biology, anatomy, engineering, and physics. He filled dozens of notebooks, which continue to surface to this day, containing hundreds if not thousands of drawings, sketches and ideas based on human anatomy, architecture, and mechanics. Whilst most of his work was not experimental – rather based on theoretical concepts, his work went into extreme detail, and provide some of the first explorations of many fields.

Under the apprenticeship of Andrea del Verrocchio, Da Vinci began what would become a lifelong appreciation of anatomy and physiology, which show up repeatedly in his notebooks; some of his most famous sketches include pictures of a foetus in a womb, the human brain and skull, and a series of topographic images describing muscles, tendons, and other visible anatomical features. It’s a common myth that to carry out these studies, Da Vinci stole corpses on which to perform illegal autopsies – the truth is much less exciting. He was in fact given permission, first by hospitals in Florence, and then later in Milan and Rome, to dissect human corpses. As well as studying ‘healthy’ specimens, disease also fascinated Da Vinci, being the first person to define atherosclerosis (thickening of the arterial wall) and liver cirrhosis, and is known to have constructed models that depicted the flow of blood through the vessels of the heart. His work was published in De humani corporis fabrica (The Human body) in 1543.

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Anatomical Drawings of the Neck and Shoulders

Perhaps Da Vinci’s most famous scientific exploits come from the field of Engineering. In 1488, he developed a design for a flying machine, whilst also developing plans for a parachute, giant crossbow, and what has been described a ‘tank’, but which represents a moveable cannon. He worked as an Engineer, when, in 1499 he was forced to flee to Venice, where he developed a system of moveable barricades to shield the city. He worked with Niccolo Machiavelli on a project to divert the flow of the Arno River near Florence, as well as a design, produced in 1502, of a 720-foot bridge developed for the Sultan of Constantinople intended to cross the mouth of the Bosporus, the straight that separates the bulk of Turkey from central Europe. Whilst never constructed, Da Vinci’s work would later be vindicated, when, in 2001, a bridge based on his design was constructed in Norway.

Da Vinci also worked in botany – where he paid attention to the action of light on plants. He also had an excellent understanding of geology, a particularly famous story exists of him frequently exploring caves around the Apennine mountain range. His observations of layered rock also convinced him the biblical story of the great flood could not be true. In addition, he was an accomplished cartographer, producing a map of Chiana Valley in Tuscany from eye, rather than using any modern surveying equipment. Elsewhere, he studied mathematics heavily, becoming particularly interested in geometric forms such as the rhombicuboctahedron, a 26-sided object made up of both square and triangular faces. An accomplished musician, Da Vinci also invented the viola organist, the first bowed keyboard instrument to ever be designed and developed.

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Map of the Chiana Valley, Tuscany.

Da Vinci kept his personal life very secret. As a result, his sexuality has been the subject of much analysis and speculation. Whilst he had few close relationships with women, his most intimate relationships are said to have been with his pupils Salai and Melzi. Court records from 1476 show that Da Vinci and three other young men were charged with sodomy – whilst the charges were dismissed for lack of evidence, there remains considerable speculation around his presumed homosexuality. In any case, the influence of Da Vinci cannot be understated; he made enormous contributions to a vast range of scientific disciplines, not to mention his artistic endeavors not mentioned here. As a result, to this day he remains an iconic figure and a key player in the Renaissance period.

The Science of Jet Lag

airplaneJonathan James

It’s only been in the last few decades that long distance travel has become commonplace in our lives. With it has come the phenomenon of desynchronosis, a combination of symptoms including headaches, fatigue, and loss of concentration. This is better known as Jet Lag. Resulting from the disruption of our bodies circadian rhythms –  the collection of processes that ensure that all our body functions follow a roughly 24-hour clock, Jet Lag can make travelling on holiday or to a business meeting on the other side of the world a nightmare for even the most seasoned traveler. But what exactly is it about travelling across multiple time zones that so badly disrupts our systems, and are there ways to minimise its impact?

What is Jet Lag?

Our bodies internal clocks are regulated by a hormone,melatonin, in an area of the brain called the pineal gland. As night time approaches, the pineal gland produces more melatonin, which has lots of effects on our body – the most obvious being that we become tired, triggering us to sleep. This system relies on us being exposed to different light levels during the day – as light levels begin to fall in the early evening, different genes are switched on or off, getting us ready for sleep. This is all overseen by an area of the brain called the hypothalamus, which scientists refer to as the ‘master clock.’

Travelling across multiple time zones completely messes up the regular system going on in our brains by either extending or reducing the amount of time we are exposed to daylight. As an example, a Flight from London to New York can take around eight hours. Because you are flying ‘backwards’ against time zones, you’ll arrive in the United States only three or four hours later than you left London, effectively creating a time ‘lag’ of over four hours.

For longer flights, these delays become even more significant, but it is ‘forward’ travel that has the greatest impact. As you travel eastward, you are shortening your day, resulting in your brain having to process the idea that it must sleep much sooner than it would normally have to. This results in a lot of internal ‘confusion’ – processes regulating everything from sleeping patterns to digestion are thrown out of kilter, resulting in the typical symptoms we associate with Jet Lag.

How might we minimise its effects?

Research carried out by a group of scientists at the Nuffield Laboratory in Oxford in mice has shown that a protein, SIK1 plays a role as a kind of natural brake mechanism in the mouse, responding to light exposure and stopping the mouse’s body clock. By inactivating this protein, the scientists could produce mice which can adjust to changes in time zones much quicker. Work done by these scientists, as well as research carried out in Japan, has opened the door to the idea of a jet lag ‘cure’ – a medication able to block a similar protein found in humans. However, with much of their work in the experimental stage, the idea of a wonder cure to jet lag is some way off.

Is it possible that there might be other, more easily adopted ways to minimise the effects of Jet Lag? One way might be to take melatonin orally in small quantities – work at Rush University Chicago has been exploring the impact of giving small doses (0.5milligrams) along with exposure to ‘light boxes.’ They’ve demonstrated remarkable results, resetting subject’s circadian rhythms and minimising the impact of Jet Lag. Since then, there’s been an explosion in mobile apps and programmes such as Entrain, designed to help travelers adjust to crossing time zones by telling them when to expose themselves to bright light. Many of these programs have had limited testing, so it’s good to be wary of so called ‘miracle cures.’

In retrospect,  Jet Lag is unavoidable, with the advent of long distance travel in the last few decades meaning we’ve had little time to evolve to the challenge, and whilst we might try to avoid light exposure at certain times and try to maintain a normal sleep cycle, overcoming our own natural body clocks is a pretty big ask all the same.

Why Do So Many Drugs Fail?

Jonathan James

Major pharmaceutical companies like AstraZeneca and GlaxoSmithKline (GSK) invested a staggering 140 billion US dollars between 1997 and 2011 in drug research and development. The cost to the consumer also varies widely, with the drug Copaxone (used to treat multiple sclerosis) costing nearly $4,000 a dose in the US, compared to just $862 in the UK. Even so called ‘affordable’ drugs, like Nexium (used to treat stomach acid) cost several hundred dollars per dose. Why are these drugs so expensive?

In part it is due to the competitive and profit driven nature of pharmaceuticals; but the major reason is that so many drugs fail during development. As a result, in order to continue researching and producing new drugs, pharmaceutical companies have to charge enormous amounts to recoup the amount of money lost on failed drugs. AstraZeneca, which spent nearly 60 billion dollars between 1997 and 2011, had only five drugs approved in that time. To put that in perspective, it cost them approximately 12 billion dollars to produce one usable drug! Clearly it’s in the best interest of both the consumer and the drug companies to see more drugs successfully make it to market. With that in mind, what are the major reasons why so many drugs fail, and can we do anything about it?

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Image Credit: Public Domain Pictures

The drug discovery process is tightly regulated by different bodies depending on what country the company is operating in, but, as most major pharmaceutical companies are multinational, they effectively all follow a similar set of rules. Drug discovery begins by identifying a particular target – be it a protein to inactivate, a bacterium to kill, or a tumour marker to attack. From this, scientists can spend anywhere between three and 20 years working on new compounds. A lot of the time, they won’t even find anything useful!

Let’s assume that the company has found a useful compound it thinks could be a drug. The next step involves a series of trials. These begin with pre-clinical trials in non-human subjects such as mice and rats, and may progress onto dogs, cats, and primates. While controversial, drug companies are forced by law, to carry out animal testing – it’s not something they can just get away with ignoring. The Thalidomide tragedy, which resulted in severe birth defects in thousands of children, came about in part due to a lack of testing in model organisms.

Once the drug passes pre-clinical trials, and only about 10% make it this far, it then passes into three phases of clinical trials. This involves testing the drug on progressively larger groups of both healthy and affected patients to check safety, dosage, and side effects. Only when they are satisfied it’s an effective drug, can a pharmaceutical company apply for a licence to market their drug – and these are not cheap either! By the end of the process, a company may have spent billions investing in a potential drug, although only five per cent of them reach the end point.

Now that we know what’s happening, we have to ask why. Why do so many drugs fail clinical trials? There are a number of reasons. Firstly, model organisms such as rats and mice have different metabolic pathways to humans. This means that the way a drug interacts in one animal may be different from how it behaves in another. This doesn’t mean that animal testing is useless – it just means that more is needed to understand the differences.

Another major reason is that the theory behind a disease is wrong. At the beginning of the drug development process, we might understand very little about the disease. By the time the drug enters clinical trials (maybe 10-15 years later) we might have a much better understanding, only to realise that this means our original drug won’t work. Or we might not understand the disease at all (and this is surprisingly common). This is very true of Alzheimer’s, and is a major reason behind the lack of effective drugs. Whilst we might have a basic understanding of the factors at play, we still don’t know enough to make a drug that will actually work.

Side effects must also be considered. A drug might be very effective at treating an illness, only for it to have devastating side effects that make it a no-no for human use. For example, cancer researchers must try to limit the effects of chemotherapy agents (a tough job) in order to try and give the patient the best quality of life.

With all that in mind, you might be forgiven for thinking it’s a losing battle. Don’t despair. Our knowledge of disease is progressing at an ever increasing rate, and with it comes the hope of wonderful new ways of treating them. In the future, researchers hope to be able to better utilise specific cell cultures, taken from a patient, to better understand their unique disease profile and develop personalised medicines. Other technologies, such as gene editing, and nanotech, may also offer hope to millions of people suffering from disease.

Editing Human Embryos: The Science And The Ethics

Jonathan James

For a long time, the much discussed idea of editing human embryos to eradicate genetic defects has been seen as something of an extremely controversial pipe dream. Until recently, scientists had been unable to successfully edit the genome of a human embryonic cell, both for scientific and ethical reasons. That is until recently, when a team lead by researcher Junjiu Huang at the University of Guangzhou in China announced in the journal Protein and Cell that they had successfully edited out the gene for β-thalassaemia, a condition that affects the production of oxygen-carrying haemoglobin in the blood. However, it is important to note that this was only successful in a couple of a total of 78 cells used, all of which had been designed so that they could not develop into viable offspring. Due to the low success rate, Huang’s team have stopped further work, believing that at the moment the techniques are too inefficient to have any practical real world applications.

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Image Credit: Public Domain Pictures

The technique itself relies on a system called CRISPR/Cas9. This technique works by targeting a specific DNA sequence within the cell’s genetic makeup, and specifically cutting it out, replacing it with a correct copy of the gene, or an inactive, neutral replacement. It, along with all such similar techniques, are very inefficient, although a more recent development, TALENS, promises to reduce this inefficiency.

Of course, the controversial side of this development is not the science itself, but the ethical implications. For some, gene editing in this way is seen as a fantastic opportunity to combat disease; for others it only creates an ethical minefield. So who exactly is right, if anyone?

On the one hand, if restricted to specific cases, there is great hope that gene modification in this way will allow us to overcome all manner of genetic disorders, from Huntington’s disease to cystic fibrosis, by simply removing the offending gene from the developing embryo. George Church, a geneticist at Harvard Medical School, sees no issue once the practical problems have been solved. The fact that manipulation in this way will be passed onto to offspring (via the germ line – sex cells; sperm and egg.) is of little consequence, as Craig Mello of the University of Massachusetts believes altered germ lines will ‘protect humans against cancer, diabetes and other age-related problems’ in the future.

Yet one issue remains – the wider effects of such widespread alteration to our genes. It is incredibly difficult to assess what impact modifying a particular gene might have on the next generation – a risk many consider too great. After all, what good would it be if you remove risk factors for diabetes, only for that individual’s offspring to develop another disease like cancer?

What most scientists (and the wider public at large) agree on is the need for a serious discussion over the use of this technology. Many argue that altering embryos in this way goes too far, beyond what can be considered ethically correct. Edward Lanphier, president of pharmaceutical company Sangano, believes there are ‘fundamental ethical issues’ involved, concerned that the techniques could be exploited for ‘non-therapeutic modifications’ such as eye colour and hair. This underlies a familiar argument in genetic manipulation – the development of so called ‘Designer babies’ – infants that have been specifically designed by their parents and scientists to have specific traits; whether it be increased intelligence or a specific appearance.

So where do you stand on the ethics? For many, this is a very divisive topic. Clearly it offers the potential for great benefit – helping people, who would otherwise be resigned to suffering at the hands of a particular genetic disease, the chance at a happier life. And still there are enormous ethical and moral problems which need to be understood if not solved. Yet it is worth remembering just how remarkable it is that we are now on the brink of having the ability to directly change the way humans are coded. With each passing day, scientists are developing a better and better understanding of the way genes influence our lives. So even if we end up disagreeing on whether it’s right or wrong, let’s all appreciate just how amazing it is that we can even contemplate it.