Are you sick of the lazy stereotypes that surround scientists? That we are all old, white men in lab coats, with fuzzy hair and safety goggles, and that the only thing that we find fashionable are tank tops and boiler suits? Well I was, and so that is why my colleague Sophie Powell and I have created a new blog, to challenge these conventions.
I have always been extremely interested in fashion, and at one point I believe that I had the largest collection of bowties in the North West. As well as being a PhD student at the University of Manchester, Sophie is also a keen fashion blogger, posting regularly on her website, The Scientific Beauty. We were both sick of seeing articles such as this one from the Guardian portraying scientists as socially inept and modishly incompetent troglodytes, and so we decided to create Sartorial Science.
The idea behind this blog is that any scientist, from undergraduate to professor can send us a photo of them in their resplendent best, and then answer some basic questions about their research and their fashion influences. It is supposed to be a bit of fun, but like similarly minded projects ‘This is What a Scientist Looks Like’ and ‘STARtorialist’, it aims to showcase to the wider public that scientists are real people, and that many of them have a variety of interests outside of science, including fashion and looking fabulous!
Many might think that sites such as this are a waste of time, and that scientists should only
concern themselves with doing their research, publishing results, and applying for grants. However, it is extremely important to humanise the people behind the science, not least because it will help to inspire a future of generation of scientists. If younger students think that being a scientist is all about working in a laboratory and conforming to stereotypes, then many of them might not decide to pursue science any further than compulsory education.
As well as showcasing the sartorial merits of our contributors, we also hope to gather enough data to be able to start investigating the relationship between scientists and fashion, in a more detailed study that would be suitable for publication. But in order for that to happen we need lots more posts, so come on scientists show us your style!
With the summer holidays in full swing and the sun making (intermittent) appearances, it’s time to start lathering on the suntan cream! Despite the hassle and general “greasiness” of these products, suntan cream is essential to protect our skin from damaging ultraviolet (UV) A and UVB rays which can lead to sunburn, premature skin aging and cancer. But while we’re busy trying not to stick to our beach towels, it may be interesting to note that not all organisms share our sticky plight: many bacteria, algae and marine invertebrates are known to produce their own sun protection. Now, research suggests that even fish may share this useful ability.
The sun is vital for maintaining life on Earth. It provides us with essential light and heat, without which our planet would be a lifeless rock covered in ice. But sunlight comprises different forms of light, including UV radiation which is invisible to the naked eye. It is this UV radiation (specifically the UVA and UVB forms) that can be harmful to our health, causing damage to the skin’s DNA. In humans, this can result in detrimental DNA mutations occurring, leading to various skin cancers such as basal cell carcinoma and squamous cell carcinoma.
But UV radiation is also harmful to other organisms, and many bacteria, algae and invertebrates that inhabit marine environments are exposed to high levels of sunlight (e.g. reefs, rock pools, etc.), meaning they need to protect themselves against this damaging UV radiation. While we humans need to lather on the suntan cream, these clever organisms produce their own sunscreens in the form of mycosporine-like amino acids and gadusols, which are able to absorb UV radiation and provide photoprotection. Such compounds are made by an enzyme called DDGS for short, a member of the sugar phosphate cyclase “superfamily” of proteins which are involved in synthesising natural therapeutic products (e.g. the antidiabetic drug acarbase).
While mycosporine-like amino acids and gadusols have been found in more complex marine animals, such as fish, it was originally thought that these compounds had been acquired through the animal’s diet. Recently, however, a group of scientists from Oregon State University in the United States have discovered that fish can produce gadusol themselves. Interestingly, this seems to be achieved through a different pathway to that used by bacteria.
Rather than DDGS, the group found that fish (in this case, zebrafish) possess a gene responsible for making an enzyme similar to another member of the sugar phosphate cyclase superfamily, EEVS. This EEVS-like gene is found grouped with a functionally unknown gene termed MT-Ox. In fact, the researchers were able to produce their own gadusol by adding both genes to a modified strain of E Coli and growing the cells in an environment rich in the necessary components for gadusol production. This suggests the EEVS-like and MT-Ox genes are involved in the production of this UV-protective compound in fish. Importantly, both the EEVS-like and MT-Ox genes are expressed during embryonic development, providing further evidence that fish are able to synthesise gadusol, rather than simply acquiring the compound through their diet.
Unfortunately for us, the EEVS-like and MT-Ox genes are not present in the mammalian or human genome, but they do appear in other animals including amphibians, reptiles and birds, inferring that the production of UV-protective compounds may be even more widespread than once thought. And while this does not save us from the dreaded, yet essential exercise of putting on suntan cream, it certainly acts as a friendly reminder that we may not be as evolutionarily superior to these animals as we might think…which I suppose is a good thing.
Have you ever thought about being a scientist? The growing movement of citizen science encourages public volunteers to contribute towards ‘the doing’ of scientific research, all without giving up the day job, undergoing extensive training or putting on a white coat. Topics and activities involved can vary widely, but typically ‘citizen scientists’ get involved in collecting, processing and/or interpreting data in some way, all under the direction of professional scientists or researchers. For example, you could be asked to record observations about the natural environment, track human or animal behaviours, perform logging or mapping activities, or interpret images and patterns.
Galazy Zoo (a study to investigate the properties and histories of galaxies) is regarded as one of the most well-known and successful citizen science projects. Launched in 2007, the project started life as a website that invited members of the public to sort images of galaxies into different categories (ellipticals, mergers and spirals). Stunned by the speed and scale of the initial response (over 70,000 classifications received within 24 hours), the project has continued to attract an army of willing volunteers who perform ever more skilled tasks. Furthermore, they have developed a growing number of online resources to engage schools and the general public in astronomy. Meanwhile, in Old Weather, volunteers delve into and transcribe the contents of historical logbooks from ships. Transcribing handwritten entries about weather readings taken at sea from thousands of logbooks into a digital (and analysable) format would clearly be a mammoth, and potentially impossible, task; yet, opening it up to the public has made it feasible.
So, citizen science can be a valuable way of both advancing scientific inquiry and engaging the public in science. The general public can indulge their own interests whilst getting the feel-good factor of knowing they’ve contributed towards science. Basically, it’s a win-win situation. Or is it? Cynics may argue that some projects are little more than crowdsourcing, enabling scientists to achieve what would otherwise be too expensive, time consuming or intensive for researchers working alone. Whilst it’s true that there may be pragmatic reasons for using citizen science approaches, projects can offer opportunities for genuine dialogue and collaboration between scientists and the public. For example, members of the public with hay fever are now involved in designing #BritainBreathing, a citizen science project aimed at understanding more about seasonal allergies such as hay fever. So far, individuals have been involved in ‘paper prototyping’ workshops, to sketch out the design of a mobile phone app that will capture data about allergy-related symptoms such as sneezing, breathing and wheezing. Hence, the goal is to engage citizens in multiple roles whereby they can act as co-designers and collaborators, and not just as passive sensors.
Citizen science is not a new concept. Indeed, the first project has been traced back to 1833, when the astronomer Denison Olmsted invited the public to submit first-hand accounts of a spectacular meteor shower. Nonetheless, the term ‘citizen science’ only entered the Oxford English Dictionary In 2014 and it is enjoying a ‘boom period’ at the moment, with an explosion of projects emerging. Why the sudden popularity, you might ask? Two factors stand out. First, advances in information technology and the widespread availability of internet-enabled devices (e.g. smartphones and tablets) have enabled individuals to contribute data online in real-time, on the move, and with minimal effort. Second, there is growing recognition that the public have a stake in science and that research should be more democratic, shaped by the interests and needs of the people. Whilst the former is certainly useful in enabling projects, personally it is the latter that most excites me. Citizens have more opportunities (and power) than ever to shape research to generate the knowledge and solutions we want for our futures. So go on, indulge your inner scientist. Power to the people.
Guest post by: Lamiece Hassan
Lamiece is a health services researcher and public involvement specialist at The University of Manchester. With a background in psychology, her research has explored topics such as health promotion, mental health in prisons and psychotropic medicines. Her current work focuses on how we can use digital technologies and health data in trustworthy ways to empower patients and improve health.
I’m not sure about you but, for me, Sunday hails the end of one long week and the beginning of another *yawn! So, just in time to brighten up your Monday morning, the Brain Bank team have complied a list of 20 of the finest nerdy jokes to keep you smiling through the coming week!
In reverse order:
20) A mathematician walks into a bar and orders a root beer in a square glass.
19) A statistician gave birth to twins, but only had one of them baptised. She kept the other as a control.
18) A psychoanalyst shows a patient an inkblot, and asks him what he sees. The patient says: “A man and woman making love.” The psychoanalyst shows him a second inkblot, and the patient says: “That’s also a man and woman making love.” The psychoanalyst says: “You are obsessed with sex.” The patient says: “What do you mean I am obsessed? You are the one with all the dirty pictures.’’
17) Potassium and oxygen had a boxing match, it ended in a KO
16) There are 10 kinds of people in this world, those who understand binary, and those who don’t.
15) Einstein, Newton and Pascal are playing hide and seek. lt’s Einstein’s turn to count so he covers his eyes and starts counting to ten. Pascal runs off and hides. Newton draws a one meter by one meter square on the ground in front of Einstein then stands in the middle of it. Einstein reaches ten and uncovers his eyes. He sees Newton immediately and exclaims “Newton! I found you! You’re it! ” Newton smiles and says “You didn’t find me, you found a Newton over a square meter. You found Pascal!”
14) What does a subatomic duck say? Quark!
13) A photon walks into a hotel and the porter asks “do you need any help with your luggage?” The photon replies “no thanks I’m traveling light.”
12) Know any good sodium jokes? … NA
11) What does DNA stand for? National Dyslexia Association.
The Higher Education Funding Council for England (HEFCE) have recently announced that they are lessening their proposed stance in relation to Open Access (OA) for the next round of the Research Excellence Framework (REF). If that opening sentence seems like it contains far too many acronyms to be of relevance to you then think again, as effectively what it means is that scientific research will be less accessible by the general public than had previously been hoped for.
What a lot of non-researchers don’t realise is that a lot of scientific articles sit behind a pay wall, which like that of news outlets such as The Times, means that you have to pay in order to access them. These fees vary from journal to journal, but are normally somewhere in the £15-£25 price range (per article), which means that if you wanted to look at four separate articles you could be paying upwards of £100. Of course you may be asking yourself, “yes, but when am I going to actually want to read one of these articles?” But, imagine that you have a terminally ill relative and have just heard of a new miracle cure, or that you are a potato farmer wanting to fully investigate the efficiency of a new type of pesticide. Would you be able to shell out for each of these articles, no matter how spurious the abstracts (which ARE free to access) might appear? Of course you could take up an annual subscription for some of these journals but, with the Nature brand of journals having 91 publications alone, and with most of these subscription costs in excess of £200 per journal, these costs soon become insurmountable.
I have written more extensively on the topic elsewhere, but the whole point of the OA movement is to make these journal articles freely available for all, with either the researcher or the central government bearing the cost. And, it was supposed to be HEFCE that was helping to bring about the change by implementing restrictions for the REF. For those of you who do not know, the REF is basically a giant study that is conducted every six years, in which the research output of every UK university is assessed and ranked, with funding awarded from HEFCE based on that ranking. Again, more details on REF can be read about here, but the idea was that in order for publications to qualify for REF2020, they would need to be made OA, either by publishing in OA journals, or placing them in a freely-accessible repository within three months of the journal article being accepted for publication.
However, under the new guidelines (which can be read here, with highlighted track changes from the original document), which have been revisited after consultation with several leading research institutes, the rules have been changed, and the period of grace is now three months since publication. This may seem like quite a subtle difference, but in some cases it will mean that there is a period of several more months before the research is made freely available. There have also been some other changes, including the admittedly sensible decision that any article that is published via the gold route (i.e. in an OA journal) need not be uploaded to the repository until the final published version has been created. However, I think that there is a very real danger that any softening of the rules is indicative of the fact that HEFCE are probably likely to bend the rules, probably to ensure that any of the larger, and less OA mobilised, research institutes don’t miss out on their slice of the REF pie. The fact that “this additional flexibility will be reviewed in 2016” means that we need to monitor these developments very carefully indeed, in order to make sure that the door is not just slightly ajar, but ripped clean off its hinges so that everyone is welcome.
Please note that, due to its content, readers may find this article distressing.
I had been kidnapped by depression and killed.
A couple of months ago my friend died by suicide. A vivacious, kind and gentle guy, he was one of the six thousand people who kill themselves every year in the UK (Samaritans, Suicide Statistics Report 2015). Every such death affects on average 10-15 people, including family, friends, neighbours and work colleagues (Dyregrov, 2011). Even though the poet Gwyneth Lewis, cited at the beginning of this article, did not attempt a suicide, depression is a major contributor to lethal self-injury. In fact, suicidality is one of the symptoms of this illness. Most of us can probably imagine how loss of hope and prolonged despair can make us want to escape life. However, not all depressed people desire death; among those that do, only about half will attempt to take their lives (May et al., 2012).
Why is it then that people kill themselves? According to the interpersonal theory of suicide it is because of the combination of three factors: thwarted belongingness, perceived burdensomeness, and the capability for lethal self-injury (Joiner, 2005; Van Orden et al., 2010). Thwarted belongingness is a subjective feeling of being disconnected from others, loneliness and lack of mutual care: “I have no one to turn to”, “I am not a support for others”. For example, prisoners kept in single cells are more likely to attempt a suicide. Thwarted belongingness does not necessarily mean that we truly do not belong; it could just be the case of interpreting the behaviour of others as rejecting.
The second factor, perceived burdensomeness, is the feeling that we are a burden to others. It arises from self-hatred and from the belief that we are inadequate, that we let others down and therefore our family and friends will be better off without us: “I make things worse for the people in my life”, “I am useless”. Perceived burdensomeness plays an important role in suicides of terminal cancer patients. Of course, the subjective feeling of being a burden, or being ‘expendable’ does not mean that others also see us as a burden; often it is part of a distorted view of the self and others. Such bias towards negative signals and the perception that we are ‘stuck’ can be remedied with cognitive-behavioural therapy, which helps us to restructure the way we interpret information, how we make sense of the world and how we approach problems.
I dreamt about a creature, a cross between a beaver and a rabbit had landed between my shoulder blades, biting in so deeply that it hung there. Whenever I moved to try and catch the creature its weight would make the flesh gape even more, as if it were unzipping my back. (…) Of course, the creature on my back was me and it was pointless trying to get away. (…) If you met me you’d think I was perfectly nice, but (…) it’s what you are at two in the morning when you’ve been pushed off a cliff again and have nothing to hold on to as you fall.’
Thwarted belongingness and perceived burdensomeness, accompanied by loss of hope, together create the desire to die (suicidal ideation). However, in order to complete a suicide we also need the capability for lethal self-injury. In other words, people kill themselves not only because they want to, but also because they can; after all, suicide is painful and violent, and therefore very difficult to carry out. The interpersonal theory proposes that self-killing becomes easier if we lose our fear of death and if we are less sensitive to pain. This is why previous attempts, as well as previous experience of violence make us more likely to die by suicide. However, the capability for lethal self-injury also increases with increased access to information about suicide and the means to complete it. For example, military people, when choosing a mean of suicide attempt, opt for the method they have been exposed to: members of the army prefer guns, those in the navy – hanging and air force individuals – falling from heights. Consider also the phenomenon of suicide contagion (Wray, 2012). It has also been termed the Werther effect after the suicide of the main character in the famous novel by Goethe led to a wave of copy-cat deaths. Golden Bridge in the US attracts suicidal people from all over the country and from abroad. Kevin Berthia was one of the two hundred people coaxed back from its railings by a police officer. He chose the bridge for the ease of death it offered. He also admitted that erecting a suicide net under the bridge would definitely discourage him from jumping.
The interpersonal theory of suicide can help explain the links between lethal self-injury and age, as well as some personality aspects. Loss of health and independence, sometimes combined with limited financial means puts older people at greater risk of ending their lives (Jahn and Cukrowicz, 2011). This is because having to rely on the help of others, especially children and grandchildren, makes older people feel that they are a burden. Perceived burdensomeness also appears to be important in linking perfectionism with suicidal tendencies (Rasmussen et al., 2012). Perfectionist individuals tend to set themselves standards which are so high that it is often impossible for them to reach their own expectations. As a result they may fall prey to feelings of incompetence, self –blame and inadequacy, and start to see themselves as a burden on others.
On the other hand, it has been shown that mindfulness as a personality trait can help prevent suicide in veterans (Serpa et al., 2014). Mindfulness is an awareness of present moment with non-judgemental attention, almost the opposite of rumination and worry. It makes it easier to cope with negative emotions, alleviates the severity of mental illness and reduces the risk of suicide.
The interpersonal theory of suicide provided me with a partial explanation for my friend’s death. Ending one’s life is said to be the permanent solution to the temporary problems; the sense of hopelessness blinds us to the fact that no matter how bad things are, nothing lasts forever. Sometimes it takes a while to find the right treatment or the right approach to help those in despair. However, mindfulness and cognitive-behavioural therapy are only some of the treatments that can be tried and that work for many people. Perhaps we should also come up with effective ways to teach ourselves and our children how to better manage our emotions, look after our psychological selves and how to find meaning in life.
In memory of Stephen
If you or someone you know needs help, contact Samaritans at 0845 790 9090.
Dyregrov, K. (2011). What do we know about needs for help after suicide in different parts of the world? A phenomenological perspective. Crisis, 32(6), 310–318.
Jahn D.R., Cukrowicz, K.C. (2011) The Impact of the Nature of Relationships on Perceived Burdensomeness and Suicide Ideation in a Community Sample of Older Adults. Suicide and Life-Threatening Behavior 41(6) 635-49
Joiner, T.E. (2005) Why people die by suicide. Cambridge: Harvard University Press.
Lewis, G. Sunbathing in the rain. A cheerful book about depression.
Rasmussen, K.A., Slish, M.L., Wingate, L.R., Davidson, C.L., Grant, D.M. (2012) Can Perceived Burdensomeness Explain the Relationship Between Suicide and Perfectionism?
Suicide and Life-Threatening Behavior 42(2): 121-128.
Serpa, J.G., Taylor, S.L., Tillisch, K. (2014) Mindfulness-based stress reduction (MBSR) reduces anxiety, depression, and suicidal ideation in veterans. Medical Care 52(12 Suppl 5):S19-24. doi: 10.1097/MLR.0000000000000202.
Van Orden, K.A., Witte, T.K., Cukrowicz, K.C., Braithwaite, S.R., Selby, E.A. & Joiner, T.E. (2010). The interpersonal theory of suicide. Psychological Review 117, 575–600. doi:
People are unaware that diabetes mellitus, either type 1 or type 2, goes hand in hand with increased susceptibilities to oral health problems. Even diabetics themselves know little about the risks of bacterial infections such as Porphyromonas gingivalis, a primary cause of periodontitis; the correct term for gum disease. Although P. gingivalis is not normally found in subjects with good dental health, the presence of other bacteria is far more common. Streptococcus mutans and Streptococcus gordonii are both found within the oral setting and form biofilms on the tooth surface. Regular brushing and flossing removes these unwanted visitors but if the accumulated bacteria remain undisturbed for a long period of time they can begin to destroy the gum tissue surrounding the teeth. Interestingly this is where the P. gingivalis comes in. A shift in normal ecological balance in the microenvironment allows the bacteria to act as a secondary invader of the gums, and more specifically the gingival sulcus, the part where the tissue contacts the tooth. Colonisation of P. gingivalis arises via its ability to adhere to salivary molecules, matrix proteins in the gum and other bacteria present in the mouth. It is clearly an opportunistic pathogen.
So, why do diabetics have an increased risk of developing periodontitis? Well, Advanced Glycation End Products (AGEs) arise from chronic hyperglycaemia and therefore are common in diabetes. It is these glycated proteins or lipids which have been shown to impact on periodontal deterioration. Although the exact mechanism behind the interactions of AGE with the disease are unknown there is general consensus suggesting a couple of important points;
An accumulation of AGEs affects the host immunological response. The products can disrupt an important nuclear transcription factor called NF-κβ, one which is involved in many inflammatory responses. IL-6 and TNF-α are also just two important pro-inflammatory cytokines which have been shown to be upregulated in the presence of AGEs.
AGEs will not only upregulate the production of certain cytokines, they also affect the chemotactic properties of mono and polynuclear cells. This enhances the inflammatory response at a given site of infection, in this case at the gums and surrounding tissue.
One final problem in diabetic patients is a drop in salivary pH. Xerostomia, or hypo-salivation is a main cause of the low pH. Maintaining the correct level of fluid in the body perhaps is the greatest problem for individuals with diabetes mellitus. The presence of AGEs and glycated haemoglobin, the latter being another result of high blood sugar levels, disrupts the balance of fluid and electrolytes in the blood stream. Diabetes is a condition that is associated with polyuria (frequent urination), which occurs because the excessive glucose found in the blood changes the normal osmolarity gradient within the body. Simple GCSE Biology states that water will move from an area of high concentration to low concentration. Therefore the increased movement of water into the bloodstream will effectively force the kidney to produce more urine. It’s a vicious cycle – high glucose levels mean more urine produced, causing the person to become dehydrated which leads onto hypo-salivation, leaving an environment perfect for bacterial infection.
The low pH and reduced salivary rate contributes to an increase in tooth decay and as a consequence bacterial/fungal infections are more common in individuals with diabetes mellitus. This is because most oral bacteria and yeast thrive in the acidic conditions of the mouth, the reason why dental experts warn against sugary diet rich in carbohydrates – the main source of food for all mouth dwelling species. This is an alarming problem for experts and scientists worldwide, with an estimated 1 in 3 individuals with either form of diabetes mellitus having some degree of periodontitis during their lifetime. Of course the deterioration of dental health concerns everybody, but more attention must be paid to those that are at a higher risk. Managing the condition as a whole will pay dividends but are there any further precautions which should be taken to preserve the oral wellbeing for diabetics? This remains the most difficult question. Antimicrobial management and regular periodontal treatment is common in the general population, but both should be more prevalent in controlling diabetes related infections.
This post, by author Jason Brown, was kindly donated by the Scouse Science Alliance and the original text can be found here.
Goyal, D. et al (2012) Salivary pH and Dental Caries in Diabetes Mellitus. International Journal of Oral & Maxillofacial Pathology. 3(4):13-16
Griffen, AL. et al (1998) Prevalence of Porphyromonas gingivalis and Periodontal Health Status. J Clin Microbiol. 36(11):3239-3242
Lamont, RJ. Jenkinson, H. (1998) Life Below the Gum Line: Pathogenic Mechanisms of Porphyromonas gingivalis. Microbiol. Mol. Biol. Rev. 62(4):1244-1263
Takeda, M. et al (2006) Relationship of Serum Advanced Glycation End Products with Deterioration of Periodontitis in Type 2 Diabetes Patients. J.Periodontol. 77(1): 15-20.
The science blogosphere has been awash this past week with articles exploring a link between depression and damage to part of the brain known as the hippocampus. News outlets, such as IFLS, are claiming that: “Depression Damages Parts of the Brain”. But, where does this assertion come from, is it really so cut and dry, and what impact will this research have on those currently living with major depression?
Firstly, as with many science news stories, the ideas discussed here are far from a new. What is new and exceptionally clever, is the way this study was performed:
As you might imagine, imaging the living brain is not an easy task and different researchers tackle this problem in different ways. This means that data analysis and imaging methods can vary a lot between research groups. Sadly, this lack of standardisation makes it hard to compare data across different studies, which limits the number of patients each study can look at. This is where this new work really shines. Through a massive international collaborative effort, this study has been able to standardise imaging protocols across a number of international labs. The study examines data from a whopping 1728 major depression patients and 7199 healthy controls, meaning that statistically these findings really pack a punch.
Their findings corroborate what other researchers already suspected – that recurrent depressive episodes seem to be accompanied by shrinking of a brain region known as the hippocampus. The hippocampus is best known for its role in memory formation, specifically in the conversion of new experiences to permanent long-term memories (think 50 First Dates or Memento). This region is arguably also integral to our sense of self. Without memories of our pasts how do we know who we are or what we want for the future? So, hippocampal damage could hold far reaching implications beyond that of simple memory loss and perhaps even contribute to many aspects of depression.
Now, the question scientists really want to answer is – what happens in the brain to cause depression? This study finds that hippocampal shrinkage is only significant in patents who have suffered from multiple depressive episodes, while patients who have only experienced a single episode have relatively normal hippocampi. This suggests that depression causes hippocampal shrinkage, rather than hippocampal shrinkage leading to depression.
Could this mean that we need to look beyond this brain region for the cause of depression?
It’s necessary to keep in mind that this work is not conclusive and may only represent part of a bigger picture. Large scale changes in the brain’s morphology, visible on MRI brain scans (as studied here), indicate significant cell loss. It is quite reasonable to assume that in the early stages of major depression, as with many long-term illnesses, changes in the body/brain may be more subtle – think alterations in brain chemistry and communication rather than large scale cell loss. So, although it’s useful to know that major depression can lead to hippocampal cell loss, we cannot yet rule this region out as a main player in the early stages of depression.
But, most importantly, will this research change anything for the >350 million people suffering from depression worldwide?
Well, actually this work feeds rather nicely into another hypothesis of depression known as ‘the neurotrophic hypothesis of depression’. In brief: It is known that stress and depression cause cell loss in limbic brain regions (including the hippocampus). Neurotrophic factors are proteins in the brain which encourage cell growth and multiplication, these are depleted in depressed patients and animal models of the disorder (often specifically within the hippocampus). Some scientists believe that a reduction in neurotrophins, such as BDNF (Brain Derived Neurotrophic Factor), begins a cascade which ultimately leads to cell damage and death. Therefore, it is possible that repeated episodes of major depression cause an additive loss of BDNF and perhaps subsequent hippocampal damage. Interestingly, a number of studies also suggest that antidepressants may increase BDNF in depressed patients, suggesting the effects of depression on the brain may be reversible.
So, it seems that when it comes to depression, scientists are slowly piecing together large parts of the puzzle. Although many uncertainties still exist (the brain is a tricky organ to understand), with continued research it is hoped that better treatments may be just around the corner.
Having grown up in a South Eastern European country, where fruits are abundant and make up probably about half of our diet during the summer, I’m used to many different kinds of fruit. However, a banana was probably the most exotic fruit that I came across until the age of about sixteen. So, I was pretty intrigued when a couple of months ago a friend of mine bought a mango for us to try. We googled ‘how to eat a mango’, cut it into those cute hedgehogs like they do and tasted it. But, since neither of us had ever tried this fruit before, we didn’t realise that it wasn’t ripe, so the taste was far from nice. Except for the part just around the pit it was like chewing on pine needles. Since then I have learned how to pick more or less ripe mangos and developed quite a taste for them but, I still can’t help noticing a hint of pine in the flavour. Every time this makes me ask myself, what is it that makes two plants that are so different in terms of their habitat and their taxonomic position taste or smell similar?
To get to the bottom of this lets start by looking at how the sense of taste operates and how it is linked to the sense of smell. The flavour of our food is determined by these two senses
combined: try holding your nose whilst eating, you’ll find even familiar foods don’t taste right. Our tongue, the roof, sides and the back of our mouth are covered with taste buds – small receptors sensitive to so called flavorants. The receptors that allow us to detect and recognise odors are somewhat similar to these taste receptors. The two systems rely on chemoreception, which means that the receptors involved are able to capture the chemical compounds that make up a certain smell or taste and transform this information into a nerve impulses in the brain. Information regarding both taste and smell combine in your brain allowing you to enjoy a multi-sensory flavour experience.
Now back to the mango/pine problem. I decided to start my investigation by finding out what chemicals produce the familiar smell of pine. A quick trip to the nearest pharmacy and a scan through the ingredients of pine-scented essential oils revealed that the main components were: α-pinene, β-pinene, limonene, myrcene, camphene cadinene with very little variation from one brand to another. These compounds belong to a larger group known as terpenes, or more precisely monoterpenes, which are most commonly, but not exclusively, found in the resin of coniferous trees.
More than thirty different chemicals make up the flavour of mango and, surprisingly enough, α-pinene, β-pinene, limonene, myrcene and camphene are among them. So, five out of six compounds that are found in pine needles are also found in mango pulp.
Due to their strong smell, high viscosity and antiseptic properties, terpenes act as a repellent that drives away herbivores and insects, thus protecting the plant from predation. The native land for mangos is South and South East Asia and, while there are several varieties of pines that grow in the same part of the world, these plants are only distantly related. Pines are gymnosperms – even though they produce seeds, they develop neither a flower nor a fruit. Mangos on the other hand are flowering plants. From an evolutionary point of view they are considered to be more advanced than gymnosperms since they have flowers that facilitate pollination and their seed is protected by a fruit. Flowering plants diverged from gymnosperms more that 200 million years ago. So how did such different plants develop such a similar defense mechanism?
The first thing that pops to mind is convergent evolution. It is very common in nature for different animals which occupy very different habitats and never even come near each other to develop similar adaptations when faced with a similar obstacle. A classic example is the structure of an eye of vertebrates (e.g. mammals) and cephalopods (e.g. octopus): both these groups have independently developed camera eyes astonishingly similar in their structure and way of functioning. Therefore, an efficient system is very likely to develop in parallel across unrelated species.
So, in the case of pines and mangos, terpenes provide not only a reliable defense against predators but also a mind-bending taste anomaly.
Guest Post by: Daria Chirita.
Originally from Moldova, I am currently in my second year at university in France, Université Jean Monnet , St Etienne, studying Biology. My scientific interests include Molecular Biology and Genetics, in which I am hoping to pursue a Master’s degree. Other than that I enjoy learning and speaking foreign languages, knitting and cinema.
We humans are social creatures. We love to meet up with our friends, family and partners, and rely on them for support through the good times and the bad. But it turns out we may also rely on our loved ones for our health. Our social ties may be helping us to keep sickness at bay and aiding a longer happier life.
There is no shortage of studies that suggest a potential link between feelings of social isolation and declining health in humans. In a study of 2,101 adults aged 50 years and over, a US-based group of scientists found that over a 6-year period, feelings of loneliness predicted higher rates of depression, a reduction in self-reported health and an increased risk of mortality. In 2010, an analysis of 148 separate studies showed that among the 300,000 plus participants, those with stronger social ties had an increased likelihood of survival.
Although the precise biological mechanisms behind the impact of loneliness on our health remain unclear, there is a growing body of evidence to suggest this feeling may affect a number of key systems in our bodies, including the hypothalamic-pituitary-adrenocortical (HPA) axis. The HPA axis is responsible for the release of important hormones called glucocorticoids – cortisol in humans and corticosterone in rodents. These hormones help regulate such things as our sleep, blood sugar, heart function and immune response. However, chronic high levels of glucocorticoids have also been linked with disease. Long-term increased levels of cortisol, for example, have been associated with high blood pressure, diabetes and an increased susceptibility to infection, as well as a number of other chronic diseases.
Interestingly, both urinary cortisol levels and HPA activation have been found to be increased in individuals who feel lonely, with higher levels of loneliness associated with greater cortisol increases. However, this effect only appears to be significant in individuals who are chronically lonely, suggesting the length of time one feels lonely for may play an important role in how this impacts upon our health.
Given the detrimental effect loneliness appears to have on our physical and mental well-being, one must wonder what the function of this feeling is? What is the benefit of making us feeling bad?
From an evolutionary point of view, the aversive nature of loneliness is pretty logical. When we feel socially isolated or our social ties start to waver, we get the desire to reconnect with others. Back when we lived in tribes, maintaining social relationships allowed us to protect each other from predators and hunt more efficiently, thus ensuring the survival of our species. Similarly, our desire to find a mate allowed us to reproduce and ensure our genetic legacy. This is strengthened by an innate desire to care for our children as without a parent’s nurture and love, children would die.
So, it seems loneliness may not just be an unpleasant feeling we all experience from time to time. Evidence suggests feelings of social isolation – particularly if these are chronic – could put us at risk of high blood pressure, diabetes and other health-related co-morbidities, not to mention possibly sending us to an early grave! Despite the negative feeling of loneliness coming with an evolutionary function – i.e. promoting the survival of the species – it certainly seems to be a feeling one may want to avoid. So pick up a phone and call your friends, reach out to your family and organise a meet up. Most importantly, keep those all important social ties strong – it may be good for your health!