Category Archives: Science news

Guardians of the brain under pressure

By Sevda Boyanova, @boyanova_sand Hao Wang, @olivia_hao, King’s College London, UK

In England, more than 1 in 4 adults are affected by high blood pressure, making it the third most common cause of premature death, after smoking and poor diet. Globally, 1.5 billion people are expected to have high blood pressure by 2025. This ‘silent killer’ usually occurs without symptoms, and contributes to more than half of heart attacks and strokes.

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Recently, scientists have revealed a connection between high blood pressure and the disruption of the gateway to the brain’s blood circulation, called the blood-brain barrier. These disruptions might lead to problems in the part of our nervous system involved in heart rate and blood pressure regulation (called the autonomic nervous system), thus contributing to high blood pressure.

So, how exactly does the blood-brain barrier work? The blood-brain barrier is the boundary between the blood flow that is circulating around our body, and the brain. Its function is two-fold: it regulates the balance of molecules flowing in and out of the brain, and also protects the brain from toxic substances. It’s formed by the cells that make up the walls of capillaries, tiny blood vessels in the brain. These cells, called endothelial cells, are joined together tightly so that blood contents cannot cross into the brain like they do in other parts of the body. The cells of the brain capillaries also contain transporters which move specific molecules across the walls of the capillaries. Surrounding the capillaries are three types of cells – astrocytes, pericytes and microglia – which work together with them to maintain a stable blood composition, allowing the brain to function properly. Scientists have implicated three players in the link between the blood-brain barrier and high blood pressure.

Blood Brain Barrier

This cake, submitted to our #BioBakes competition, represents the blood-brain barrier, with the cells of the blood vessel wall (blue) tightly joined by adhesive molecules (green squares) so that potentially harmful components in the blood cannot cross.

The first is a molecule involved in increasing blood pressure by constricting blood vessels (called angiotensin II). Angiotensin II can make the blood-brain barrier more porous which may affect the nervous system’s control of blood pressure. However, at the moment it is not clear if blood-brain barrier disruptions happen prior to or as a result of high blood pressure.

The second is molecules involved in the immune response. High blood pressure is related to low levels of inflammation (the first response when a threat to the body is detected), which is enough to activate the immune system. This activation leads to more inflammatory cells and molecules in the blood. These molecules can affect the structure of the blood-brain barrier, weakening it. Researchers have shown an increase in molecules that take part in the inflammatory response and in the production of white blood cells, during high blood pressure and heart failure. Therefore, these factors may play a part in the initial dysfunction in the blood-brain barrier, and may work alongside angiotensin II to worsen the disease.

The final player comes from the brain itself, in the form of cells that mediate inflammation. These are some of the brain cells that aren’t neurons, called astrocytes and microglia. These cells are normally involved in maintenance, surveillance and repair of the brain. However, researchers have found that microglia might be responsible for sustaining high blood pressure and astrocytes might work together with the microglia to release inflammatory molecules in response to infection by bacteria or viruses. Therefore, glial cells might have an effect on the blood-brain barrier’s ability to keep harmful molecules out. Also, there is evidence that glia could influence the activity of the autonomic nervous system (involved in heart rate and blood pressure regulation); in animal models, increased glial activation happens in brain regions important for the control of blood pressure.

The growing area of research on the link between the blood-brain barrier and high blood pressure is exciting because the blood-brain barrier is a very important target for new therapeutics. Further investigation of the mechanisms involved in maintaining the integrity of the blood-brain barrier will be useful for developing interventions targeted at treating or limiting the progression of conditions such as high blood pressure.


Reference:

Setiadi, A. et al., 2017. The role of the blood-brain barrier in hypertension. Experimental Physiology.

How loud is loud: the physiology of ear ringing

by Thomas Tagoe, Accra College of Medicine, @Tom_DAT

Benedicta took in the sweet smell of flowers in the field as she felt the chill of a cool breeze blowing over her. She could hear the sound of rushing waters from the stream nearby as she lay in the grass biting into a freshly baked doughnut and marvelling at the birds flying high over-head.

In the space of a few seconds, Benedicta had all her five main senses stimulated, providing her with information about the world outside her body. Each of these senses is specialised to a specific part of the body; nose to smell and skin to touch, eyes to sight, ears to hearing, and tongue to taste. Although each of these senses is assigned to a specialised part of the body, it is all interpreted by one part of the body: the brain.

Brain

The five organs respond to different stimuli and convert it all into one type of signal, electricity, which the brain can understand. Light, sound, touch, and odours are all converted to electrical signals which the brain interprets to let us see beauty, hear melodies, and experience the world. This is part of why the brain uses 25% of the body’s energy although it makes up only 2% of the body weight.

Of all the organs and systems which convert a given sense to electrical signals, the auditory system is one of the most impressive. It converts vibrations in the air, better known as sound, into an electrical signal for the brain. Like any finely tuned machine, the auditory system can start to fall apart if abused, such as through exposure to prolonged periods of loud sound. To understand how this can happen, it is best to appreciate how the system works under normal conditions.

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The outer part of the ear, known as the pinna, funnels sound in the air towards the ear canal. This is the reason cupping your hands behind your ears makes hearing better. Once the sound is channelled into the ear canal, it vibrates the ear drum which is connected to three small bones known as the malleus, incus and stapes. These three continue the chain of vibrations which ends in the cochlea, a spiral-looking organ where specialised hair cells are attached to a surface which is tuned like a guitar string. Different frequencies of sound cause vibrations in various sections to bend these hair cells; high frequency sounds like that of a whistle vibrate the bottom end while low frequency sounds like a bass drum vibrate the top end.

These hair cells are the pivotal point in the whole auditory system. Each one that bends from vibrations sends a unique electrical signal. The louder the sound, the more they bend, sending a stronger electrical signal to the brain. Once the electrical signal is in the brain, various bits of information are teased out of it to help us identify language, music, tones and much more.

Ear hair cells

So how can the whole system go wrong? Imagine the difference between beating a drum with open palms and pounding on it with clenched fists; that’s the difference between the effects of normal and loud sound. Loud sounds cause strong vibrations which can eventually destroy the hair cells. This primarily leads to hearing loss but can also lead to tinnitus, the perception of sound in the absence of an external stimulus, typically experienced as a “ringing in the ears”.

Tinnitus is an interesting condition because it suggests that somewhere in the brain, a false signal is being generated in response to a sound which does not exist in the outside world. There are a number of researchers working to understand how this occurs. Their findings suggest that after exposure to loud sound, some of the cells in the brain area called the dorsal cochlear nucleus become easily stimulated, making them respond inappropriately to signals. This and other findings could be traced back to the hair cells in the cochlea, suggesting that once these hair cells get damaged, irrevocable changes follow in the brain.

How loud is loud

The dangers posed by prolonged exposure to loud sound have been known for a while now. So much so that many countries require by law that people who work under conditions of loud sound wear ear protection. Now isn’t it quite curious that as one group of people are required by law to wear ear protectors, while another group willingly expose themselves to the same dangerous levels of sound. Think of the last time you were at a concert, on a night out, or better yet, turned up the volume in your head phones while travelling home.  The short or long-term damage caused by prolonged exposure to loud sound, whether from headphones or planes remains the same: hearing loss and tinnitus.

How do pain meds lose their effect?

By Julia Turan, Communications Manager

You know something’s not right when more Americans are dying from pain medications than illegal drugs. This opioid crisis is filling headlines, and rightly so. However, for patients with chronic pain, tolerance to opioids such as morphine, not addiction, is the real issue. Tolerance is not usually a problem for acute pain after injuries or surgery, but for chronic pain, the patients need the drug to work over a long period.

Most studies have focused on how tolerance affects individual brains cells (neurons). New research from The Journal of Physiology clarifies a piece of the puzzle of how opioid tolerance changes the communication between neurons. This brings us one small step closer to one day developing pain therapies that avoid the development of opioid tolerance.

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Tolerance to a drug means that larger and larger amounts are required to achieve the desired effect. Patients can become tolerant regardless of whether or not they are addicted. Tolerance does not result from abusing the drug, but rather, it can occur even when the patients follow their course of treatment as required.

The research, led by Adrianne Wilson-Poe and Chris Vaughan at The University of Sydney looked at rat brain slices after giving the animals a low dose treatment of morphine that produces tolerance. To study this, the researchers used a technique that records electrical activity in an area called the midbrain that plays an important role in the pain-relieving effects of opioids. Rather than examine individual neurons they measured how neurons talk to each because this communication is how the brain works.

BrainDiagram

To understand their findings, we need to understand a bit about how our neurons talk to each other. To send a signal, molecules travel from the sender brain cell to the receiver across a gap called the synapse. The synapse has two sides, the pre-synapse and the post-synapse. The pre-synapse is part of the brain cell sending the message, and the post-synapse is part of the receiving cell.

One of the molecules sent between neurons is called GABA. Opioids normally decrease the release of GABA. After chronic treatment with opioids, the researchers found that their dampened effect was due to fewer molecules of GABA being available on the sending side. Consequently, opioids had less of an effect on GABA release from the sending side, as there were fewer molecules around. This reduced communication between neurons is likely to contribute to reduced effectiveness of opioids after chronic treatment.

Diet, exercise or drugs – how do we cure obesity?

by Simon Cork, Imperial College London, @simon_c_c

October 11th is officially “World Obesity Day”, a day observed internationally to promote practical solutions to end the obesity crisis. The term “obesity crisis” or “obesity epidemic” is often repeated by the media, but how big is the problem? Today, over 1.9 billion adults worldwide are overweight or obese. By 2025, this is projected to increase to 2.7 billion with an estimated annual cost of 1.2 trillion USD. Of particular concern is that 124 million children and adolescents worldwide are overweight or obese. In the UK, this equates to 1 in 10 children and adolescents and is projected to increase to 3.8 million by 2025. We know that obesity significantly raises the risk of developing 11 different types of cancer, stroke, type 2 diabetes, heart disease and non-alcoholic fatty liver disease, but worryingly, we now know that once someone becomes obese, physiological changes to the body’s metabolism make long-term weight loss challenging.

Our understanding of the physiology of food intake and metabolism and the pathophysiology of obesity has grown considerably over the past few decades. Obesity was seen, and often still is seen, as a social problem, rather than a medical issue: a lack of self-control and willpower. We now know that physiological changes occur in how our bodies respond to food intake. For example, hormones which are released from the gut following food intake and signal to the brain via the vagus nerve normally reduce food intake. However, in obesity, the secretion of these hormones is reduced, as is the sensitivity of the vagus nerve. The consequence of this is a reduced sensation of feeling full.

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Imaging of the hypothalamus (a key region for keeping food intake at a balanced level) shows a reduction in activity following food intake in lean men, an effect which was absent in obesity. This effect may relate to a reduction in the body’s responses observed following food intake in obesity, such as balancing blood sugar and signalling that you are full. Furthermore, numerous studies have shown that obese individuals have a reduced availability of dopamine receptors, the structures on cells that respond to the pleasure chemical dopamine, in key brain regions associated with reward. Whether the reduction in dopamine receptor availability is a cause or consequence of obesity remains to be fully explored, but it is likely to be a combination of both of these factors. Individuals with a gene called the Taq1 A1, associated with a decreased availability of dopamine receptors, are more likely to become obese, suggesting that decreased responsiveness to high calorie foods leads to increased consumption in order to achieve the same level of reward. (Interestingly, this same gene is also associated with an increased risk of drug addiction). However, much like drug addiction, hyper-stimulation of the dopamine system (i.e. by consuming large quantities of dopamine-secreting, high calorie foods) can in turn lead to a reduction in dopamine receptor levels, thus creating a situation where more high calorie foods are required to stimulate the same level of reward.

It is therefore clear that obesity is not simply a manifestation of choice, but underpinned by complex changes in physiology which promote a surplus of food consumption, called positive energy balance. From an evolutionary standpoint, this makes sense, as maintaining a positive energy balance in times of abundant food would protect an individual in times of famine. However, evolution has failed to keep up with modern society, where 24-hour access to high calorie foods removes the threat of starvation. The good news is that we know that weight loss as small as 5% can yield significant improvements in health, and can often be managed without significant modification to lifestyle.

 

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Presently, treatment options for obesity are limited. The first line treatment is still diet and exercise; but as the above examples of how our physiology changes show, maintaining long term weight loss through self-control alone is almost always impossible. However, the future does look bright, with new classes of drugs either recently licenced, or in production. Saxenda (a once-daily injectable drug which mimics the gut hormone GLP-1 made by Novo Nordisk) has recently been licenced for weight loss in patients with a BMI greater than 30. However, after 56 weeks treatment, average weight loss was a modest 8kg. Likewise Orlistat (which inhibits absorption of dietary fat, made by Roche) has been on the market for a number of years and shows average weight loss of around 10%. However, it is associated with unpleasant side effects, such as flatulence and oily stools. Presently, bariatric surgery is the only treatment that shows significant, long term weight loss (around 30%, depending on the surgical method used) and is also associated with long-term increases in gut hormone secretion and vagus nerve sensitivity.  Research is currently underway to assess whether the profile of gut hormones observed post-surgery can be mimicked pharmacologically. Studies have shown that administering select gut hormones in combination results in a reduction in body weight and food intake greater than the sum of either hormone when administered in isolation. This observed synergy between gut hormones will undoubtedly form the basis for future pharmacotherapies with improved efficacy, with various combinations currently in both clinical and pre-clinical trials.

For healthcare policy makers, the future obesity landscape does not make for happy reading. A combination of better therapies and improved public health messages are undoubtedly needed to stem the rising tide. However, both policy makers and society as a whole should be mindful that changes in ones physiology mean maintaining long-term weight loss through diet and exercise alone are unlikely to be the whole answer.

Nobel Prize 2017: Our 24 hour body clock

By Professor Hugh Piggins
Professor of Neuroscience, The University of Manchester

The winner of the Nobel Prize in Physiology or Medicine was announced today (Monday 2nd October). Physiologist Hugh Piggins of the University of Manchester explains why the research is vital to understanding how our bodies respond to health and disease.

The Nobel Prize winning research by Jeffrey Hall, Michael Rosbash and Michael Young has transformed our understanding of how our bodies work.

In simple terms, they have discovered that molecules in our body have a clock that represents a 24 hour day. They first found this in fruit flies in the 1980s and then later other researchers showed that these fundamental components were also present in cells and tissues of mammals, including humans.

All mammals have a master clock in the brain that receives input from the eye that synchronises it to day and night. We now know that, having evolved on a planet with changing conditions across roughly a 24 hour cycle, our bodies are designed to anticipate when these changes should happen. Thus the 24 hour cycle is called our circadian rhythm and we all feel the impact of this, for example, when our bodies signal to us in the morning and we find ourselves awake just before our alarm clock.

As so much of our brain and body relies on this 24 hour rhythm, it needs to be kept in good order to ensure optimum health. As our bodies are programmed to operate in 24 hour periods then deviation from this can cause problems.

This is felt by shift workers or those suffering from jet lag. The result of forcing our body to operate abnormally means our internal clock clashes with external signals. This means the body is not ready and we see the sometimes tragic consequences of this with industrial accidents more likely to occur with those working long shifts.

Longer term, this disruption in the body clock causes health issues such as obesity or heart disease. There is lots of evidence to show that night shift workers are at greater risk of developing obesity, partly due to the fact that night shift patterns disrupt the metabolism and sleep cycles of employees.

This research also points the way towards new treatment routes. Now that we know the disruption of these clocks can cause illness, it opens the door to targeting particular components of the clock to stop the development of disease. There is also evidence that the body can be more sensitive to certain drugs at specific times of the day, which could help us deliver more effective treatments.

Finally, our internal clock changes over time, which means a teenager’s clock runs differently to that of an older person. By recognising this biological reality and, for example, changing school start times, there is increasing evidence that the performance of school pupils will improve.

This is an exciting and important area of scientific research. It highlights why an understanding our daily physiology –the science of biological timekeeping – is vital to understanding how our bodies respond to health and disease.

More information about this year’s Nobel Prize in Physiology or Medicine is available on the Nobel Prize website.

Watchers on the wall: Microglia and Alzheimer’s Disease

By Laura Thei, University of Reading, UK

The watch, worn by years of use, sits ticking on our table for the first time in two years. It has a simple ivory face and is the last memorabilia my partner has from Grandad Percy. Percy passed from us after a long personal battle with dementia, specifically Alzheimer’s disease. It is in his name that my partner and I will take to the beautiful winding pathways beside the Thames, to raise money for the Alzheimer’s Society.

We will be taking part in a 7 km Memory Walk, with thousands of others, some my colleagues from the University, each sponsored generously by friends and families, each who has had their life touched by this disease in some way. Last year nearly 80,000 people took part in 31 walks, raising a record £6.6 million. As a researcher in Alzheimer’s disease, I am acutely aware of every penny’s impact in helping to solve the riddle of dementia.

AlzheimersWalk

Alzheimer’s Society Memory Walk

Alzheimer’s disease is ridiculously complicated. Oh, the premise is simple enough: two proteins, amyloid beta and phosphorylated tau, become overproduced in the brain and start to clog up the cells like hair down a plug. This causes these cells to be deprived of nutrients, oxygen and other vital factors that keep them alive. This eventually causes regional loss in areas specific to memory and personality. It’s simple in theory, but the reality is that we still have much to learn.

Current, extensive research is starting to answer these questions and whilst there is a growing list of risk factors – genetic (APOE4, clusterin, presenilin 1 and 2) and environmental (age, exercise, blood pressure) – confirmation only occurs when a brain scan shows the loss of brain region volume in addition to the presence of amyloid beta and tau. This means that by the time someone knows they have the disease, it’s possible that it’s already been chugging away at their brains for some time.

So we need to push diagnoses earlier. To do that we need to look at the very early stages of the disease, down to a cellular level, to find out how we can prevent the build-up of amyloid and tau in the first place. This is what I, the group I’m in, and many other researchers nationally and globally are striving to do.

AlzheimersWatch

In a non-active state, microglia lie quietly surveying their local area of the brain. ©HBO

I am specifically focusing on the immune cells of the brain, microglia, and their contribution. Microglia are the most numerous cells in the brain. They act as the first line of defence, so their involvement and activation is often seen as an early sign of disease progression. Like all good defences, they tend to be alerted to damage before it becomes deadly. But, like the neurons (the basic building blocks of the brain), microglia are also susceptible to the disease. If they die, does that leave the brain more vulnerable to further insult? That is what I would like to know too!

In a non-active state, microglia lie quietly surveying their local area of the brain. When activated by a threat to the brain, they cluster around the targeted area, changing shape in the process. They then enter one of two states. The pro-inflammatory state releases molecules that attack the harmful pathogens directly, and the anti-inflammatory state releases ones that promote healing and protection of the area.

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Microglia can change shape to either attack pathogens or protect the area. ©Nickelodeon

With Alzheimer’s, microglia are activated by the accumulation of amyloid, not damage. They absorb the amyloid beta, and in the process, trigger the pro-inflammatory response. This then increases the permeability of the brain’s blood supply, allowing immune cells into the brain to assist removal of the excess protein. However, in the brain of Alzheimer’s patients, the amyloid beta production outdoes the microglia’s ability to remove it. This creates a perpetual cycle of pro-inflammatory response, releasing molecules that can kill cells in the brain. It is unclear whether there is a threshold between beneficial or detrimental in the microglial response.

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Microglial response to fight Alzheimer’s Disease can become detrimental. ©2011 Scott Maynard

Given the importance of microglia in neurodegenerative diseases, a new field of microglial therapeutics has recently emerged, ranging from pharmacologically manipulating existing microglia by switching their response status, to inhibiting microglial activation altogether. Continued research and clinical efforts in the future will help us to improve our understanding of microglial physiology and their roles in neurological diseases.

We’re making progress, but there’s still a long way to go, which is why every penny counts!

Shark Diary, Episode III: The oldest living vertebrate

The Greenland shark’s scientific name is Somniosus microcephaly, which means ‘sleepy small brain’.  They live in the cold waters of the North Atlantic and Arctic Oceans, and are members of the family Somniosidae – the Sleeper Sharks. This name implies their slow growth and low levels of activity. In some ways they live up to their name, but in many other ways they are anything but sleepy, small-brained creatures!

Native range of the Greenland shark. Source: FishBase

How old is old? 

These sharks were known by Greenlanders to grow slowly and the fact that they can reach lengths of 5.5 metres implied they may also be very old. It wasn’t until a few years ago that a Danish team led by Prof John Steffensen was able to confirm their extreme longevity, and publish the findings last year in the journal Science.

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Calculating the age of a cartilaginous shark is more complicated than it is for a bony fish. This is because bony fish have otoliths, bones of the inner ear which grow in rings, much like that of a tree. By counting the rings of the otolith, you can determine the fish’s age. Cartilaginous fish like sharks (and rays) do not have otoliths, nor do they have any other true bones.

To overcome this challenge, John and his team used carbon dating techniques to determine the age of 28 female sharks (81 to 502 cm total length) collected during expeditions to Greenland between 2010 and 2013. Carbon dating is famously used to determine the age of fossils, but they used this same technique on the carbon in lenses in the sharks’ eyes. This carbon comes from the  “bomb-pulse” that entered the ecosystem following the nuclear tests of the 1950s. The carbon in body parts formed during that time is in a different form.

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From these sharks, growth curves were established linking a shark’s age to its size. Using these, we can now calculate the age of live sharks from their measurements, which we took on the expedition. Current estimates suggest that the average Greenland shark grows less than one cm per year. That makes animals longer than 5 metres between 275 and 510 years old!

How does living so long affect the shark’s bodies?

Aging is decay, at least in humans. Indeed, the biggest risk factor for a large number of diseases like heart disease and cancer is advancing age. So how is it that the Greenland shark can live for so long?

At the moment, we know very little. Very early evidence from previous work suggests these sharks do not have any special strategies for surviving damage from free radicals. Another health concern specific to top oceanic predators is accumulation of toxic substances in their bodies. However, recent work on accumulation of organic pollutants does not suggest that they accumulate with age in the Greenland Shark either. We hope to learn much more about how these sharks age as we process the samples from our expedition. For instance, Takuji Noda, Bob Shadwick and Diego Bernal are studying movement and skeletal muscle function in sharks of different ages. This could tell us whether Greenland sharks deal with frailty, another plague of human aging.

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Most sharks caught have this parasite hanging from their eye.

Some aspects of a shark’s long life bear no comparison to humans. Although dimming eyesight might feel like an inevitable part of aging to us, Greenland sharks contract a parasite on their cornea, so they may need more than a pair of reading glasses as they age! A 4-6 cm long crustacean dangling from the centre of a shark’s eye is off-putting, but also intriguing. It raises obvious questions about how the parasite affects vision and how the fish survives with potential vision-impairment. General consensus is that the parasite severely impairs the ability of the eye to form images, but how important is vision in animals living 1 kilometer below the surface? Perhaps they rely more on their other senses, like smell. In any case, gut contents show these sharks eat everything from small fish to whole seals, suggesting they forage successfully even with a large crustacean dangling from their eye!

Conserving this old shark 

The Greenland shark is slow-growing and thus also slow to reach reproductive age. A member of our team on the expedition, PhD student Julius Nielsen, from the University of Copenhagen has been trying to understand how body length relates to reproductive maturity in both males and female sharks. Their current estimate is that females reach sexual maturity at lengths of over 400 cm, which makes them at least 150 years old. Males, who are smaller than the females, may reach reproductive maturity at slightly shorter lengths.

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Ovaries and uteri recovered from an injured female shark humanely euthanised during the expedition. Watch Julius talk you through them, and what he hopes to learn from tracking shark’s movements after their release, below.

This slow maturation means it takes at least 150 years for shark pups to start reproducing! This has big implications for the population, and for conservation. Indeed, the Greenland shark population may still be recovering from being over-fished before World War II, when their livers were used for machine oil. Calculating back from the amount of machine oil produced suggests that between 50,000 and 150,000 animals were caught per year between 1900 and 1938. Prices of shark-liver oil fell in 1949 as other options became viable, and the fishery then collapsed. Hatchlings born to parents who were caught for their livers are now teenagers and still not quite at reproductive age. That may be the reason why there are very few reports of juvenile Greenland sharks.

Slow growth leading to late reproductive maturity is a big factor for conservation strategies in this animal. At present, the Greenland shark is a common by-catch, meaning it’s unintentionally caught along with other fish, in the North Atlantic and Arctic Oceans. This suggests that its population is still quite strong. But as it takes so long to increase the population of adult animals, they are vulnerable to increased fishing pressure in a warming Arctic environment. Thus they are listed as near-threatened on the ICUN list and there is a growing need to understand their physiology, life history and their role as top predator in the Arctic marine ecosystem.

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The tag on this shark will transmit data via satellite about where it goes after being released.

Follow #SharkDiary on Twitter to see all the updates about the expedition.


This expedition was made possible by funding from the Danish Centre for Marine Research, the Greenland Institute of Natural Resources, The Danish Natural Science Research Council and the Carlsberg Foundation.