It doesn’t matter how carefully you monitor your fluid intake before a dive, or how close to dive time you leave the last toilet visit, we have all got out from a dive ready to rugby tackle anyone standing between us and the toilet. It’s well known that going for a dive causes an increased need to urinate. There are some interesting physiological changes that come to play. Immersion and temperature changes cause a narrowing of the blood vessels in the extremities. This results in an increased volume of blood to the central organs which is interpreted by the body as fluid overload. This causes the production of antidiuretic hormone (ADH) to stop, signalling to your kidneys that they need to produce urine to lower the blood volume. So even if your last toilet visit was only minutes ago, you can quickly find yourself feeling the need to go again.
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It’s almost impossible to give an exact measurement for the volume of the human bladder as everyone’s ability to hold urine varies. Normal adult bladders hold between 300 and 400ml but can hold up to 600 or even 1000ml in some cases. The need to urinate is stimulated by the expansion of the bladder which triggers the Micturition reflex centre in the spinal cord. Most adults will feel the need to urinate when their bladder is only around a quarter to a third of its normal capacity. In normal circumstances, adults will feel the need to empty their bladder about every 3 hours, but as divers we know the effect that immersion plays.

There’s always a big debate in the wetsuit diving community about whether peeing in a wetsuit is acceptable or not. In a drysuit, the debate becomes somewhat redundant unless you have a P-valve fitted. But is there any danger to ‘holding it in’? When you first feel the need to pee, your bladder probably has quite a way to go before it’s completely full. As your bladder fills up the muscles around it will contract to keep urine from leaking out until you’re ready – just make sure you can get out of your suit fast enough!

The dangers of holding your pee are mostly cumulative, so the occasional episode probably isn’t harmful. However, if you are diving frequently and often find yourself ignoring the need to pee you run the risk of urinary tract infections, urinary retention (the muscles can’t relax even when you want to pee) or bladder atrophy (leading to incontinence). But for most people, you can hold your bladder full for a few hours without serious complications, even though its uncomfortable.

If you dive in a wetsuit, you can of course make the call as to whether you pee in your suit or not. The old saying is that 50% of divers pee in their wetsuits and the other 50% are liars. So whichever camp you fall into, just make sure you flush your suit through before you get out of the water and start to take it off, and please wash your suit thoroughly between dives.  If you’re a drysuit diver, there’s always the option of adult nappies to ensure that you can relieve yourself. If that seems a little retrograde, or as you march middle age a little too prophetic, then perhaps a P-valve is an option.

Not surprisingly there are hazards associated with P-valves too. Ignoring the issues with getting a stick-on condom or the female cup attached successfully, so that the urine does actually enter the tubing to leave suit, there are reported cases of urinary sepsis. The tubing used to connect the urine to the P-valve is the ideal breeding ground for Pseudomonas bacteria, and it only takes a small amount of backward flow to introduce those bacteria into the body. If you think rinsing your wetsuit is a bit of a faff, syringing antiseptic through P-valve tubing should give you some perspective.

​As I child I had a budgerigar called Dinsdale. Dinsdale was a pretty happy bird who would cheerfully run round my desk, leaving special presents on my homework (!) and hop back into his cage on command. He loved hitting the bell that was attached to a little round mirror and pecking hard at his cuttlefish.  Of course, he didn’t really have a whole cuttlefish in the cage with him, just the hard, bony bit.

Cuttlefish bones aren’t actually bones at all, they are a special kind of shell.  And while we are at it, cuttlefish aren’t fish either. Cuttlefish are one of the Cephalopods and they have their own family name Sepiidae. The early ancestors had a shell for protection and existed before the first fish had evolved. Modern cuttlefish don’t have an external shell but rely on camouflage for evading predators. 

The common cuttlefish (Sepia officinalis) also produces a brown ink, which can be harvested from their ink sacs.  Most of us would recognise the colour of the ink from old fashioned brown sepia photos, and that’s how the ink got its name. The chemistry and biosynthesis of ink in cephalopods is fairly complex. It is a form of the common biological pigment melanin which is the same molecule responsible for your skin developing a tan after exposure to sunlight. Who’d have thought you and the cuttlefish would have so much in common? The eumelanin in the ink sacs is also found in fossils from the early Jurassic period around 200 million years ago.

For a soft bodied animal, it seems strange that there should be a good fossil record. The cuttlebone is generally well preserved. When the cuttlefish are alive the cuttlebone is a mix of chitin (a really large structural sugar molecule) and aragonite (one of the three forms of calcium carbonate). After the animal dies, the chitin will break down fairly readily but the aragonite persists. That means that it is possible to find fossilised remains of cuttlefish that are readily identifiable and from modern catches of cuttlefish, your budgie gets a calcium supplement.

The cuttlebone has a very specific function in the cuttlefish. It’s clearly not for defence – what use would an internal bone be? Cuttlefish have a short life span, maybe only 1-2 years and during that time they have a phenomenal growth rate (up to 10 kg) so for a cuttlefish conserving energy is critically important. The cuttlebone structure is full of holes and the cuttlefish can control liquid or gas into those spaces to effortlessly control its buoyancy.

The cuttlebone is a long oval structure made of around 100 chambers, with the chamber lying at the head end being the oldest, other layers are added as the cuttlefish grows. Lying along the cuttlebone is the siphuncle, which is a strand of tissue that connects all the small chambers.  In order to add water to the cuttlebone, the cuttlefish makes the blood in the siphuncle more salty by pumping salt out of the chamber. Water in the chamber is drawn out of the chamber and into the blood by osmosis and oxygen and carbon dioxide come out of solution and make up the volume in the chamber by diffusing from the siphuncle.  So it’s not true to say the siphuncle pumps the water….more that it pumps the salt and that causes the water to be drawn out. Siphuncles rarely get preserved in fossil records but you can usually see the notches in the cuttlebone where the siphuncle used to be.
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Removing water from the chambers of the cuttlebone reduces the overall density and causes the cuttlebone to float. Cuttlefish aim to maintain neutral buoyancy and will swim up or down with the minimum of effort. In addition to this, the cuttlefish can control whether the chambers towards the head or the tail end are water filled or gas filled, making it’s journey from depth towards the surface even easier as it adjusts its trim. Next time you’re diving, be more cuttlefish, perfect buoyancy and perfect trim.
 

​While reviewing some marine survey videos lately I found myself mesmerised by watching an octopus move across my survey area, settling and changing colours before moving again and changing yet again. The colour change was so rapid and the octopus completes three quick changes before scooting off out of the video.  It got me to thinking that colour changing is a pretty cool skill to have. The most us puny humans can manage is to develop a tan, producing melanin in the skin to try and prevent the damage that UV radiation can cause.

Colour in cephalopods (octopus and squid) depends on 4 different types of cells.  The first layer of colour controlling organs in the skin are the chromatophores.  Each chromatophore consists of a small balloon like sac filled with pigment. Each sac is connected to around 20 muscles, and each muscle is controlled by 2-6 nerves linked directly to the brain of the octopus. The octopus can stretch the balloon-like sac and allow the pigment to cover a large surface area, so we get to see the black, brown, orange, red or yellow colour just under the surface of the skin. When the muscles around the sac relax, it shrinks and the colour is hidden.  Chromatophore sacs are individually controlled so the cephalopod can control which colours are displayed and where, hence the patterns seen in cuttlefish.  Deep water cephalopods have very few chromatophores as colour isn’t much use in an environment with little light.

The next layer of colour organs under the chromatophores are the iridophores. Iridescence is the property of luminous colours that change depending on the angle they are viewed from. Iridophores are the key to how cephalopods create the metallic green, blue, silver and gold colours. Iridophores work by reflecting light from stacks of very thin cells.  It’s not certain how iridophores are controlled, but they are slower to respond than chromatophores so it’s unlikely to be controlled by nerves but more possibly by hormones.

Then there’s the leucophores. These are cells that scatter full spectrum light, so they appear white. In fact, they will reflect any light that is shone on them, and the light doesn’t change with the angle that you view at. It’s thought that having leucophores underlying the chromatophores increases the intensity of the colours that we observe. Leucophores also help with the cephalopods ability to colour match because they reflect the surrounding light.

Cephalopods have 3 types of specialised colour creating organs in their skin to mimic their background for camouflage and communicate. The cephalopod eye is remarkably similar to a vertebrate eye consisting of an iris, lens and photoreceptor cells. The similarity is often cited as an example of convergent evolution, both vertebrates and cephalopods need to observe their environment and they have solved how to do this in a similar way. But there is a critical difference, cephalopods are colourblind, so their eyes only see in black and white. How on earth does that make sense? An animal with the ability to make a myriad of colours, metallic sheens and mesmerising patterns can’t actually see in colour?

The explanation for this apparent contradiction is that the cephalopod eyes have wide pupils in a strange variety of shapes, U-shaped, W-shaped or dumbbell shaped. When light passes through the wide pupil, the lens in the eye acts as a prism and splits the light into different colours, a large pupil allows for more splitting, known as chromatic aberration.  Cephalopods use their wide pupils to create the maximum chromatic aberration and focus on these different wavelengths by changing the depth of their eye ball (altering the distance between the lens and the retina). So, cephalopods can detect colour, not by using special proteins embedded in cells in the retina (like we do) but by changing whether the light focusses on the retina at all. They find it easy to focus distinguishing between bright and dark colours, so that probably explains why display patterns are usually colour separated by black bars.
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But if a cephalopod can’t really see so well, how on earth do they mimic their environment? The secret to this lies in the presence of opsin (light detecting protein) in the skin. Its thought that its possible for some cephalopods to sense how much ambient light is present across their periphery and adjust their skin colour and brightness accordingly. To camouflage yourself, you don’t have to be a perfect match for your surroundings, you just have to match it slightly more than your predator can distinguish. 

Sea hares (Aplysia punctata) are a common find on dives around the south, west and northern British Isle. They are usually around 7cm long but can grow up to 20cm in length. The colour of Sea hares varies from olive, brown, red and purplish black depending on the algal diet. At the head end, two slender rhinophores stand up like the ears of a hare, hence their common name.
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At first sight, Sea hares would appear to be an easy target as a meal, there’s no shell, no spines like an urchin, no claws and they move at a fairly slow pace. Sea hares have a mucous coating containing acid and other nasty compounds which might deter some predators, but their party piece is to release a cloud of sticky, purple ink when attacked by hungry predators.

The cloud of purple ink is in fact a mixture of two secretions. On the back of the Sea hare the central structure is called the mantle with an opening called the foramen. Just under the surface there’s the last remnants of what was probably a shell in the Sea hare’s evolutionary history, a protein disc which acts as an internal shell. On the roof of the mantle is the Purple Gland above the gills. The Purple Gland is responsible for storing and secreting the ink. The building blocks for noxious chemicals are obtained from their algal food, particularly from red algae, metabolised and stored here. This strategy is quite common in marine gastropods and a number of these substances are being actively tested for pain killing, antibacterial, antiviral and anticancer activity. It’s powerful stuff.

Beneath the gill on the floor of the mantle cavity is the Opaline Gland. This gland secretes a white liquid that becomes viscous upon contact with water. If you’ve ever seen the videos of Hagfish (Myxini sp.) producing copious volumes of slime as a way of evading predators, then you will already have seen opaline in action.

The ink and the opaline are secreted into the cavity in the mantle where they mix and are expelled towards the predator. The ink has an intriguing role in that it has been shown to be a phagomimetic decoy (phago = eat, mimetic = to mimic). Some species of lobster will drop the sea hare and try to manipulate and eat the ink cloud, thinking that it is food. Whilst testing this idea scientists found another ink effect. The lobsters tried to rub the ink off their antennules. The opaline in the ink blocks the receptors and response to food odours, thereby preventing the predator from recognising that Sea hares are food. It’s the lobster equivalent of a stuffy nose. Whilst the lobster is busy removing the sticky ink, the Sea hare can make its escape. So, in this aspect the ink is rather more than just a cloud to hide the escape of the Sea hare, it is an active cloud which has the effect of blinding the predator.

It can take quite a bit of stimulation to persuade a Sea hare to produce ink. The threshold depends on factors such as the environment (living in a turbulent environment makes inking less likely), how full the gland is and what the stimulus is (inking occurs more rapidly near anemone tentacles that it does in response to an electric shock). If a Sea hare has full ink glands then it will release nearly half of its ink at the first stimulation. Each subsequent stimulation will release 30-50% of the contents. It will take at least 2 days to replenish the gland.

Whilst aquarium owners like the grazing tendencies of Sea hares, they panic about the effect that any inking has on the fish and other residents inside their tank. The jury is out on how much effect the Sea hare ink can have. Sea anemones retract their tentacles, but the evidence for the toxic effect of the ink inside an aquarium is limited, perhaps because the Sea hares aren’t feeding on red algae that are the source of the most potent toxins.
 
 

​It’s a popular misconception that lobsters are red in colour. That’s because most people have never seen a live lobster, and what gets served up in their lobster thermidor is distinctly red in colour. It’s one of my pet hates when media shows lobsters as red, right up their with the reporter talking about the oxygen tanks worn by the scuba divers. Grrr! As divers we are well positioned to know that lobsters are a dark shade of blue-green, but it’s not just the shell that’s blue, so is the lobster’s blood.

Technically the lobster doesn’t have blood in the way that we would understand it. They have haemolymph, a fluid equivalent to blood that circulates inside arthrpods. Haemolymph is mostly watery with some salts and nutrients dissolved in. There are some cells known as haemocytes, but in arthropods these play a role in the immune system of the organism. There aren’t any red blood cells containing haemoglobin to carry oxygen like we have. Instead invertebrates have some special proteins in their haemolymph called haemocyanins that transport oxygen for them.

Haemocyanins are metalloproteins that have two copper atoms which can reversibly bind to a single oxygen molecule. Oxygenation causes a colour change from the colourless deoxygenated form to the blue oxygenated form. Haemocyanins are only found in molluscs and arthropods but aren’t limited to marine animals and can be found in tarantulas, scorpions and centipedes too. Haemocyanins turn out to be rather more efficient than haemoglobin at binding to oxygen in cold environments and when the oxygen pressure is low. Sounds ideal for the average marine crustacean.

Lobster haemolymph has been shown to have antiviral properties, but only in the uncooked state. In research it was shown to be effective against the viruses that cause shingles and warts. In fact, there is an American based company that has developed a blood-based cream for treating cold sores and skin lesions, although it’s yet to get approval from the regulatory authorities.

So, we’ve established that copper coloured proteins give lobsters their blue blood, but that’s not the explanation for the shell changing colour when the lobster is cooked. For this we have to look at another protein called crustacyanin, and its best buddy astaxanthin. Astaxanthin is a carotenoid pigment so it absorbs blue light and gives off red/orange colour. Astaxanthins are mostly synthesised by microalgae and enters the marine food chain. In shellfish the astaxanthin becomes concentrated in the shell. Its likely that astaxanthins have a string antioxidant and anti-inflammatory effect and may protect against age-related degeneration. Astaxanthins are also found in some sponges, starfish and in species of octopush and cuttlefish. They give the muscle tissue of the salmon its characteristic colour.

Crustacyanin is a very interesting chromoprotein, that changes colour depending on whether it is in water or dehydrated. When it’s bound to the lipid like astaxanthin it has a distinctly blue colour. While a lobster is alive, crustacyanin stays bound tightly to astaxanthin, so tightly that the astanxanthin’s light-absorption properties are quashed and the complex appears to be blue-green in colour. That all stops when the lobster hits the boiling water.
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Crustacyanin is not heat stable, so the boiling temperatures cause it to unravel and lose its grip on astaxanthin. The true colours of the astaxanthin then shine through in the red lobster shell. In fact, they were there all the time, you just couldn’t see them. It’s the same mechanisms for cooking shrimp too. Flamingos rather cleverly digest the crustacyanin protein to release the astaxanthins that colour their feathers soft pink.

​In 1973, four hostages were seized in a bank robbery in Stockholm, Sweden. A convict on parole attempted to rob the bank but as the siege situation developed he negotiated the release of his friend from prison to help him.  The hostages were held for 6 days in the vault. When the siege was finally over none of them would testify against their captors and they even started raising money for the defence’s legal team. Baffled by the responses of the hostages, further assessment was sought.

A Swedish psychiatrist examined the hostages and described ‘Stockholm Syndrome’. In cases where Stockholm syndrome is present, victims start out as powerless, but go on to develop positive feelings towards their captors. Sympathy for the cause and goals an often follow hostages back into their real life. This can cause cognitive and social problems, and a feeling of dependence on the captor.

Stockholm syndrome probably arises as a coping mechanism.  The victim wants to survive, and that is a stronger instinct than hating the person who has created the hostage situation. A positive emotional bond will help survival, but there’s a danger of being spotted as a fraud. So the victim ends up believing that they really do like their captor.

You’re by now, probably wondering why I’m writing about this topic…and whether you’ve accidentally picked up a copy of Psychiatrist Monthly. But actually, Stockholm syndrome is an extreme example of how an imbalance of power in any relationship can have a massive influence on how the parties behave.  For this reason, educational establishments (from schools to universities) have very strict guidelines about appropriate relationships between teaching staff and students.  Teaching staff (or instructors) occupy a position of power over the student. Instructors grade work, give personal feedback, ensure standards for the course are met. And students will hold the instructors in high esteem because of their position and experience. Most educational establishments would require a member of teaching staff to remove themselves from teaching any student who they were having a relationship with. In this case the student may be so overwhelmed by the instructor’s attention that they may feel unable to say no, concerned about the impact on their progress. And the student will normalise this behaviour in their future life.

When would-be instructors first attend a BSAC Instructor Foundation Course, we run a session on what the ideal instructor would look like. Usual (and valid) responses include knowledgeable, patient, approachable, organised and skilful. Rarely does anyone mention ethical. In PADI’s instructor manuals, there’s a small section on ethics, although it seems to deal more with the ethics of business than the relationship between an instructor and a student. And yet, instructors are in a position of extreme power. On smaller courses, especially technical ones, there may only be one instructor for 2 students. That instructor will play a variety of roles during the course, mentoring and assessing the student.
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Diving at all levels in built on trust. Instructors that build a positive relationship with a student will achieve more as they work to develop the student’s skills. But whilst this relationship can be hugely beneficial, they are in a situation where a massive imbalance of power in possible. The risks for student infatuation with the instructor are real. Ask any experienced instructor and they will be able to tell you of the students who came a little too close. In the stress of the course with the worry of whether you’ll pass, those evolutionary survival mechanisms kick in. The need to survive outweighs the desire to fight back against the demands of the course (and the instructor delivering it). Scuba instructors get idolised, and that’s not always a healthy situation. Stockholm syndrome may be at the extreme end of the scale, but the potential imbalance of power exists. Treat carefully my fellow instructors. 

​No ship yard ever built a ship with the intention that it should end up on the seabed. By design ships are intended to keep the water on the outside (or in controlled areas like ballast tanks). From the earliest hollowed logs and coracles to the ocean going supertankers, the aim is to find materials that create a good airspace and allow the vessel, cargo and crew to stay on the surface. As construction methods have evolved, so have the materials that are used. For any vessel owner, the necessary maintenance to keep the water out is an ongoing and relentless battle.

Once a ship sinks, the process of decay inevitably starts. There are a number of parameters that affect how quickly a wreck will break up. A shallow wreck is exposed to the mechanical shearing forces of wave action and the remarkably destructive scouring of sand. Many wrecks become wrecks because the end up punctured on shorelines. In the battle between the rock and the metal hull, rocks often come out the winner. However, deeper wrecks evade the action of the weather and therefore will remain intact for longer.

Any biological material on a wreck which will decay very quickly. Body flesh is quickly scavenged by crustacea and fish. The hard matrix of the bones that are left behind is mostly hydroxyapatite (a mixture of calcium and phosphate) which is soluble in the sea and becomes more soluble at depth. This is why the deep ocean isn’t several metres deep in fish and whale bones, they dissolve.
The next most fragile structure on any ship wreck is the wooden components. Modern ships with chipboard partitions fare particularly badly once submerged, and can fall apart within a very short space of years. Wood is made up of cellulose and lignin molecules. Cellulose is the main part of the cell wall from the tree that the wood came from. Cellulose isn’t water soluble but the chains of cellulose are held together by hydrogen bonds which water helps to promote. Surrounding the cellulose chains are lignins. These are complex polymers that give wood rigidity and resist rotting. The levels and type of lignin vary between different species of tree. Teak, the beloved material for decks of many vessels, has a high lignin content, which helps it to resist degradation.

For the metal components of a wreck to decay there are several factors that will affect the rate of decay. Salt minerals dissolved in the ocean, particularly sodium chloride (the same stuff you sprinkle on your chips) is a major player. In salt water metals will corrode about 5 times faster than in fresh water. Salts break into charged ions which allow the conduction of electricity and metal ions from the ship will enter the water, gradually thinning the metal plates of the hull. Salinity levels can vary massively depending on the location. A nearby source of freshwater can reduce decay. Salinity is maximum at the surface and decreases down to 500 metres, although it rises again around 2500 metres down.

Oxygen levels in the water will also affect the rate of decay.  Oxygen reacts with metals to produce metal oxides eg iron reacts to produce iron oxide ie rust. Metal oxides are weaker than the metal they derive from.  So gradually the layer of metal turns to rust, which will thin the metal hull even further. Oxygen levels are at a maximum near the surface and decrease down to about 1000m, and then they increase with depth.

Finally, let’s consider temperature. A higher water temperature means all the water molecule are moving faster and at a molecular level, all these reactions occur more quickly. Deeper wrecks in colder waters have a slower decay pathway.
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So for a shipwreck to survive, we require a well-constructed, high quality metal in thick sheets, sunk in fairly cold water, deep enough to avoid wave action and sand scouring, so somewhere sheltered would be ideal……welcome to the wrecks of Scapa Flow! 

​Stefano Lorenzini was an Italian physician born in Florence in 1652. One of his teachers at the medical school in Pisa was Francesco Redi who as well as being a physician spent time experimenting to prove that spontaneous generation (life just appears) was a myth, mostly with maggots and flies. As part of his work Redi, like all scientists of a time without cameras, made incredibly detailed anatomical drawings. Redi inspired Lorenzini, who in 1678 published the work that he is best remembered for, an in-depth study on the anatomy and physiology of sharks. This work contained the discovery of the Ampullae of Lorenzini, the special electromagnetic sense organs found in sharks and rays. But although Lorenzini described and drew the Ampullae, it would take nearly 300 years before modern science could explain how sharks had an additional sensory organ not seen in most other animals.

The Ampullae of Lorenzini form a network of jelly filled canals that open in small pores through the surface of the skin which can be seen as dark spots on the skin. At the back end of the canal is a collection of receptor cells that have a unique structure and allow the shark to sense electric and magnetic fields. The gel in the canals is keratan sulfate which has one of the highest known conductivity of any known biological material (about 1.8 milliSiemens/cm). The ampullae are clustered and each cluster connects to a different part of the skin, so the shark can get detailed directional information from this network.

The cells that actually detect the electrical field have a very special structure. There is a single layer of excitable cells closely packed together. The membrane of these cells facing into the canal is packed with voltage dependent calcium channel proteins. The rest of the canal lining has a very high resistance, which means that any voltage difference is effectively concentrated on the electroreceptor cells. A change in the electric field in the jelly allows these proteins to open and calcium floods into the cells. This causes the other side of the cell (away from the canal) to release neurotransmitter signalling to the shark.

Sharks have been shown to be more sensitive to electric fields than any other animal, possibly as low as 5 nanoVolts/cm – that’s 5/1,000,000,000 of a volt detected in a 1cm long ampulla. All living creatures produce an electric field by muscle contractions and as a result of the internal body chemistry. So being able to detect weak electrical stimuli probably allows sharks to hunt prey animals, including those buried in sand. Basking sharks have been observed swerving around jellyfish whilst feeding, after all the last thing you’d want clogging up your gill rakers would be lots of jellyfish and their stinging nematocysts.
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It’s likely that the Ampullae of Lorenzini also allow sharks to sense magnetic fields.  Any moving conductor will induce an electric field, so seawater moving on ocean currents, with the Earth’s magnetic field will produce electric fields well within the range that sharks can detect. Behavioural studies have shown that magnetic fields can change the behaviour of sharks. The ability to sense and orientate along magnetic field lines may help explain some of the large distance migrations that have been found using shark tagging experiments. Great white sharks have been shown to migrate over 2000 miles in open ocean to feeding grounds in the Pacific Ocean. Whale sharks have been tracked on journeys over 4800 miles. That is an astonishing figure considering that they don’t have sat nav guiding the way! So next time you’re up close and personal with any shark or ray, have a look for the black dots around their snout and remember that 340 years ago an Italian doctor and fish fanatic spotted the same thing.

In Japan it takes 3 or more years or rigorous training to become a Fugu chef and the pass rate for the exam is less than 40%. Fugu is a dish prepared from pufferfish, which is potentially lethal due to the presence of Tetrodotoxin (TTX). Budding chefs learn how to carefully remove the most toxic parts of the fish without contaminating the meat. Even though the liver of the fish is considered by some to be the tastiest part, its also the most poisonous organ. With such high stakes, restaurants serving Fugu are controlled by law, but there are around 20-40 incidents a year in Japan, with a fatality rate of around 7%.  Most of the fatalities aren’t associated with restaurants, but with home preparations. Never has the phrase “I’m dying to eat” been more apt.

The symptoms of ingesting a lethal dose of TTX include dizziness, exhaustion, headache, nausea and difficulty breathing. The victim remains conscious but cannot speak or move. Breathing stops and asphyxiation follows.  There is no known antidote. Treatment consists of emptying the stomach, giving the victim activated charcoal to absorb the TTX and putting them on life support until the poison has worn off. You can add in whatever prayers you feel like at that point. If the patient survives the first 24 hours then recovery over a few days is common.

So, what on earth is the pufferfish doing with this potent neurotoxin? It turns out that in the marine environment pufferfish aren’t alone. TTX is also found in blue ringed octopus, Astropecten star fish, Xanthid crabs and some newts and toads too. But despite its widespread appearance in the animal kingdom, none of these creatures are actually synthesising the TTX. The toxin is produced by bacteria that infect or live in the animal, and the animal concerned uses the TTX as a defensive biotoxin, and sometimes also as a venom eg octopus and arrow worms (Chaetognaths).
TTX acts by blocking sodium ion channels. Nerve cells have to pump sodium ions outside of the cell in order to be ready to transmit a signal. Sodium ions can’t cross cell membranes, so a special protein gateway exists in the nerve cell membrane that helps move the sodium out. Block this protein and the nerve cells will lose their ability to send a signal. This prevents the nerve from being able to send messages to muscles, resulting in reduced muscle movement. There are slightly different sodium ion channel proteins in the nerves controlling skeletal muscle and those controlling cardiac muscle. Victims of TTX poisoning will experience progressive paralysis throughout their body, whilst remaining conscious until shortly before death. A truly awful way to go.

TTX turns out to be remarkably toxic. The lethal dose of cyanide is 8.5mg per kg of bodyweight, but it would take only 4% of that amount of TTX to be lethal. TTX can be absorbed orally, by ingestion, by injection or through abraded skin. As the TTX levels are due to bacteria, there is a seasonal, geographical and species variation. It’s no wonder that the Fugu chefs need years of training. Poisonings from TTX are almost exclusively associated with the consumption of pufferfish from Indo-Pacific regions, but this is mainly because pufferfish just aren’t eaten as commonly elsewhere. In New Zealand in 2009 several dogs died after eating grey side gilled seaslugs (Pleurobranchus maculate) found washed up on beaches. The slugs were found to have ingested high levels of TTX.
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Naturally occurring TTX has been used in traditional Chinese medicine for over 4000 years to treat convulsive disease. In 1774 Captain James Cook recorded that his crew ate locally caught tropical fish and fed the left overs to the pigs kept on board. The crew had mild symptoms (numbness and shortness of breath) but by the morning all the pigs were dead. The crew had a very lucky escape, although its not known if they had pork for lunch the next day!

​One of the hardest skills for some divers as their diving career progresses is learning to use a compass. Once you’ve mastered the technical aspects of making sure it’s moving freely and not locked off inside the casing, the biggest hurdle is trust. You need to gain a Jedi like perspective as you accept Obi-Wan’s guidance to “Use the Force”. And generally, that’s fine, until there’s a nearby wreck and your compass stops being attracted to the earth’s magnetic field and starts interacting with the ship’s magnetic field instead.

When iron hulled ships were introduced, the effect of the metal hull on steering compasses was first observed. During construction the metal in the ship adopts the magnetic field of the dockyard used for construction. In modern construction methods, the high currents used for welding the steel plates together create magnetic dipoles in the steel, thus magnetising the ship…

During the American Civil War, mines were developed that were activated by contact. The target ship hits the horn on the mine. The soft metal of the horn buckled under impact, smashing a glass ampoule with battery acid inside. The acid electrolyte dropped into the waiting battery, energizing it and heating a platinum wire inside the mercury fulminate detonator. Boom.

At the start of WW2, the Germans developed a new magnetic trigger for mines. For a while the British were stumped as to how these mines worked. But in November 1939 a German mine was dropped from an aircraft and landed on mudflats in the Thames estuary at low tide. The mine was disarmed and taken to Portsmouth, where the mechanism was examined.  A magnetic needle which was pulled by the target ship’s magnetic field completed the circuit and fired the mine.  Later sophisticated versions would use a counter that didn’t fire for the first few ships to pass.

Establishing how the mine worked held the secret to protecting vessels, you just need to wipe out the magnetic signal. Magnetic field strength is measured in units named after Carl Guass, so the process of removing the magnetic signature is known as degaussing. Remove the magnetic field from the ship and it can safely pass over the mines without triggering an explosion.

There were two ways of cancelling out the ship’s magnetic field.  The permanent one was to put thick bands of electrical wire around the length of the vessel, known as coiling. Passing an electrical current through these cables generated an electromagnetic field that cancelled out the ship’s own field, thus rendering the ship invisible to the mine mechanism. Royal Navy Commander Charles Goodeve oversaw this system, and it even allowed for the polarity to be reversed when ships were in the southern hemisphere so that the ship appeared to have the same magnetic field as the natural background.  But this equipment was expensive and difficult to install.

Measuring a ships natural magnetic field was a complex business. A series of magnetometers are anchored to the seabed about 5 metres apart for a 150 metre run. Each magnetometer wa connected to a fluxmeter on the shore. The ship passed over the magnetometers and the readings from the fluxmeter were used to create the ship’s signature.  From this starting point the number of turns of the degaussing cable could be increased or decreased, or the current altered until the signature was minimised.
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A second quicker method was to wipe the hull of the ship, with a current carrying cable running a pulse at about 2000 amps.  The large cable was dragged down the sides of the ship in a process known as deperming.  This wasn’t a permanent solution though, as the ship travelled through the Earth’s magnetic field it slowly became magnetised again. This started in late 1939 and helped protect many of the vessels that carried out the evacuation from Dunkirk.  In a 4 day marathon session prior to the evacuation over 400 ships were ‘wiped’ in this way, though there are concerns that some of the ‘wiping’ may have not been as effective as hoped.  The Isle of Man vessel Mona’s Queen was lost to a magnetic mine on 29th May 1940 just outside Dunkirk harbour, and stories persist to this day among the relatives of the crew that the ship wasn’t properly protected.