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Cognition Switch: Mind An Artefact for the Transmission of New Ideas on Mind and Mental Well-Being Issue #1: December 2018 Featuring Articles by: Gaia Vince, Michael Regnier, Jenny Diski, Geoff Watts, Lucy Maddox, Emma Young, Jo Marchant, Peter Aldhous, Mary O’Hara, Shayla Love, and Will Storr
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COGNITION SWITCH: MIND #1
Featuring Articles by:
Gaia Vince, Michael Regnier, Jenny Diski, Geoff Watts, Lucy Maddox, Emma Young, Jo Marchant, Peter Aldhous, Mary O’Hara, Shayla Love, and Will Storr
This work is licensed under a Creative Commons Attribution-NoDerivatives 4.0 International License
Originally published by Mosaic
Published 2018 by Blackmore Dennett
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1 2 3 4 10 8 7 6 5 00 000
Hacking the nervous system
The Alzheimer’s enigma
Blackness ever blackening: my lifetime of depression
In other words: inside the lives and minds of real-time translators
“I saw things children shouldn’t see” – surviving a troubled childhood
Secrets of the strong-minded
You can train your body into thinking it’s had medicine
People are animals, too
Psychosis in Parkinson’s: now we can treat it without making other symptoms worse
My grandparents survived the Cultural Revolution: have I inherited their trauma?
The male suicides: how social perfectionism kills
Gaia Vince is a writer and broadcaster specialising in science and the environment. She has been the front editor of the journal Nature Climate Change, the news editor of Nature and online editor of New Scientist. Her work has appeared in newspapers and magazines in the UK, USA and Australia, including the Guardian, Science, Scientific American and Australian Geographic. She writes for BBC Online and devises and presents science programmes for BBC radio. Her first book, Adventures in the Anthropocene: A journey to the heart of the planet we made, is out now. She blogs at WanderingGaia.com and tweets at @WanderingGaia. She lives in London.
When Maria Vrind, a former gymnast from Volendam in the Netherlands, found that the only way she could put her socks on in the morning was to lie on her back with her feet in the air, she had to accept that things had reached a crisis point. “I had become so stiff I couldn’t stand up,” she says. “It was a great shock because I’m such an active person.”
It was 1993. Vrind was in her late 40s and working two jobs, athletics coach and a carer for disabled people, but her condition now began taking over her life. “I had to stop my jobs and look for another one as I became increasingly disabled myself.” By the time she was diagnosed, seven years later, she was in severe pain and couldn’t walk any more. Her knees, ankles, wrists, elbows and shoulder joints were hot and inflamed. It was rheumatoid arthritis, a common but incurable autoimmune disorder in which the body attacks its own cells, in this case the lining of the joints, producing chronic inflammation and bone deformity.
Waiting rooms outside rheumatoid arthritis clinics used to be full of people in wheelchairs. That doesn’t happen as much now because of a new wave of drugs called biopharmaceuticals – such as highly targeted, genetically engineered proteins – which can really help. Not everyone feels better, however: even in countries with the best healthcare, at least 50 per cent of patients continue to suffer symptoms.
Like many patients, Vrind was given several different medications, including painkillers, a cancer drug called methotrexate to dampen her entire immune system, and biopharmaceuticals to block the production of specific inflammatory proteins. The drugs did their job well enough – at least, they did until one day in 2011, when they stopped working.
“I was on holiday with my family and my arthritis suddenly became terrible and I couldn’t walk – my daughter-in-law had to wash me.” Vrind was rushed to hospital, where she was hooked up to an intravenous drip and given another cancer drug, one that targeted her white blood cells. “It helped,” she admits, but she was nervous about relying on such a drug long-term.
Luckily, she would not have to. As she was resigning herself to a life of disability and monthly chemotherapy, a new treatment was being developed that would profoundly challenge our understanding of how the brain and body interact to control the immune system. It would open up a whole new approach to treating rheumatoid arthritis and other autoimmune diseases, using the nervous system to modify inflammation. It would even lead to research into how we might use our minds to stave off disease.
And, like many good ideas, it came from an unexpected source.
Kevin Tracey, a neurosurgeon based in New York, is a man haunted by personal events – a man with a mission. “My mother died from a brain tumour when I was five years old. It was very sudden and unexpected,” he says. “And I learned from that experience that the brain – nerves – are responsible for health.” This drove his decision to become a brain surgeon. Then, during his hospital training, he was looking after a patient with serious burns who suddenly suffered severe inflammation. “She was an 11-month-old baby girl called Janice who died in my arms.”
These traumatic moments made him a neurosurgeon who thinks a lot about inflammation. He believes it was this perspective that enabled him to interpret the results of an accidental experiment in a new way.
In the late 1990s, Tracey was experimenting with a rat’s brain. “We’d injected an anti-inflammatory drug into the brain because we were studying the beneficial effect of blocking inflammation during a stroke,” he recalls. “We were surprised to find that when the drug was present in the brain, it also blocked inflammation in the spleen and in other organs in the rest of the body. Yet the amount of drug we’d injected was far too small to have got into the bloodstream and travelled to the rest of the body.”
After months puzzling over this, he finally hit upon the idea that the brain might be using the nervous system – specifically the vagus nerve – to tell the spleen to switch off inflammation everywhere.
It was an extraordinary idea – if Tracey was right, inflammation in body tissues was being directly regulated by the brain. Communication between the immune system’s specialist cells in our organs and bloodstream and the electrical connections of the nervous system had been considered impossible. Now Tracey was apparently discovering that the two systems were intricately linked.
The first critical test of this exciting hypothesis was to cut the vagus nerve. When Tracey and his team did, injecting the anti-inflammatory drug into the brain no longer had an effect on the rest of the body. The second test was to stimulate the nerve without any drug in the system. “Because the vagus nerve, like all nerves, communicates information through electrical signals, it meant that we should be able to replicate the experiment by putting a nerve stimulator on the vagus nerve in the brainstem to block inflammation in the spleen,” he explains. “That’s what we did and that was the breakthrough experiment.”
Operating far below the level of our conscious minds, the vagus nerve is vital for keeping our bodies healthy. It is an essential part of the parasympathetic nervous system, which is responsible for calming organs after the stressed ‘fight-or-flight’ adrenaline response to danger. Not all vagus nerves are the same, however: some people have stronger vagus activity, which means their bodies can relax faster after a stress.
The strength of your vagus response is known as your vagal tone and it can be determined by using an electrocardiogram to measure heart rate. Every time you breathe in, your heart beats faster in order to speed the flow of oxygenated blood around your body. Breathe out and your heart rate slows. This variability is one of many things regulated by the vagus nerve, which is active when you breathe out but suppressed when you breathe in, so the bigger your difference in heart rate when breathing in and out, the higher your vagal tone.
Research shows that a high vagal tone makes your body better at regulating blood glucose levels, reducing the likelihood of diabetes, stroke and cardiovascular disease. Low vagal tone, however, has been associated with chronic inflammation. As part of the immune system, inflammation has a useful role helping the body to heal after an injury, for example, but it can damage organs and blood vessels if it persists when it is not needed. One of the vagus nerve’s jobs is to reset the immune system and switch off production of proteins that fuel inflammation. Low vagal tone means this regulation is less effective and inflammation can become excessive, such as in Maria Vrind’s rheumatoid arthritis or in toxic shock syndrome, which Kevin Tracey believes killed little Janice.
Having found evidence of a role for the vagus in a range of chronic inflammatory diseases, including rheumatoid arthritis, Tracey and his colleagues wanted to see if it could become a possible route for treatment. The vagus nerve works as a two-way messenger, passing electrochemical signals between the organs and the brain. In chronic inflammatory disease, Tracey figured, messages from the brain telling the spleen to switch off production of a particular inflammatory protein, tumour necrosis factor (TNF), weren’t being sent. Perhaps the signals could be boosted?
He spent the next decade meticulously mapping all the neural pathways involved in regulating TNF, from the brainstem to the mitochondria inside all our cells. Eventually, with a robust understanding of how the vagus nerve controlled inflammation, Tracey was ready to test whether it was possible to intervene in human disease.
In the summer of 2011, Maria Vrind saw a newspaper advertisement calling for people with severe rheumatoid arthritis to volunteer for a clinical trial. Taking part would involve being fitted with an electrical implant directly connected to the vagus nerve. “I called them immediately,” she says. “I didn’t want to be on anticancer drugs my whole life; it’s bad for your organs and not good long-term.”
Tracey had designed the trial with his collaborator, Paul-Peter Tak, professor of rheumatology at the University of Amsterdam. Tak had long been searching for an alternative to strong drugs that suppress the immune system to treat rheumatoid arthritis. “The body’s immune response only becomes a problem when it attacks your own body rather than alien cells, or when it is chronic,” he reasoned. “So the question becomes: how can we enhance the body’s switch-off mechanism? How can we drive resolution?”
When Tracey called him to suggest stimulating the vagus nerve might be the answer by switching off production of TNF, Tak quickly saw the potential and was enthusiastic to see if it would work. Vagal nerve stimulation had already been approved in humans for epilepsy, so getting approval for an arthritis trial would be relatively straightforward. A more serious potential hurdle was whether people used to taking drugs for their condition would be willing to undergo an operation to implant a device inside their body: “There was a big question mark about whether patients would accept a neuroelectric device like a pacemaker,” Tak says.
He needn’t have worried. More than a thousand people expressed interest in the procedure, far more than were needed for the trial. In November 2011, Vrind was the first of 20 Dutch patients to be operated on.
“They put the pacemaker on the left-hand side of my chest, with wires that go up and attach to the vagus nerve in my throat,” she says. “I waited two weeks while the area healed, and then the doctors switched it on and adjusted the settings for me.”
She was given a magnet to swipe across her throat six times a day, activating the implant and stimulating her vagus nerve for 30 seconds at a time. The hope was that this would reduce the inflammatory response in her spleen. As Vrind and the other trial participants were sent home, it became a waiting game for Tracey, Tak and the team to see if the theory, lab studies and animal trials would bear fruit in real patients. “We hoped that for some, there would be an easing of their symptoms – perhaps their joints would become a little less painful,” Tak says.
At first, Vrind was a bit too eager for a miracle cure. She immediately stopped taking her pills, but her symptoms came back so badly that she was bedridden and in terrible pain. She went back on the drugs and they were gradually reduced over a week instead.
And then the extraordinary happened: Vrind experienced a recovery more remarkable than she or the scientists had dared hope for.
“Within a few weeks, I was in a great condition,” she says. “I could walk again and cycle, I started ice-skating again and got back to my gymnastics. I feel so much better.” She is still taking methotrexate, which she will need at a low dose for the rest of her life, but at 68, semi-retired Vrind now plays and teaches seniors’ volleyball a couple of hours a week, cycles for at least an hour every day, does gymnastics, and plays with her eight grandchildren.
Other patients on the trial had similar transformative experiences. The results are still being prepared for publication but Tak says more than half of the patients showed significant improvement and around one-third are in remission – in effect cured of their rheumatoid arthritis. Sixteen of the 20 patients on the trial not only felt better, but measures of inflammation in their blood also went down. Some are now entirely drug-free. Even those who have not experienced clinically significant improvements with the implant insist it helps them; nobody wants it removed.
“We have shown very clear trends with stimulation of three minutes a day,” Tak says. “When we discontinued stimulation, you could see disease came back again and levels of TNF in the blood went up. We restarted stimulation, and it normalised again.”
Tak suspects that patients will continue to need vagal nerve stimulation for life. But unlike the drugs, which work by preventing production of immune cells and proteins such as TNF, vagal nerve stimulation seems to restore the body’s natural balance. It reduces the over-production of TNF that causes chronic inflammation but does not affect healthy immune function, so the body can respond normally to infection.
“I’m really glad I got into the trial,” says Vrind. “It’s been more than three years now since the implant and my symptoms haven’t returned. At first I felt a pain in my head and throat when I used it, but within a couple of days, it stopped. Now I don’t feel anything except a tightness in my throat and my voice trembles while it’s working.
“I have occasional stiffness or a little pain in my knee sometimes but it’s gone in a couple of hours. I don’t have any side-effects from the implant, like I had with the drugs, and the effect is not wearing off, like it did with the drugs.”
But what about people who just have low vagal tone, whose physical and mental health could benefit from giving it a boost? Low vagal tone is associated with a range of health risks, whereas people with high vagal tone are not just healthier, they’re also socially and psychologically stronger – better able to concentrate and remember things, happier and less likely to be depressed, more empathetic and more likely to have close friendships.
Twin studies show that to a certain extent, vagal tone is genetically predetermined – some people are born luckier than others. But low vagal tone is more prevalent in those with certain lifestyles – people who do little exercise, for example. This led psychologists at the University of North Carolina at Chapel Hill to wonder if the relationship between vagal tone and wellbeing could be harnessed without the need for implants.
In 2010, Barbara Fredrickson and Bethany Kok recruited around 70 university staff members for an experiment. Each volunteer was asked to record the strength of emotions they felt every day. Vagal tone was measured at the beginning of the experiment and at the end, nine weeks later. As part of the experiment, half of the participants were taught a meditation technique to promote feelings of goodwill towards themselves and others.
Those who meditated showed a significant rise in vagal tone, which was associated with reported increases in positive emotions. “That was the first experimental evidence that if you increased positive emotions and that led to increased social closeness, then vagal tone changed,” Kok says.
Now at the Max Planck Institute in Germany, Kok is conducting a much larger trial to see if the results they found can be replicated. If so, vagal tone could one day be used as a diagnostic tool. In a way, it already is. “Hospitals already track heart-rate variability – vagal tone – in patients that have had a heart attack,” she says, “because it is known that having low variability is a risk factor.”
The implications of being able to simply and cheaply improve vagal tone, and so relieve major public health burdens such as cardiovascular conditions and diabetes, are enormous. It has the potential to completely change how we view disease. If visiting your GP involved a check on your vagal tone as easily as we test blood pressure, for example, you could be prescribed therapies to improve it. But this is still a long way off: “We don’t even know yet what a healthy vagal tone looks like,” cautions Kok. “We’re just looking at ranges, we don’t have precise measurements like we do for blood pressure.”
However the technology develops, our understanding of how the body manages disease has changed for ever. “It’s become increasingly clear that we can’t see organ systems in isolation, like we did in the past,” says Paul-Peter Tak. “We just looked at the immune system and therefore we have medicines that target the immune system.
“But it’s very clear that the human is one entity: mind and body are one. It sounds logical but it’s not how we looked at it before. We didn’t have the science to agree with what may seem intuitive. Now we have new data and new insights.”
And Maria Vrind, who despite severe rheumatoid arthritis can now cycle pain-free around Volendam, has a new lease of life: “It’s not a miracle – they told me how it works through electrical impulses – but it feels magical. I don’t want them to remove it ever. I have my life back!”
Michael Regnier is a science writer and editor at the Wellcome Trust, having previously worked as a writer for the Medical Research Council and as a press officer for the Wellcome Trust and Cancer Research UK. As well as a degree in natural sciences, he has a Master’s in science communication, which included a brief stint helping to develop public exhibitions at CERN. Before writing about science for a living, Michael wrote plays, the best of which was Time Out Critic’s Choice when it was performed in London.
The King of Crete demanded that, to atone for the death of his son, the city of Athens send him seven young men and seven young women every seventh year. When they arrived in Crete, they were sent into the Labyrinth, at the centre of which lived the Minotaur, a monstrous creature with the body of a man but the head of a bull. If the Minotaur didn’t kill the young Athenians, they were condemned to wander the tortuous maze, losing first their way and eventually their lives.
This human tribute had been paid twice when Theseus, a prince of Athens, took his place among the 14 youths. In most retellings of the myth, it is taken for granted that the hero will defeat the Minotaur in combat. But the physical fight is not the point of this story – it’s how Theseus overcame the mental challenge of navigating the Labyrinth. As well as his sword, he took with him a ball of thread, a clew, to line his path. No matter how deep into the maze he had to go, the thread would bring him out safely.
Theseus’s clew is the root of the modern English word clue, and clues are the best way to solve a mystery. They are signposts showing that a puzzle, no matter how convoluted it seems, has a straightforward solution. Real life is messier than myth or fiction, but we still tend to believe that our problems can be reduced to something manageable, if we only gather enough clues.
“Auguste D–” was the name on the blue cardboard case file. Auguste Deter, admitted to the Hospital for the Mentally Ill and Epileptics in Frankfurt on 25 November 1901. Senior physician Dr Alois Alzheimer examined her the next day and over three days after that.
“What is your name?”
“What is your husband’s name?”
“Auguste, I think.”
“Ah, my husband.”
Aged 51, Deter had an unusually severe and progressive dementia. Her first symptom had been intense jealousy towards her husband. Soon her memory had begun to fail, she was often disoriented and would hide things in her flat; sometimes she felt someone wanted to kill her and she would start screaming. She died within five years.
By then, Alzheimer had taken a job in Munich but, unable to forget Deter, he arranged for her brain to be sent to him after her death. He wanted to get inside her head, literally, and see what 32 pages of medical notes had failed to show: the cause of her mental degeneration. Alzheimer cut thin slices from her brain and examined them under the microscope, looking for clues.
Your brain is a dark, damp maze. The 1.5 kg or so of soft brain tissue that is folded and pleated in your skull holds within it another, more complex labyrinth of nerve cells reaching out to each other in the darkness, making electrical and chemical connections, forming pathways and circuits that somehow give rise to consciousness and cognition, the memories and thoughts that define you. In Deter’s brain, that labyrinth had become a trap. Connections were lost, cells missing, memories wiped, intellect destroyed. As its order and organisation broke down, her brain made desperate attempts to reroute signals, wandering the same loop of thought over and over or generating bizarre, frightening delusions. The interweaving neural paths that once allowed her to interact with the world eventually became impassable, overgrown with knotty plaques and tangles – these were the clues Alzheimer found.
In Deter’s otherwise healthy nerve cells, many of the fibres along their branch-like extensions were unusually thick and impregnable – the ‘tangles’. At the same time, lying between her cells were small, round clumps, or ‘plaques’. It seemed obvious that these plaques and tangles – the twin hallmarks of what is now called Alzheimer’s disease – made the difference between a healthy brain and a diseased one.
Detective fiction was invented in 1841 by Edgar Allan Poe. Inspired by the burgeoning sciences of the early 19th century, the American writer created Monsieur C Auguste Dupin, a Parisian sleuth. Dupin was supremely intelligent, observant and rational. He was also reclusive and boastful, but capable of astounding leaps of deduction that cut through the most mystifying crimes. Literary commentators of the day said Poe had moved the focus of storytelling from the heart to the head: romance and drama were sacrificed for logic and reasoning; thoughts counted more than actions.
Dupin’s first case was The Murders in the Rue Morgue: two women had been brutally murdered in a fourth-storey room from which there was apparently no possible exit – the windows were fastened from the inside, the chimneys too narrow for even a cat to climb, and a crowd of neighbours had blocked the stairs to the locked door, the key on the inside, as they listened to the horrific shrieking within. One woman’s head was almost completely severed from her body; the other’s body was crammed head-down up a chimney. Insoluble to all of Paris, not least the police, the mystery becomes transparent to Dupin thanks to the clews (Poe uses this spelling throughout) he finds at the scene of the crime. The killer is indeed an inhuman brute – it turns out to be an escaped orang-utan.
As the fictional construct of an author solving constructed crimes, Monsieur Dupin was infallible. Real life would prove more challenging.
“Alzheimer’s disease is a construct; all diseases are constructs,” says Simon Lovestone, Professor of Old Age Psychiatry at the Institute of Psychiatry, King’s College London. “They’re our best attempt to explain the world.”
Alois Alzheimer’s descriptions of Deter added a new construct to the medical textbooks: a rare form of dementia that attacked memory, self-awareness and rational intellect, was accompanied by plaques and tangles in the brain, and developed much earlier than ‘senile dementia’, the gradual loss of mental faculties that was all but accepted as a natural part of old age.
This definition came under threat in the 1930s, as it was discovered that some apparently healthy old people also had plaques and tangles in their brains when they died. If Alzheimer’s clues were red herrings, not specific to the dementia at all, it would leave nothing else on which to start building an understanding of the disease.
From the 1960s, scientists took a more rigorous approach. Rather than noting merely the presence or absence of plaques and tangles in people’s brains, they began to measure how many there were and how these quantities related to performance in standardised tests of cognitive ability. In general, more plaques and tangles were present in cases of more severe dementia, suggesting they were indeed linked. Where people had plaques and tangles but no dementia, it may have been that they died before symptoms appeared, or that our brains could compensate up until a certain point. Overall, researchers were now satisfied that Alzheimer’s disease was real.
In fact, Alzheimer’s disease was redefined in the 1970s to include anyone with dementia who was then found to have plaques and tangles in their brain when they died. This turns out to include many people who would previously have been diagnosed with ‘senile dementia’ as well as those who fit Alzheimer’s original description. This new construct became by far the most common form of dementia – according to the charity Alzheimer’s Research UK, about half a million people in the UK have Alzheimer’s disease, accounting for more than 60 per cent of all people with dementia.
“To me as a scientist, Alzheimer’s disease is a process in the brain which is manifested by plaques, tangles and neuronal loss,” says Lovestone. “It is defined by progressive loss of cognition and an ability to function in the daily world.
“People lose their memories and then they lose their ability to do complex tasks and then increasingly simple tasks, and this results in them needing care. And it is frequently accompanied by behavioural and psychological symptoms, which can be everything from sleep disturbance to frank psychotic features.
“To me as a clinician, Alzheimer’s disease is a patient before me with a set of characteristic symptoms, who I’m currently unable to help very much.”
The body of Mary Rogers had been found floating in the Hudson river, off the shore of New Jersey, in July 1841. A tobacconist’s clerk, she was referred to in the press as the “beautiful cigar girl”. The ensuing investigation gave the American journalists ample opportunity to come up with a slew of sensational theories. Some papers claimed Rogers’s former employer was the culprit, some that she was the victim of a gang rape and murder; others had more far-fetched ideas.
Edgar Allan Poe thought he knew better. The following year, he translated the salient details of the case to Paris so that Monsieur Dupin could tackle the analogous Mystery of Marie Rogêt, serialised in Snowden’s Ladies’ Companion. Before he could publish the final instalment and reveal the culprit, however, real life intervened: a woman confessed on her deathbed that Rogers had not been murdered but had actually died during a botched abortion on her premises.
No one was ever convicted in the Rogers case, largely because no one could ever be sure what had happened. In Poe’s story, Dupin never commits to a solution. Poe left his ending inconclusive, instead discussing the nature of probability and error when choosing between competing theories.
The 1970s redefinition of Alzheimer’s disease attracted more attention, more money and more researchers. Everyone had their own pet theory. John Hardy, a scientist who has come as close as anyone to finding a convincing explanation of Alzheimer’s disease, says it was the land of anything goes: “People said it was aluminium, ‘slow viruses’, oxidative damage – not that any of these are necessarily 100 per cent wrong but it was just an anarchic ideas mush.”
Out of the mush, however, came a simple theory that led to the first set of treatments for Alzheimer’s disease. Scientists had discovered that we need a neurotransmitter called acetylcholine to form memories. Since memory is the first thing to go in Alzheimer’s disease, and nerve cells that used a lot of acetylcholine seemed especially vulnerable, researchers were convinced this could be the basis of a treatment. They designed drugs such as Aricept to bolster acetylcholine and help maintain the function of those specific nerve cells.
It would have been a relatively simple solution to Alzheimer’s disease – if it had worked. Unfortunately, the benefit to patients is short-lived before the disease regains the upper hand and mental degeneration continues. And yet there is still no better treatment available today than these imperfect drugs.
Poe returned to the elegant simplicity of a constructed crime for Dupin’s third and final case. In it, the detective must locate The Purloined Letter, which has been brazenly stolen from the Queen of France. The thief, a politician referred to only as Minister D–, turns out to be Dupin’s mirror image, his arch-rival: both detective and crook renowned for their genius and distinguished in mathematics and poetry. These similarities are deliberate, Poe’s point being that a detective has to be able to understand and think like his quarry to catch him.
By the time Dupin is asked to help, the police are on the Minister’s trail, surreptitiously searching his home nearly every night for three months. They have used microscopes to examine the walls, floors, tables and even the rungs of the chairs for signs that the letter had been secreted within. Only Dupin understands that Minister D– would have anticipated such thoroughness and avoided any attempt to conceal the letter: therefore, unlikely as it seems, he must have not hidden it at all.
Donning a pair of green spectacles as a disguise, Dupin calls on the Minister. He spots a soiled and crumpled letter lying carelessly in a cheap plasterboard card-rack. Despite not matching the police’s description, this, he deduces, is obviously the stolen object. He is, of course, proved right when he later steals back the letter, which had simply been folded over on itself.
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