Isegoria

Most people transition in and out of paralysis multiple times per night, Charles Duhigg explains (in The Power of Habit), but some experience switching errors and end up sleepwalking:

“Sleepwalking is a reminder that wake and sleep are not mutually exclusive,” Mark Mahowald, a professor of neurology at the University of Minnesota and a pioneer in understanding sleep behaviors, told me. “The part of your brain that monitors your behavior is asleep, but the parts capable of very complex activities are awake. The problem is that there’s nothing guiding the brain except for basic patterns, your most basic habits. You follow what exists in your head, because you’re not capable of making a choice.”

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Sleepwalkers can behave in complex ways — for instance, they can open their eyes, see, move around, and drive a car or cook a meal — all while essentially unconscious, because the parts of their brain associated with seeing, walking, driving, and cooking can function while they are asleep without input from the brain’s more advanced regions, such as the prefrontal cortex.

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However, as scientists have examined the brains of sleepwalkers, they’ve found a distinction between sleepwalking — in which people might leave their beds and start acting out their dreams or other mild impulses — and something called sleep terrors. When a sleep terror occurs, the activity inside people’s brains is markedly different from when they are awake, semi-conscious, or even sleepwalking.

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Because sleep deactivates the prefrontal cortex and other high cognition areas, when a sleep terror habit is triggered, there is no possibility of conscious intervention. If the fight-or-flight habit is cued by a sleep terror, there is no chance that someone can override it through logic or reason.

In Germany, one researcher thinks he has found what is triggering the clots in patients who have received a COVID vaccine:

Andreas Greinacher, a blood expert, and his team at the University of Greifswald believe so-called viral vector vaccines — which use modified harmless cold viruses, known as adenoviruses, to convey genetic material into vaccine recipients to fight the coronavirus — could cause an autoimmune response that leads to blood clots. According to Prof. Greinacher, that reaction could be tied to stray proteins and a preservative he has found in the AstraZeneca vaccine.

Prof. Greinacher and his team has just begun examining Johnson & Johnson’s vaccine but has identified more than 1,000 proteins in AstraZeneca’s vaccine derived from human cells, as well as a preservative known as ethylenediaminetetraacetic acid, or EDTA. Their hypothesis is that EDTA, which is common to drugs and other products, helps those proteins stray into the bloodstream, where they bind to a blood component called platelet factor 4, or PF4, forming complexes that activate the production of antibodies.

The inflammation caused by the vaccines, combined with the PF4 complexes, could trick the immune system into believing the body had been infected by bacteria, triggering an archaic defense mechanism that then runs out of control and causes clotting and bleeding.

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One reason vaccine-induced clotting might not have been reported in the past is because shots using viral vector technology haven’t been administered at scale. The Russian vaccine Sputnik V and the shot by CanSino Biologics from China use the same technology as AstraZeneca and Johnson & Johnson, but haven’t been linked to the condition so far.

The only similar shot widely administered before the pandemic is one against Ebola by Johnson & Johnson, which was given to at least 60,000 people as of last July.

Clotting occurs between one in 28,000 and one in 100,000, according to European data — extremely rare amid the hundreds of millions of doses administered so far, yet higher than one in 150,000 previously assumed by some medical authorities, Prof. Greinacher said. Most of the hundreds of people who have been diagnosed recover, but between a fifth and a third have died, and others could suffer permanent consequences.

Athena Aktipis and Joe Alcock suggest that SARS-CoV-2 is a sort of zombie virus, turning people not into the undead but rather into the unsick:

People typically think of zombies as the stuff of science fiction. But in the biological world, zombies are all over the place, from the Ophiocordyceps fungus that perpetuates itself by zombifying ants; to Toxoplasma gondii, a single-celled parasite that completes its life cycle by leading rodents into the jaws of predators. Zombie viruses are also a real thing, influencing their host’s behavior in ways that enhance the viruses’ evolutionary fitness.

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About 40% of those with SARS-CoV-2 are asymptomatic spreaders, never showing symptoms at all. And those who do show symptoms are most contagious in the two days before symptoms appear. Why people don’t feel sick earlier – or sick at all – might be part of the evolutionary strategy of SARS-CoV-2.

A look under the hood of the virus reveals more about that manipulative machinery. SARS-CoV-2 interferes with a person’s immune response; this is why people don’t necessarily feel sick and withdrawn as they would in a typical viral infection. Instead, SARS-CoV-2 silences the body’s alarm signals that otherwise would orchestrate anti-viral defenses. It blocks interferons, a set of molecules that help fight viruses. Interferon activity makes people feel more depressed and socially withdrawn – so when the novel coronanvirus impedes interferon activity, mood is lifted, sociality is increased and you feel less sick.

The virus also decreases pain perception. Normally, pain motivates us to hunker down when we need to heal. But SARS-CoV-2 blocks this response by preventing the transmission of pain signals. This is why people feel fine even when they are teeming with virus before the onset of symptoms.

At the same time, SARS-CoV-2 dampens the body’s response to infection. It hinders pro-inflammatory cytokines, molecules that help spur the immune response. This too makes hosts feel better than they should. Typically, feeling sick helps our bodies prioritize healing by making us reduce our energy expenditure. With SARS-CoV-2, unsick hosts have the energy to do as much as they used to, maybe more.

The human body uses 30% to 50% less water per day than other primates:

The study compared the water turnover of 309 people with a range of lifestyles, from farmers and hunter-gatherers to office workers, with that of 72 apes living in zoos and sanctuaries.

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When they added up all the inputs and outputs, they found that the average person processes some three liters, or 12 cups, of water each day. A chimpanzee or gorilla living in a zoo goes through twice that much.

Pontzer says the researchers were surprised by the results because, among primates, humans have an amazing ability to sweat. Per square inch of skin, “humans have 10 times as many sweat glands as chimpanzees do,” Pontzer said.

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But the researchers controlled for differences in climate, body size, and factors like activity level and calories burned per day. So they concluded the water-savings for humans were real, and not just a function of where individuals lived or how physically active they were.

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One hypothesis, suggested by the data, is that our body’s thirst response was re-tuned so that, overall, we crave less water per calorie compared with our ape relatives. Even as babies, long before our first solid food, the water-to-calories ratio of human breast milk is 25% less than the milks of other great apes.

Another possibility lies in front of our face: Fossil evidence suggests that, about 1.6 million years ago, with the inception of Homo erectus, humans started developing a more prominent nose. Our cousins gorillas and chimpanzees have much flatter noses.

Our nasal passages help conserve water by cooling and condensing the water vapor from exhaled air, turning it back into liquid on the inside of our nose where it can be reabsorbed.

Having a nose that sticks out more may have helped early humans retain more moisture with each breath.

A junior doctor in the UK explains that the Covid pandemic didn’t feel real there in the first few months of 2020:

Then in early March it began to feel far more real. We’d had one confirmed Covid case in my hospital so far when I went to review a patient in Accident and Emergency. He’d had a fall here in England while on holiday from Milan — the epicentre of Europe’s outbreak — and needed an operation to fix a fracture.

I asked the A&E consultant if he had screened the man for any Covid symptoms and he laughed, admonishing me — semi-jokingly — for my “racism” against Italians. I suggested that we should isolate him until we had tested for the virus, to be on the safe side.

At this point I was told sharply “whatever next? We test everyone who walks through the doors for covid?” Looking back, that comment feels entirely absurd — today, of course, every patient has a rapid Covid swab before they are admitted to the hospital — but a year ago such an idea didn’t even occur to anyone.

While it was not within my powers to question a senior A&E doctor, I was able to suggest to my surgical consultant that the patient should be isolated “just in case”. We moved him from the open ward, alongside all of the other elderly patients with fractures, to a side room.

At the time tests were hard to get and results took 48hrs, although our hospital had developed a more informal 24-hour test which was “not yet clinically validated”. The result came back negative, although in block capitals underneath the result was written DO NOT DEISOLATE PATIENT UNTIL FORMAL 48h TEST. And so… we deisolated the patient immediately, because, so I was told, “He has a fracture that we need to fix. He’s got no symptoms anyway!”

The following day the result of the clinically-validated second test came back — the patient had coronavirus. By this point he had already been intubated and ventilated in theatres, itself an aerosol-generating procedure, and on several separate open bays full of patients. It’s hard to know how many infections resulted; how many deaths.

It’s worth remembering at this stage that masks were strictly Not Allowed when reviewing patients, unless they had either tested positive or had symptoms, and had also recently returned from China, Italy or Iran. When we were assessing our Italian patient in A&E, we were told sternly to remove our masks, lest we “scare the patients and other staff”.

My colleague, who had reviewed the patient with me, developed a cough several days later. Initially she stayed at work, since she had neither shortness of breath nor fever; when she called in sick the next day, many of the consultants laughed at how she had clearly been scared by her Covid contact, and was being ridiculous to not work through her “mild cold”. She was later admitted to our hospital with moderate “Covid pneumonitis”, as we would now say, requiring oxygen to help her breathe.

Tests of simple reaction time had done astonishingly little to help explain expert sports performance, David Epstein notes (in The Sports Gene):

The reaction times of elite athletes always hovered around one fifth of a second, the same as the reaction times when random people were tested.

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So, in 1975, as part of her graduate work at [the University of] Waterloo, [Janet] Starkes invented the modern sports “occlusion” test.

She gathered thousands of photographs of women’s volleyball games and made slides of pictures where the volleyball was in the frame and others where the ball had just left the frame. In many photos, the orientation and action of players’ bodies were nearly identical regardless of whether the ball was in the frame, since little had changed in the instant when the ball had just exited the picture.

Starkes then connected a scope to a slide projector and asked competitive volleyball players to look at the slides for a fraction of a second and decide whether the ball was or was not in the frame that had just flashed before their eyes. The brief glance was too quick for the viewer actually to see the ball, so the idea was to determine whether players were seeing the entire court and the body language of players in a different way from the average person that allowed them to figure out whether the ball was present.

The results of the first occlusion tests astounded Starkes. Unlike in the results of reaction time tests, the difference between top volleyball players and novices was enormous. For the elite players, a fraction of a second glance was all they needed to determine whether the ball was present. And the better the player, the more quickly she could extract pertinent information from each slide.

In one instance, Starkes tested members of the Canadian national volleyball team, which at the time included one of the best setters in the world. The setter was able to deduce whether the volleyball was present in a picture that was flashed before her eyes for sixteen thousandths of a second. “That’s a very difficult task,” Starkes told me. “For people who don’t know volleyball, in sixteen milliseconds all they see is a flash of light.”

Not only did the world-class setter detect the presence or absence of the ball in sixteen milliseconds, she gleaned enough visual information to know when and where the picture was taken. “After each slide she would say ‘yes’ or ‘no,’ whether the ball was there,” Starkes says, “and then sometimes she would say, ‘That was the Sherbrooke team after they got their new uniforms, so the picture must have been taken at such and such a time.’”

One woman’s blink of light was another woman’s fully formed narrative. It was a strong clue that one key difference between expert and novice athletes was in the way they had learned to perceive the game, rather than the raw ability to react quickly.