Newspaper Accounts of Memory Marvels (Part 4)

 The credibility of claims that memory recollections come from brains is inversely proportional to the speed and capacity and reliability at which things can be recalled. There are numerous signal slowing factors in the brain, such as the relatively slow speed of dendrites, and the cumulative effect of synaptic delays in which signals have to travel over relatively slow chemical synapses (by far the most common type of synapse in the brain). As explained in my post here, such physical factors should cause brain signals to move at a typical speed very many times slower than the often cited figure of 100 meters per second: a sluggish "snail's pace" speed of only about a centimeter per second (about half an inch per second).  Ordinary everyday evidence of very fast thinking and instant recall is therefore evidence against claims that memory recall occurs because of brain activity, particularly because the brain is totally lacking in the things humans add to constructed objects to allow fast recall (things such as sorting and addressing and indexes). Chemical synapses in the brain do not even reliably transmit signals. Scientific papers say that each time a signal is transmitted across a chemical synapse, it is transmitted with a reliability of 50% or less.  (A paper states, "Several recent studies have documented the unreliability of central nervous system synapses: typically, a postsynaptic response is produced less than half of the time when a presynaptic nerve impulse arrives at a synapse." Another scientific paper says, "In the cortex, individual synapses seem to be extremely unreliable: the probability of transmitter release in response to a single action potential can be as low as 0.1 or lower.")  The more evidence we have of very fast and very accurate and very capacious recall (what a computer expert might call high-speed high-throughput retrieval), the stronger is the evidence against the claim that memory recall occurs from brain activity. 

It is therefore very important to collect and study all cases of exceptional human memory performance. The more such cases we find, and the more dramatic such cases are, the stronger is the case against the claim that memory is a neural phenomenon. Or to put it another way, the credibility of claims that memory is a brain phenomenon is inversely proportional to the speed and reliability of the best cases of human mental performance.  The more cases that can be found of humans that seem to recall too quickly for a noisy address-free brain to do ever do, or humans that seem to recall too well for a noisy, index-free, signal-mangling brain to ever do,  the stronger is the case that memory is not a neural phenomenon but instead a spiritual or psychic or metaphysical phenomenon.  In part 1  and part 2 and part 3 of this series, I gave many newspaper clips giving examples of such exceptional human memory performance. Let us now look at some more of such newspaper clips. 

The 1906 account below is one that is rather hard-to-believe, as it is a claim that a man memorized the entire Bible.

You can read the claim on the newspaper page here:

https://chroniclingamerica.loc.gov/lccn/sn84026843/1906-08-24/ed-1/seq-5/

It is well known that quite a few Muslim scholars memorized the entire Quran, a work of 6236 verses. In the newspaper story here, we read of a 90-day scripture memorization contest; and we have the claim that the winner memorized the entire New Testament (a work of 7,957 verses) and also a good deal of the Old Testament: 

"On the day of the award it was found that among the older competitors the winner was Miss Leste May Williams, a young woman 16 years of age. With these ninety days, during which she had an attack of measles, she committed to memory and recited to the committee 12,236 verses of Scripture, covering the entire New Testament ...and including liberal selections from Genesis, Psalms, Ecclesiastes and other parts of the Old Testament."

The length of memorization claimed above (roughly 10,000 verses) is in the same league as the claim made in a scientific paper that between age 59 and age 67 a person memorized all 10,565 lines of Milton's Paradise Lost, recalling the entire work over a three-day period. But the total number of verses in the Bible is about 31,102.  So a person memorizing the entire Bible would seem to display an unprecedented human ability of memorization, in terms of the total length. 

The 1923 news story here in the Washington Times claimed that  H. H. Halley had memorized the entire New Testament. The 1926 newspaper account here claims that H. H. Halley of Chicago, USA memorized the entire Bible. The same paper (the Indianapolis Times) had made the same claim in the 1925 newspaper account here. 

In the 1888 newspaper article here, we read of a Rev. Nathan Smith here, and it claimed that he had memorized the entire Bible. We are told he can name the verse, chapter and book of any Bible quotation. 

The newspaper page here has in its "Lived Under All Presidents" article a claim that an old woman named Elizabeth Freeman "memorized nearly the entire Bible."

The newspaper account below appeared in 1925.

"Germans believe that a member of the staff of the Prussian State library has the finest memory in the world. He has specialized in weather reports and from memory he can describe the weather of any day from 1881 up to the present time. His wonderful memory recently was tested by the Berlin Meteorological society and he came through with flying colors. Colonel Charratle of England once memorized the entire Issue of a newspaper on a wager; a stoker memorized Haydn’s  'Dictionary of Dates,' and Lord Randolph Churchill, also of England, was able to repeat a page of print after a single reading."

You can read the account on the page below:

https://chroniclingamerica.loc.gov/lccn/sn83032307/1925-08-27/ed-1/seq-5/

The account above refers to a perfect recall of weather reports over a period of 44 years (1881 to 1925), involving about 16,000 days. If we assume that each weather report would require on average a number of words equal to a single verse, the claim above is roughly equivalent to a claim that a man memorized  a body of material about as long as 16,000 verses.

Below are some accounts of extraordinary memory powers held long ago, from the newspaper account here:

The newspaper account claims that Thomas Cranmer memorized an entire translation of the Bible, and that Lord Granville memorized the entire New Testament. We also have a claim that a Corsican could repeat in order 36,000 names, and could also repeat the names in reverse order. 

In the newspaper account below, from the page here, we have a claim that a man memorized a catalog of more than 1,100 pages, and that he demonstrated his memorization of the catalog:

In the 1963 newspaper account here, we read of a man who every week would memorize the entire Saturday Evening Post, a magazine that at that time would have very many pages in each edition, with a page typically consisting of three of four columns of small print adding up to more than 700 words per page.

In the newspaper account here, we read of an opera singer with an astonishing memory: 

"Julia Rosewald, the prima donna with the Abbott opera company, has, perhaps, the most astonishing memory on the lyric stage. Her repertoire consists of sixty-eight operas, in nine of which she sings double roles. Besides this marvelous selection she adds ten oratorios, and what is more wonderful still, she memorizes the entire work and will instantly detect the slightest error in harmony or instrumentation. The rapidity with which she studies is almost incredible. On one occasion, to save the company, she studied an entirely new role in twenty-four consecutive hours, and without rest appeared in the part without an error. This is vouched for by the conductor, Tomasi, and the entire company."

Derek Paravicini was born 25 weeks early, with severe brain damage, but he has reliably demonstrated countless times the ability to very accurately play back on a keyboard any song that is played to him, note for note, even if he has never heard the song before. In the newspaper account below, which can be read here, the claim is made that such an ability was demonstrated repeatedly by an entire orchestra, which could play from memory some newly written march it had only heard once.. We read this:

"Practically all Latin Americans possess, in marked degree, what is known as ‘musical memory'....This ability to memorize has been exemplified on many occasions in San Antonio, Tex., when the visiting Mexican band has been asked to ‘stand by’ while the latest march from the United States is being played by the American band. With all standing at attention, the Mexican bandsmen have waited until the finish of the first strain and then came the marvelous test; the playing of this number in harmony by the entire group. Audiences have been astounded at this exhibition and some in the audience have expressed the thought that ‘there was some trick in it.’ That is absolutely true, for there is a trick, but it has taken thousands of years to produce it, and it is in the form of this musical memory . .. Leaders of the great orchestras in Latin America, with but little effort, are able to memorize the entire scores of dozens of operas.”

In support of such a claim, you could cite the huge number of opera roles memorized by Placido Domingo, who knew 151 opera roles in several different languages. 

On the newspaper page here, we have the claim that the Belgian shcolar Joest Lips (also called Justus Lipsius) memorized the entire text of the Histories of Tacitus, a work of 50,000 words. The page also claims that he once challenged a man to stand over him with a dagger, and to stab him if he transposed a single word. 

When Neuroscientists Doing Shoddy Studies Make Grandiose Boasts

Misleading statements are extremely abundant in neuroscience literature. One incredibly common type of misstatement is when neuroscientists produce scientific papers that claim in their titles and abstracts to have shown things that their research never showed.  You should never forget that you simply cannot take for granted the truth of achievement claims made in the titles or abstracts of biology papers, which often do not correspond to any achievements made in the paper. Then there are the huge number of misstatements made in university and college press releases announcing new science research. Such press releases often make grand achievement claims not matching any claims made by the scientific papers the press releases are promoting. 

In such cases a neuroscientist may be able to semi-credibly claim that it was not him who was deceiving people. Neuroscience papers typically have many different authors. So if you are one of seven authors of a neuroscience paper with a title claiming to have shown something the study did not actually show, you might be able to make a claim such as: "It was not me who wrote the title." If you are a co-author of a paper that is incorrectly described by a university press release making groundless boasts, then maybe you can semi-credibly say something like, "Well, you know how those PR guys are -- they are always making crumbs sound like castles." I don't find such excuses to be very credible. If you are a researcher at a university, and a press release is being written to announce your research, you should be able to review that press release for accuracy, and to make sure it does not make boastful misstatements about your research. 

In the case of a personal narrative in which one individual scientist makes untrue claims that something was done by him or his team of scientists, we have a case in which such excuses for misstatements cannot be used. If scientist Joe Smith says, "My colleagues and I have shown..." and makes a claim that is untrue, then we have very clear evidence that scientist Joe Smith has not told us the truth. In such a case Joe Smith cannot excuse his misstatement by using some "joint authorship" excuse or some excuse in which misstatements are blamed on overenthusiastic "hype everything" public relations writers. 

In the article here, we have an example of a neuroscientist personal narrative with some accuracy shortfalls. The article entitled "While do some memories stick while others fade" is written by neuroscientist Sadegh Nabavi.  Referring to a recently published study that he co-authored (a very bad example of poorly-designed junk science), Nabavi makes some grand boasts of achievement that are untrue. 

Nahavi starts out by stating a half-truth. He states this: "Research shows that emotionally impactful events strengthen the neural connections in the brain that store our memories." It is true that emotions help us remember things better and longer, but there is no scientific basis for the claim that it is "neural connections in the brain that store our memories." No memories have ever been found in a brain by microscopic examination. 

Nahavi then begins boasting, telling us this:

"My colleagues and I conducted a study using mouse models, whose brain functions are remarkably similar to humans. Our findings offer new insights into what happens in the brain during memory formation and help explain why some things are remembered while others are not."

Mice have brain functions remarkably similar to humans? This is not a story line that a "brains make minds" persons should feel comfortable making, given the gigantic difference between the intellectual capabilities of mice and humans. The paper referred to offers no such insights, because of defects in it I will soon list. 

Nahavi then makes this claim:

"Scientists agree that memories are formed (and lost) by changes in the strength of these synapses—a process known as synaptic plasticity. Synaptic plasticity can be increased or decreased in two ways: by altering the number of synapses or by making existing synapses larger or smaller."

The claim about scientists agreeing on this topic is untrue. The claim that memory is stored by changes in synapse strength is an utterly untenable theory, for a large number of reasons I explain in my post here, entitled "10 Reasons Synapses Cannot Be a Storage Place for Human Memories." Quite a few scientists have recognized that claims of memory storage by synapse strengthening are untenable or dubious, or recognized that scientists lack any well-established or credible theory of memory creation. I quote some of these scientists in the appendix of this post.

Nahavi makes this misleading claim: "At the same time, we observed that the synapses active during the event were strengthened – either by forming more channels or by expanding existing ones." Mice have billions of synapses, most of which are continually active at any given time, because neurons throughout the brain are constantly firing at random intervals, (between about 1 and 200 times a second), and that causes activity in synapses. It is utterly beyond today's technology to simultaneously study all the active synapses in the brain of a rodent, or even a hundredth of them, to tell whether they are strengthening.  And it is utterly untrue that when something is learned, particular synapses act in some distinctive way different from average synapses, some "standout" way that would allow a neuroscientist to credibly say, "Oh, I see, those are the synapses that are storing the memory just learned." 

What happens in studies like this is that scientists will arbitrarily pick some tiny fraction of a rodent's synapses to study, some miniscule fraction like .000001 of the total synapses.  It is misleading to identify some tiny fraction of these synapses (chosen for study by neuroscientists) as "synapses active during the event," when 99.99% of the synapses that were active are not being studied.  Synapses throughout a brain are continually undergoing random changes that may be interpreted as strengthening or weakening. We know this because synapses are connected to dendritic spines that have short lifetimes, and also because synapses are built from proteins that have an average lifetime of only a few weeks or less. There is no way to convincingly correlate the strengthening of some little group of synapses with an experience event of an organism. What goes on in studies such as this is that some tiny group of synapses will be chosen for study, and neuroscientists will act as if they luckily happened to have chosen some group of synapses that are being affected by something a mouse recently experienced. Such an assumption is never warranted. 

What goes on is cases like this is like what might go on if someone had the theory that his memories are stored in flowers. Such a person might choose for study a few of the flowers in Central Park, and observe that the flowers were growing stronger as he got more memories by taking a school course. This would be nonsense, because flowers getting stronger is something happening continuously and massively, and there would be no sound basis for correlating the observed strengthening of a few flowers and your memory formation. Similarly, because in every brain there are always countless synapses strengthening and countless synapses weakening, you never validate some theory of synapse memory storage by showing that some synapses strengthened when something was learned. 

Nahavi then begins to make grandiose boasts. He claims to have found a memory in a mouse brain, and to have "activated" such neurons. He claims to have observed that there was synapse strengthening that had something to do with memory. He claims to have affected memory recall in a mouse by artificially strengthening synapses. 

"We strongly activated the neurons encoding the weak memory....In this case, the mice were able to recall the aversive memory even the following day. At the same time, we observed that the synapses active during the event were strengthened ...In our experiment, we artificially strengthened certain synapses, even though they weren’t directly linked to the trivial experience. The result? The mice could recall the 'trivial' event the next day. Even more interestingly, the synapses encoding the trivial experience also became stronger."

The claims are mostly false. The claim about "neurons encoding the weak memory" does not even agree with Navavi's earlier claim that synapses store memories. Neurons are not synapses.  Nahavi and his guys did not actually find any "neurons encoding the weak memory"; they did not actually find any good evidence that memory creation strengthens synapses; and they did not actually show that memory recall in a mouse can be changed by artificially strengthening certain synapses. The main reason none of these was done is that  Nahavi's paper is a very poorly-designed piece of junk science, guilty of very bad examples of Questionable Research Practices and an unreliable measurement technique (attempting to judge freezing behavior). 

Some of the defects of the paper are these:

(1) The study group sizes were way too small for any decent statistical power to be claimed. The study group sizes were way-too-small sizes such as only 4 mice or only 6 mice or only 9 mice, and never more than 11. As a general rule, no experimental neuroscience paper should be taken seriously unless it uses at least 15 or 20 subjects per study group; and usually a higher study group size is needed to produce a decent statistical power. 

The authors would have found out that the study group sizes they used were grossly inadequate if they had done a sample size calculation, like good experimental scientists; but they failed to do such a calculation. 

(2) No blinding protocol was used, and no study of this type should be taken seriously unless a rigorous and through blinding protocol was used. 

(3) The study was totally dependent upon a very unreliable method for judging whether mice recalled, the technique of trying to judge "freezing behavior." All studies using such a technique are junk science, for reasons explained at length in my post here. 

When this utterly unreliable technique is used, observers will look at mice, and attempt to judge whether they recalled a fearful stimulus, purely based on the percentage of time that is mouse is immobile, during some arbitrary time length (which can vary between 30 seconds and 180 seconds, based on the arbitrary whim of a researcher).  Such a technique does not reliably measure fear recall in mice. Mice afraid of something are just as likely or more likely to flee as to "freeze" or become immobile. So you cannot reliably tell whether a mouse is recalling something by trying to judge their immobility during some time span, and calling that "freezing behavior." Living a decade in an apartment where mice would appear an average of maybe 5 or 10 times a year, I never once saw a mouse "freeze in fear" when suddenly seeing a human who shrieked at the sight of the mouse. Instead, the behavior would inevitably be a fleeing behavior. 

There are reliable techniques for measuring fear recall in mice. You can measure heart rate, which has a very strong spike when mice are afraid. Or you can use a simple "fear stimulus avoidance" technique like the one shown below. With such a setup, if a mouse recalls a fearful stimulus, it will take the harder path to a food reward; it if does not recall, it will take the easier path. 

Why do neuroscientists continue to use the utterly unreliable method of trying to measure fear recall in rodents by trying to judge "freezing behavior"? Because such a technique is a "see whatever you want to see" type of thing allowing a neuroscientist to report whatever he wants to report. All papers using "freezing behavior" judgments are junk science, including Nahavi's paper. 

(4) We have in the paper claims such as "Mice showed significantly increased freezing response during optical stimulation." The optical stimulation was optogenetic brain-zapping. Mice were brain-zapped, and a claim made that this was producing memory recall of a fearful stimulus, because a mouse was inactive, interpreted as "freezing behavior." But zapping a mouse's brain can itself produce freezing behavior, even when no recall is involved. A science paper says that it is possible to induce freezing in rodents by stimulating a wide variety of regions. It says, "It is possible to induce freezing by activating a variety of brain areas and projections, including the hippocampus (Liu et al., 2012), lateral, basal and central amygdala (Ciocchi et al., 2010); Johansen et al., 2010; Gore et al., 2015a), periaqueductal gray (Tovote et al., 2016), motor and primary sensory cortices (Kass et al., 2013), prefrontal projections (Rajasethupathy et al., 2015) and retrosplenial cortex (Cowansage et al., 2014).”

So any experiment trying to judge recall during brain-zapping (as judged by "freezing behavior") is guilty of doing things in a doubly-unreliable way. Trying to judge recall by judging "freezing behavior" is unreliable by itself; and doing such a thing while zapping a mouse's brain (which can produce freezing behavior by itself) is doubly-unreliable. 

Nahavi's method here seems as silly as that of some scientist who claims that memories are stored in a human's cheek, and who tries to test this claim by giving someone an embarrassing memory and then slapping him hard five times on the cheek, with the scientist claiming that the person's resulting red cheek is caused by stimulation of the memory cells in the person's cheek, which caused a blush after the embarrassing memory was recalled. This would be nonsense. The red cheek could be explained as merely a response to the slapping, without assuming any memory recall. And if mice engage in more "freezing behavior" when brain-zapped, that's just more evidence that brain-zapping tends to cause non-movement or "freezing behavior," not evidence of memory recall.  

What these kind of "memory experiments" mainly tell us about is the rather bad memory of some neuroscientists. 

Another recent example of a neuroscientist making groundless boasts of having done grand things is to be found in the article here. A neuroscientist makes these boasts:

"We wanted to know if there are cells that organise the knowledge of our behaviour, rather than the outside world, and how they work. Specifically, what are the algorithms that underlie the activity of brain cells as we generalise from past experience? How do we rustle up that new pasta dish?

And we did find such cells. There are neurons that tell us 'where we are' in a sequence of behaviour (we haven’t named the cells)."

The neuroscientist is referring to his paper "A cellular basis for mapping behavioural structure," which is an example of a junk science study because of its use of way-too-small study group sizes, and its lack of any blinding protocol.  The study group sizes were merely sizes such as 7 mice, 9 mice and 13 mice, way too small for any decent statistical power. We have in the paper the typical confession that occurs when authors fail to do a sample size calculation. We read, "No statistical methods were used to pre-determine sample sizes but our sample sizes are similar to those reported in previous publications (for example, in ref. 12)."  This is like someone saying "I cheated on my income tax, but it's okay because my friends also cheat on their income taxes."  The use of way-too-small study group sizes is a deplorable epidemic in today's neuroscience research. You do nothing to show that your study group sizes were large enough by claiming that other researchers are also using similar study group sizes. 

Appendix: The statements below show that Nahavi was not correct when he claimed "scientists agree that memories are formed (and lost) by changes in the strength of these synapses—a process known as synaptic plasticity."  There is no such agreement, and in the statements below, scientists express skepticism about such a claim or the claim that scientists know how memories are created. 

• "Direct evidence that synaptic plasticity is the actual cellular mechanism for human learning and memory is lacking." -- 3 scientists, "Synaptic plasticity in human cortical circuits: cellular mechanisms of learning and memory in the human brain?" 
• "The fundamental problem is that we don't really know where or how thoughts are stored in the brain. We can't read thoughts if we don't understand the neuroscience behind them." -- Juan Alvaro Gallego, neuroscientist. 
• "The search for the neuroanatomical locus of semantic memory has simultaneously led us nowhere and everywhere. There is no compelling evidence that any one brain region plays a dedicated and privileged role in the representation or retrieval of all sorts of semantic knowledge."  -- Psychologist Sharon L. Thompson-Schill, "Neuroimaging studies of semantic memory: inferring 'how' from 'where' ".
• "How the brain stores and retrieves memories is an important unsolved problem in neuroscience." --Achint Kumar, "A Model For Hierarchical Memory Storage in Piriform Cortex." 
• "We are still far from identifying the 'double helix' of memory—if one even exists. We do not have a clear idea of how long-term, specific information may be stored in the brain, into separate engrams that can be reactivated when relevant."  -- Two scientists, "Understanding the physical basis of memory: Molecular mechanisms of the engram."
• "There is no chain of reasonable inferences by means of which our present, albeit highly imperfect, view of the functional organization of the brain can be reconciled with the possibility of its acquiring, storing and retrieving nervous information by encoding such information in molecules of nucleic acid or protein." -- Molecular geneticist G. S. Stent, quoted in the paper here. 
• "Up to this point, we still don’t understand how we maintain memories in our brains for up to our entire lifetimes.”  --neuroscientist Sakina Palida.
• "The available evidence makes it extremely unlikely that synapses are the site of long-term memory storage for representational content (i.e., memory for 'facts'’ about quantities like space, time, and number)." --Samuel J. Gershman,  "The molecular memory code and synaptic plasticity: A synthesis."
• "Synapses are signal conductors, not symbols. They do not stand for anything. They convey information bearing signals between neurons, but they do not themselves convey information forward in time, as does, for example, a gene or a register in computer memory. No specifiable fact about the animal’s experience can be read off from the synapses that have been altered by that experience.” -- Two scientists, "Locating the engram: Should we look for plastic synapses or information- storing molecules?
• " If I wanted to transfer my memories into a machine, I would need to know what my memories are made of. But nobody knows." -- neuroscientist Guillaume Thierry (link). 
• "While a lot of studies have focused on memory processes such as memory consolidation and retrieval, very little is known about memory storage" -- scientific paper (link).
• "While LTP is assumed to be the neural correlate of learning and memory, no conclusive evidence has been produced to substantiate that when an organism learns LTP occurs in that organism’s brain or brain correlate."  -- PhD thesis of a scientist, 2007 (link). 
• "Memory retrieval is even more mysterious than storage. When I ask if you know Alex Ritchie, the answer is immediately obvious to you, and there is no good theory to explain how memory retrieval can happen so quickly." -- Neuroscientist David Eagleman.
• "How could that encoded information be retrieved and transcribed from the enduring structure into the transient signals that carry that same information to the computational machinery that acts on the information?....In the voluminous contemporary literature on the neurobiology of memory, there is no discussion of these questions."  ---  Neuroscientists C. R. Gallistel and Adam Philip King, "Memory and the Computational Brain: Why Cognitive Science Will Transform Neuroscience,"  preface. 
• "The very first thing that any computer scientist would want to know about a computer is how it writes to memory and reads from memory....Yet we do not really know how this most foundational element of computation is implemented in the brain."  -- Noam Chomsky and Robert C. Berwick, "Why Only Us? Language and Evolution," page 50. 
• "When we are looking for a mechanism that implements a read/write memory in the nervous system, looking at synaptic strength and connectivity patterns might be misleading for many reasons...Tentative evidence for the (classical) cognitive scientists' reservations toward the synapse as the locus of memory in the brain has accumulated....Changes in synaptic strength are not directly related to storage of new information in memory....The rate of synaptic turnover in absence of learning is actually so high that the newly formed connections (which supposedly encode the new memory) will have vanished in due time. It is worth noticing that these findings actually are to be expected when considering that synapses are made of proteins which are generally known to have a short lifetime...Synapses have been found to be constantly turning over in all parts of cortex that have been examined using two-photon microscopy so far...The synapse is probably an ill fit when looking for a basic memory mechanism in the nervous system." -- Scientist Patrick C. Trettenbrein, "The Demise of the Synapse As the Locus of Memory: A Looming Paradigm Shift? (link).
• "Most neuroscientists believe that memories are encoded by changing the strength of synaptic connections between neurons....Nevertheless, the question of whether memories are stored locally at synapses remains a point of contention. Some cognitive neuroscientists have argued that for the brain to work as a computational device, it must have the equivalent of a read/write memory and the synapse is far too complex to serve this purpose (Gaallistel and King, 2009; Trettenbrein, 2016). While it is conceptually simple for computers to store synaptic weights digitally using their read/write capabilities during deep learning, for biological systems no realistic biological mechanism has yet been proposed, or in my opinion could be envisioned, that would decode symbolic information in a series of molecular switches (Gaallistel and King, 2009) and then transform this information into specific synaptic weights." -- Neuroscientist Wayne S. Sossin (link).
• "We take up the question that will have been pressing on the minds of many readers ever since it became clear that we are profoundly skeptical about the hypothesis that the physical basis of memory is some form of synaptic plasticity, the only hypothesis that has ever been seriously considered by the neuroscience community. The obvious question is: Well, if it’s not synaptic plasticity, what is it? Here, we refuse to be drawn. We do not think we know what the mechanism of an addressable read/write memory is, and we have no faith in our ability to conjecture a correct answer."  -- Neuroscientists C. R. Gallistel and Adam Philip King, "Memory and the Computational Brain Why Cognitive Science Will Transform Neuroscience."  page Xvi (preface). 
• "Current theories of synaptic plasticity and network activity cannot explain learning, memory, and cognition."  -- Neuroscientist Hessameddin Akhlaghpourƚ (link). 
• "We don’t know how the brain stores anything, let alone words." -- Scientists David Poeppel and, William Idsardi, 2022 (link).
• "If we believe that memories are made of patterns of synaptic connections sculpted by experience, and if we know, behaviorally, that motor memories last a lifetime, then how can we explain the fact that individual synaptic spines are constantly turning over and that aggregate synaptic strengths are constantly fluctuating? How can the memories outlast their putative constitutive components?" --Neuroscientists Emilio Bizzi and Robert Ajemian (link).
• "After more than 70 years of research efforts by cognitive psychologists and neuroscientists, the question of where memory information is stored in the brain remains unresolved." -- Psychologist James Tee and engineering expert Desmond P. Taylor, "Where Is Memory Information Stored in the Brain?"
• "There is no such thing as encoding a perception...There is no such thing as a neural code...Nothing that one might find in the brain could possibly be a representation of the fact that one was told that Hastings was fought in 1066." -- M. R.  Bennett, Professor of Physiology at the University of Sydney (link).
• "No sense has been given to the idea of encoding or representing factual information in the neurons and synapses of the brain." -- M. R. Bennett, Professor of Physiology at the University of Sydney (link).
• ""Despite over a hundred years of research, the cellular/molecular mechanisms underlying learning and memory are still not completely understood. Many hypotheses have been proposed, but there is no consensus for any of these."  -- Two scientists in a 2024 paper (link). 
• "We have still not discovered the physical basis of memory, despite more than a century of efforts by many leading figures. Researchers searching for the physical basis of memory are looking for the wrong thing (the associative bond) in the wrong place (the synaptic junction), guided by an erroneous conception of what memory is and the role it plays in computation." --Neuroscientist C.R. Gallistel, "The Physical Basis of Memory," 2021.
• "To name but a few examples, the formation of memories and the basis of conscious  perception, crossing  the threshold  of  awareness, the  interplay  of  electrical  and  molecular-biochemical mechanisms of signal transduction at synapses, the role of glial cells in signal transduction and metabolism, the role of different brain states in the life-long reorganization of the synaptic structure or  the mechanism of how  cell  assemblies  generate a  concrete  cognitive  function are  all important processes that remain to be characterized." -- "The coming decade of digital brain research, a 2023 paper co-authored by more than 100 neuroscientists, one confessing scientists don't understand how a brain could store memories. 
• "The human brain isn’t really empty, of course. But it does not contain most of the things people think it does – not even simple things such as ‘memories’....We don’t create representations of visual stimuli, store them in a short-term memory buffer, and then transfer the representation into a long-term memory device. We don’t retrieve information or images or words from memory registers. Computers do all of these things, but organisms do not." -- Robert Epstein,  senior research psychologist, "The Empty Brain." 
• "Despite recent advancements in identifying engram cells, our understanding of their regulatory and functional mechanisms remains in its infancy." -- Scientists claiming erroneously in 2024 that there have been recent advancements in identifying engram cells, but confessing there is no understanding of how they work (link).
• "Study of the genetics of human memory is in its infancy though many genes have been investigated for their association to memory in humans and non-human animals."  -- Scientists in 2022 (link).
• "The neurobiology of memory is still in its infancy." -- Scientist in 2020 (link). 
• "The investigation of the neuroanatomical bases of semantic memory is in its infancy." -- 3 scientists, 2007 (link). 
• "Currently, our knowledge pertaining to the neural construct of intelligence and memory is in its infancy." -- Scientists, 2011 (link). 
•  "Very little is known about the underlying mechanisms for visual recognition memory."  -- two scientists (link). 
• "Conclusive evidence that specific long-term memory formation relies on dendritic growth and structural synaptic changes has proven elusive. Connectionist models of memory based on this hypothesis are confronted with the so-called plasticity stability dilemma or catastrophic interference. Other fundamental limitations of these models are the feature binding problem, the speed of learning, the capacity of the memory, the localisation in time of an event and the problem of spatio-temporal pattern generation."  -- Two scientists in 2022 (link). 
• "The mechanisms governing successful episodic memory formation, consolidation and retrieval remain elusive,"  - Bogdan Draganski, cogntive neuroscientist (link). 
• " The mechanisms underlying the formation and management of the memory traces are still poorly understood." -- Three scientists in 2023 (link). 
• "The underlying electrophysiological processes underlying memory formation and retrieval in humans remains very poorly understood." --  A scientist in 2021 (link). 
• "As for the explicit types of memory, the biological underpinning of this very long-lasting memory storage is not yet understood." -- Neuroscientist Cristina M. Alberini in a year 2025 paper (link). "

The Groundless Myth That "Floods"' or "Surges" Help Explain Near-Death Experiences

 The phenomena of near-death experiences and out-of-body experiences are strong evidence against a cherished claim of neuroscientists, the claim that your brain is the source of your mind. During near-death experiences and out-of-body experiences arising during cardiac arrest when brain activity flatlines, people often report having the most vivid experiences in which they observe their bodies from outside of the bodies. No such thing should ever occur if your brain is the source of your mind.  Under the idea that your brain is the source of your mind, nothing but unconsciousness should result from a state of cardiac arrest in which brain signals flatline.  And if the brain is the source of your mind, no one should ever observe his body from a viewing position meters away from the body, something commonly reported in near-death experiences and out-of-body experiences. 

To try and combat this evidence which so clearly refutes their most cherished dogmas, neuroscientists and materialists have resorted to spreading myths. There is the flood myth and the surge myth. 

The Flood Myth

DMT is some molecule that can produce hallucinations in humans. The main type of flood myth regarding near-death experiences is the utterly fictional claim that there occurs a flood of DMT or some other relevant chemicals when a person is dying. There is no scientific evidence for any such thing occurring in any organism.  It is sometimes claimed that some study showed that a flood of DMT occurs in rats when they die.  The claim has no basis in fact. 

The wikipedia.org article on DMT makes this claim: "A significant increase of DMT levels in the rat visual cortex was observed following induction of experimental cardiac arrest, a finding independent of an intact pineal gland."  The statement is based on a paper that failed to show any robust of such a thing. The paper is the paper "Biosynthesis and Extracellular Concentrations of N,N-dimethyltryptamine (DMT) in Mammalian Brain," which you can read here. Figure 4 of the paper has a graph that claims to show DMT levels in the brain of rats during normal times and during cardiac arrest. We see only negligible levels in both cases. The graph is below:

The nM on the left scale stands for nanomoles. The claimed amount in both cases is the negligible amount of only 1 or 2 nanomoles, something like about 1 billionth of a gram.  The "cardiac arrest" part of the graph is misleading. The measurement was not made during cardiac arrest. This should come as no surprise when you consider that cardiac arrest quickly kills an organism, within a few minutes, unless it is stopped. Within the few minutes of cardiac arrest, there would never be time to reliably make some very delicate measure of  some tiniest trace amount of a few nanomoles. 

A reading of the full caption of the figure above gives us the truth. The claimed measurement of DMT in rats did not actually occur during cardiac arrest, but between 30 minutes and an hour after cardiac arrest.  So the "cardiac arrest" in the graph is misleading. The graph should have been labeled like this. 

Should we have any confidence in the reliability of this claimed measurement, given the failure of the authors to correctly label their graph? There are three reasons we should not:

(1) The failure to correctly label the graph should cause us to doubt the reliability of the investigation. 

(2) The reported levels are so very low that they almost certainly fall within the measurement uncertainty of whatever measurement technique was used. We cannot even have confidence that there is any DMT at all in any of these rats. 

(3) The authors fail to mention any use of a blinding protocol, and their paper fails to use the word "blind" or "blinding." The very tiny difference reported is so small it can easily be explained by merely assuming that when the investigators studied the dead rats, they were more prone to report finding DMT, because of their desire to show some effect of DMT increasing when a rat dies. 

In short, we have no robust evidence here of anything that can reasonably be called a surge or a flood or even a significant increase in DMT levels in dying rats. No reliable evidence has been provided that DMT levels increase in rats when they undergo cardiac arrest. Claims of a flood of DMT in rats undergoing cardiac arrest are lies.  

The question of DMT in the brain was clarified by David E. Nichols in a paper he authored in the Journal of Psychopharmocology. Speaking of DMT (also known as N,N-dimethyltryptamine) in the paper Nichols says, “It is clear that very minute concentrations of N,N-dimethyltryptamine have been detected in the brain, but they are not sufficient to produce psychoactive effects.” Addressing speculations that DMT is produced by the tiny pea-sized pineal gland in the brain, Nichols points out that the main purpose of the pineal gland is to produce melatonin, but the pineal gland only produces 30 micrograms of melatonin per day. But the pineal gland would need to produce about 20 milligrams of DMT (about 660 times more than 30 micrograms) to produce a mystical or hallucinatory experience. “The rational scientist will recognize that it is simply impossible for the pineal gland to accomplish such a heroic biochemical feat,” says Nichols. In the article in which he states that, it is noted that “DMT is rapidly broken down by monoamine oxidase (MAO) and there is no evidence that the drug can naturally accumulate within the brain.” Strassman attempted to detect DMT in the brains of 10 human corpses, but was not able to find any.

Given these facts, it is quite absurd to suggest that near-death experiences are being produced by DMT in the brain. Judging from the amount of DMT in rat brains, we have about 100,000 times too little DMT in our bodies for DMT-produced experiences to appear. Web pages speculating that near-death experiences may be produced by DMT will typically tell us that DMT has been detected in rat brains, failing to tell us how much DMT was detected (merely trace levels 100,000 times too small to produce any remarkable mental experiences).

The latest news story to repeat the false claim about a flood of brain chemicals at the time of death is a very recent BBC Science Focus article "What Is It Like to Die? The Reassuring Science of Near-Death Experiences." After a bogus section header of "A Huge Release of Chemicals," the BBC article claims this:

"For instance, Borjigin's team have previously studied rats in a state of asphyxia (a lack of oxygen in the brain – comparable to when a human has a heart attack) and found that this triggered a sudden release of brain chemicals, including adenosine, dopamine, norepinephrine, gamma-aminobutyric acid, glutamate and aspartate. Serotonin also surged to 20 times its normal levels within just two minutes of asphyxiation. Given the key roles these chemicals play in emotions and dream-like states, scientists suggest that this swell in neurotransmitters may contribute to the intense subjective experiences reported by people who undergo NDEs."

The paper the article referred to is the 2015 Borjigin paper Borjigin "Asphyxia-activated corticocardiac signaling accelerates onset of cardiac arrest," which is a low-quality study. The main reason that the study is not reliable experimental science is that it uses a way-too-small study group size of only 7 rodents. To be robust evidence, experimental studies attempting to show the effects of interventions in rodents require a sample size of at least 15 or 20 rodents per study group, and almost always a much larger number of rodents. When such experimental studies use only much smaller study group sizes such as 7 rodents per study group, they in general deserve only scorn, particularly when they are guilty of two failures this paper was guilty of: a failure to follow a blinding protocol, and a failure to report a sample size calculation (which typically occurs when experimenters know the study group sizes are way too small). 

Another reason why this paper is not reliable evidence for any surge of chemicals in dying rodents is that it was attempting to do something that could not reliably be done in 2015: to track changes in levels of brain chemicals existing in only the tiniest trace amounts, over a time period of a few minutes. There did not exist in 2015 any technology capable of reliably tracking such chemicals over so short a time span. The relevant graph in the paper is Figure 4. There we see a graph purporting to track some brain chemicals existing at levels of only about 20 nanomoles. That's an incredibly tiny amount. In 2015 there did not exist any technology capable of reliably tracking changes in brain chemicals existing in such tiny amounts, over the span of a few minutes.  The authors state, "To probe the neurochemical basis of the heightened cortical activities, we performed minute-by-minute microdialysis in the frontal and occipital lobes of unanesthetized rats (n = 7) before and during asphyxiation and analyzed cortical dialysates using liquid chromatography-mass spectrometry (LC-MS)." In 2015 that was not a reliable technology for tracking changes in minute traces of neurotransmitters in rodents over a period of a few minutes, particularly when using a way-too-small study group size such as only 7 rodents.  For more on the unreliability of such claimed measurements, see the appendix of this post. None of the supposedly increasing chemicals listed in this 2015 paper are hallucinogens, so it makes no sense for the BBC Science Focus article to be claiming they have relevance to explaining near-death experiences. 

The recent BBC article is guilty of a particularly misleading claim by using the header "A Huge Release of Chemicals." The actual release of chemicals reported in the low-quality paper it cites is a level of something like 20 nanomoles, only the tiniest trace amount, something like 20 parts per billion. Calling that a "huge release of chemicals" is like calling a millionth of a raindrop a rain storm.  

The Surge Myth

What we can call the surge myth is the utterly fictional claim that there is a surge of some type of brain activity when a person undergoes cardiac arrest. The claim is the exact opposite of the truth. 

The claim seems to have got started after the publication of a 2013 paper with the misleading title "Surge of neurophysiological coherence and connectivity in the dying brain." The paper was based on EEG readings of dying rats. An EEG is a device for measuring brain waves, one requiring the attachment of multiple electrodes on the head.  

95% of the people reading a title of "Surge of neurophysiological coherence and connectivity in the dying brain" will think that some indication was found of increased cognitive activity in dying brains. The paper found no such thing.  The "coherence" and "connectivity" supposedly found was not a surge but merely a momentary blip, and it did not involve anything like some surge of mental activity. Nothing whatsoever was found that can help to give a neural explanation for near-death experiences. In fact, there is every reason to think that at the time when this little blip of claimed "coherence" and "connectivity" occurred, all of the rats were unconscious. 

Figure 1 of the paper is shown below. We see EEG brain wave signals from rats who were injected with a chemical causing the heart to stop. 

Nothing impressive is seen. It's just what you would expect: brain signals trailing off and dying out very quickly after the heart stops. This data offers no justification for a title of "Surge of neurophysiological coherence and connectivity in the dying brain." An honest title of the paper would have been:  "Brain waves very quickly trail off and die out after hearts stop in rats." 

After this paper with a very misleading title was published, we had innumerable misleading citations of it in the articles of materialist or mainstream writers, claiming or insinuating that the paper showed or suggested something it did not either show or suggest. An example was a National Geographic article with the misleading title "In Dying Brains, Signs of Heightened Consciousness." The 2013 "Surge of neurophysiological coherence and connectivity in the dying brain" paper had not anything whatsoever to show "signs of heightened consciousness" in the dying rats it studied. Similarly, a 2017 Big Think article linked to the 2013 paper and claimed, "One 2013 study, which examined electrical signals inside the heads of rats, found that the rodents entered a hyper-alert state just before death." This claim is totally false, and the paper suggested nothing of the sort.  

A 2023 paper discussed brain readings of coma patients in Michigan, USA who had their life-support systems turned off. Like the rat death paper described above, the paper had a misleading use of the word "surge." I previously described this paper like this:

• "Surge of neurophysiological coupling and connectivity of gamma oscillations in the dying human brain." Here we have another misleading use of the word "surge" in a science paper headline, a paper co-authored by one of the researchers who authored the equally mistitled rat study "Surge of neurophysiological coherence and connectivity in the dying brain."  The paper merely describes a little brain activity in two people after a respirator was turned off, with no evidence of brain activity continuing for more than a few seconds after the heart has stopped. The lines on brain waves charts go up and down, and there are seven or so channels of brain waves (including a gamma channel); so at any second you can usually find some little line going up and call that a "surge," although at the same time other lines (representing other brain wave channels) will probably be going down. Using the term "surge" in the title of the paper was misleading, rather like  tracking the price of Microsoft, seeing it go up 2% at 2:00, and calling that a surge. The authors of the study did not even report a surge in gamma waves, one of the brain wave channels. Eager to get something they could call a surge, the authors got their little "surge" after some statistical fiddling with the signals, to get some statistical measure that only shows up after arbitrary analytics. Almost any random ten seconds of brain wave activity can be statistically analyzed to show a little "surge" somewhere, if you're willing to dredge up secondary statistical measures. Keep torturing the data, and it will confess as you wish.  Shamefully, the journal Science has an article on this paper with the misleading headline "Burst of brain activity during dying could explain life passing before your eyes"; and the Smithsonian site has an equally misleading click-bait headline of "Surging Brain Activity in Dying People May Be a Sign of Near-Death Experiences." There is no evidence that either of these two people had an experience of "life passing before their eyes" or anything like near-death experiences. The subjects were unconscious when the respirator was turned off, and there is no evidence of any consciousness. Unconscious people have gamma wave activity (the activity reported), and you have plenty of gamma activity while you are sleeping. No "neural correlates of the NDE" were reported by the paper. As two MDs point out in a commentary on this paper, "The researchers reported no evidence whatsoever that these brain activities were correlated with conscious experiences in those two patients—and no reason to compare these results with prospective NDE studies in patients who have survived a cardiac arrest."

Innumerable false claims have appeared in the press based on these papers which made misleading uses of the word "surge" in their titles. What we have is a "give them an inch, and they'll take a mile" situation. Materialists are very eager consumers for any tiny scrap that may sound like something offering the faintest hope of some neural explanation for near-death experiences. So when a neuroscientist incorrectly uses the term "surge" in describing momentary blips that are not actual surges, then there may occur a "give them an inch, and they'll take a mile" effect, and before long the press may be talking all over the place about a surge of brain activity in dying patients. Such claims are lies. What actually happens to brains when cardiac arrest occurs is the exact opposite of a surge in brain activity. 

The latest news story to repeat the false claim about a surge in brain activity at the time of death is a very recent BBC Science Focus article  "What Is It Like to Die? The Reassuring Science of Near-Death Experiences." The article makes this false claim:  "Led by Dr. Jimo Borjigin, the team made the remarkable observation that two of the patients observed a surge of brain activity after their relatives had agreed to the removal of life support."  The untrue claim is similar to equally bogus claims made by the British newspaper The Guardian. For a very detailed discussion of the untrue claims that this newspaper  made on this topic and about these two patients who had no such surges of brain activity, read my widely read post here. I was invited by someone at a science journal to turn that post into a scientific paper, but I declined because I prefer to keep my writings entirely on my blog sites so that everyone can read them for free, without encountering any paywall or advertisements. There was no such surge of brain activity in any such patients studied by the paper mentioned.  

The term "isoelectric" or iso-electric in reference to brain waves means a flat-lining equivalent to no electrical activity in the brain, as measured by EEG readings. The paper here states, "Within 10 to 40 seconds after circulatory arrest the EEG becomes iso-electric." Figure 1 of the paper here says that such an isoelectric flat-lining occurred within 26 seconds after the start of ventricular fibrillation, the "V-fib" that is a common cause of sudden cardiac death, with "cortical activity absent." Also referring to a flat-lining of brain waves meaning a stopping of brain electrical activity, another scientific paper says, "several studies have shown that EEG becomes isoelectric within 15 s [seconds] after ischemia [heart stopping] without a significant decrease in ATP level (Naritomi et al., 1988; Alger et al., 1989)."  Another paper tells us this about brain waves and infarction (obstruction of blood flow), using CBF to mean cerebral blood flow, and the phrase "the EEG becomes isoelectric" to mean a flat-lining of brain electrical signals:

"When normal CBF declines, the EEG first loses the higher frequencies (alpha and beta bands), while the lower frequencies (delta and theta bands) gradually increase. When the CBF decreases further towards an infarction threshold, the EEG becomes isoelectric." 

Similarly, another paper refers to blood pressure, and tells us, "When flow is below 20 mL/100 g/min (60% below normal), EEG becomes isoelectric." meaning that brain electrical activity flat-lines. The 85-page "Cerebral Protection" document here states, "During cardiac arrest, the EEG becomes isoelectric within 20-30 sec and this persists for several minutes after resuscitation." Another scientific paper states this: 

"Of importance, during cardiac arrest, chest compliance is not confounded by muscle activity. The EEG becomes isoelectric within 15 to 20 seconds, and the patient becomes flaccid (Clark, 1992; Bang, 2003)."

You can find quite a few additional papers asserting that brains flat-line very quickly after cardiac arrest by doing Google or Google Scholar searches for the phrase "EEG becomes isoelectric" or "EEG becomes iso-electric." 

A recent scientific paper referring to EEG readings of brain waves states this: 

"The trajectory of EEG activity following cardiac arrest is both well defined and simple. It consists of an almost immediate decline in EEG power, which culminates in a state of isoelectricity [flatlining] within 20 s [seconds]." 

The paper refers to three studies "where gamma oscillations are essentially or mostly artifactual and non-functional biorhythms masquerading as authentic EEG signals," noting how such oscillations can be produced by muscle movements. The paper concludes by saying this about the blips reported in the papers with "surge" in their titles: "Regardless of what the electrogenesis of the gamma spikes ultimately turns out to be, it is highly unlikely that they could be responsible for generating an NDE [near-death experience]."

A recent new study I discuss here gives us additional evidence that at death brain waves flatline, the exact opposite of undergoing some surge in activity. 

We have seen above how mainstream news sources tend to be utterly unreliable in their coverage of neuroscience attempts to explain near-death experiences. The same BBC Science Focus site that misinformed us so badly on this topic (as described above) is a site that has recently been guilty of very bogus science-related headlines, as I document in my post here. 

Appendix: The 2015 paper mentioned above entitled "Asphyxia-activated corticocardiac signaling accelerates onset of cardiac arrest" claimed to use a technology called liquid chromatography-mass spectrometry (LC-MS). In 2015 there did not exist any technology for reliably tracking changes over a few minutes in neurotransmitters such as serotonin existing in only the tiniest trace amounts such as a  few nanomoles.  The pitfalls of this LC-MS technology are discussed in the 2012 paper here ("Pitfalls Associated with the Use of Liquid Chromatography–Tandem Mass Spectrometry in the Clinical Laboratory"), which states this:

"However, application of this technology is not automatically or necessarily translated into accurate results. Its pitfalls have to be recognized and must be addressed systematically. In particular interferences from in-source transformation of metabolites, differential matrix effects of analyte and internal standard and isobaric transitions can lead to inaccurate results of LC-MS/MS analyses."

Mass spectrometry does not measure the levels of neurotransmitters in a sample. As a wikipedia.org article tells us, "Mass spectrometry (MS) is an analytical technique that measures the mass-to-charge ratio (m/z) of charged particles (ions)." Attempting to deduce changes in the level of a particular neurotransmitter chemical (over a time span of a few minutes) from mass spectrometry readings would involve guesswork and some complex and largely arbitrary analysis pathway that would be very hard to get right. 

To get an analogy what it is like for some scientists trying to find traces of neurotransmitters by analyzing mass spectroscopy data from the brain of a rodent, consider the visual below:

This text consists of many different sentences, overlaid on top of each other. Imagine trying to extract a particular word from such a mess. That's pretty much impossible. It's a similar deal for a scientist analyzing mass spectroscopy data derived from the tiny brain of a rodent, because what such a person gets is signals from many different elements and compounds and chemicals, arriving all at once. Unless you are very lucky, there is almost no way to reliably extract which part is a signal from which chemical, compound or element. But with a mess like a neuroscientist gets in such a situation (or a mess like the one shown above), there are unlimited opportunities to see what you are fervently hoping to see. All that can be truthfully said about such a mess is something like this: "The data is too noisy for me to say much of anything reliable about it." 

We have seen the pitfalls of mass spectrometry analysis claiming tiniest trace amounts in the recent K2-18b affair, in which overeager scientists claimed to have found something called dimethyl sulfide in the tiniest trace amounts in a planet in another solar system. As discussed here, the claims were soon discredited by other scientists who basically said: no, your data did not show any such thing.

The LC-MS/MS technology was not designed for analyzing real-time changes over a short time span such as a few minutes. It was instead designed for a more leisurely type of analysis such as determining what is in a static sample of something.  Any claims of using such a technology in 2015 for real-time analysis of very short term in vivo changes in blood levels of neurotransmitters (over a time span of a few minutes) should be regarded with the great suspicion. To have any confidence in such claims, you would need to have best practices such as sufficient study group sizes and the use of a blinding protocol. Neither occurred in the 2015 paper "Asphyxia-activated corticocardiac signaling accelerates onset of cardiac arrest." The paper makes no mention of using any blinding protocol. 

We can make a good guess about what probably went on. One or more analysts motivated to report some increase in neurotransmitters in dying rodents analyzed some mass spectroscopy data that could be analyzed in a 1001 conflicting ways, and then claimed to see the desired result. Such an event has little value as evidence. There might have some good evidence of neurotransmitter levels if you had used a much larger number of rodents, and given the mass spectroscopy data to some independent analyst, asking him, "Tell me if you can find any reliable evidence of any chemicals, and how much of such things you see." 

It takes the human body hours or days to produce the most minute generation of the tiniest amounts of chemicals such as melatonin and serotonin. The human body produces about 30 micrograms (millionth of a gram) of melatonin daily. Rates of serotonin production in the brain are estimated at about 70 picomoles per gram per minute, which is some extremely minute amount like .000000000070 of a gram. There is no credible mechanism by which an organism could produce any strong increase in very-hard-to-produce neurotransmitters such as serotonin over the course of only a few minutes, as something like a response to death or a loss of oxygen or a stopping of a heart. If readings were to show a difference of, say, 300% over such a short interval of a few minutes, by far the best explanation would be the uncertainty and error levels and subjectivity of the claimed readings, rather than any actual increase over so short a time, which would not be time for any substantial increase. When you are attempting to measure in a tight time frame the levels of chemicals existing in only the tiniest trace amounts, the uncertainty from one attempted reading to another can easily be something like 1000%. 

A 2022 article mentions some new technology for measuring in real time changes in neurotransmitters such as serotonin. The article speaks just as if no such technology existed prior to 2022, which should make us further doubt year 2015 claims about neurotransmitter changes occurring at the minutes around death. It states this:

"Now, for the first time, UCLA scientists have attached nanoscale biochemical sensors, which are tuned to identify specific neurotransmitters, to a soft, implantable brain probe in order to continuously monitor these chemicals in real time. The new brain probe, described in a paper published in ACS Sensors, would allow scientists to track neurotransmitters in laboratory animals — and, ultimately, humans — during their day-to-day activities. 

The ability to continuously measure neurotransmitters in high resolution over long periods would provide a more accurate understanding of how serotonin, dopamine and other neurotransmitters affect psychological states, potentially leading to more effective treatments for depression and other mental health disorders, said the paper’s corresponding author, Anne Andrews, a UCLA professor of psychiatry and biobehavioral sciences and of chemistry and biochemistry."

A 2025 paper highlighting the unreliability of serotonin measurements is entitled "The Continued Mismeasurement of Plasma Serotonin: A Systematic Review." It states this:

" The review covered the period from 2010 to July 2024 and is a follow-up of a similar review published in 2011 which found that nearly all published reports of PPP 5-HT [serotonin] were clearly and markedly erroneously high. This problem has persisted unabated with nearly all retrieved 47 reports from the past 14 years also apparently being erroneously high." 

It seems rather clear that the  2015 paper mentioned above (entitled "Asphyxia-activated corticocardiac signaling accelerates onset of cardiac arrest") did not actually provide any robust evidence of a surge or even a substantial increase of cognition-relevant chemicals in the brains of dying rodents. The Figure 4 of the paper purporting to show an increase in certain neurotransmitters in dying rats is a figure reporting two statistical significances, both of only "p < .05," which is very unimpressive. It is widely regarded in experimental science that evidence listed as "p < .05" is mere borderline evidence, and when papers present such a "p < .05" other researchers may scorn it and use the derisive term "p-hacking" to describe it. Look at the error bars in the graph (indications of uncertainty in measurement) -- they are very large, and probably underestimate the uncertainty.  Even if there had been some big increase in the chemicals listed in the Figure 4 of the paper, it would do nothing to explain near-death experiences, because none of the chemicals mentioned are hallucinogens. A serotonin surge might explain a little perk in your mood, but could never explain you reporting seeing yourself out of your body, or visiting some realm of the dead or having mystical experiences. Also, Figure 5 of the paper contradicts claims of brain waves persisting after heart rate stops. In Figure 5A we see the brain waves of the rats completely flatlining by the time the red EKG reading shows a cessation of heart rate. 

The fact that the BBC Science Focus article has referred us to a 2015 paper rather than a more recent paper hints that the claimed  result of an increase in brain chemicals of dying rats has not been replicated by any high-quality paper.