Translate Interface Bug Corrected

 I was sad to discover that with the Blogger settings I had been using, it was not even possible for the users of some languages to switch to their preferred language. The problem has been fixed, and using the Translate button at the top right, you should be able to translate this blog to any desired language. 

Hyperpolyglots Intensify the Explanatory Shortfalls of "Brains Make Minds" Claims

 99% of all adult males have brains about the same size, and 99% of all adult females have brains about the same size. The average brain weight of a male is about 1336 grams, and the average brain weight of a female is about 10-15% smaller. Whenever there is a difference of some type of human mental ability that is more than 200%, this is great problem for those claiming that brains make minds -- because such a difference does not correspond to any difference in brain size or brain speed. 

One such difference is a difference in intelligence. A Reader's Digest article describes several people who had an IQ of more than 200, including William Sidis, who enrolled at Harvard at age of 11, and graduated at the age of 16. There is no evidence that having an IQ above 200 is associated with having a much larger brain. 

Then there are differences in creativity. I know of no test giving a numerical score for creativity. But anyone well-educated about the history of music, art and literature will realize that certain humans have had a level of creativity vastly exceeding that of the average man. Examples that come to mind are Shakespeare, Picasso, Mozart, Wagner, Goethe, Edison, Michelangelo, Tolstoy, Tchaikovsky and Beethoven.  None of these figures seems to have had a brain much larger than average. 

Then there are huge differences in episodic memory. Late in the 20th century there came to the attention of psychologists that a certain small number of people have levels of episodic memory dramatically better than the great majority of humans.  People with such a memory are now said to have Highly Superior Autobiographical Memory or HSAM, also called hyperthymesia. People with such an ability can typically remember details of almost every day in their adult lives. A well-studied example is the case of Jill Price. The reality of Highly Superior Autobiographical Memory had actually been documented as early as the late nineteenth century, as I document in my post here on the case of Daniel McCartney. A modern experiment showed those with Highly Superior Autobiographical Memory scoring 25 times higher on a random dates test. 

There are also huge differences in the mental calculation ability of humans. Many prodigies with normal brains (and sometimes damaged brains) have various types of extraordinary calculation ability. A widely documented ability is called calendar calculation, and consists of the ability to very quickly name the day of the week, given any date in a period that might go back 100 years or even longer, perhaps 200 years. Daniel McCartney had such an ability, as did many others, including many with autism. 

There are also huge differences in the ability of humans to recall facts or bodies of text. Many prodigies with normal brains have an ability to recall factual information to a degree many times greater than the average person. My post here documents such an ability in Daniel McCartney.  A more impressive case was that of Kim Peek, who supposedly could recall everything he had read in more than 7000 books. Then there are very many cases of people who have memorized word-for-word hundreds of pages of text, such as the entire Quran. Such people seem to have normal brains, but a memorization ability many times greater than the average person. 

Then we have the cases of what are called hyperpolyglots. These are a small number of people who can fluently speak many different languages, more than 10. An article in the New Yorker describing such people is entitled "The Mystery of People Who Speak Dozens of Languages." We read about Luis Miguel Rojas-Berscia, who can supposedly speak "fluently" 13 languages, while having a "command" of 22 languages:

"He is a hyperpolyglot, with a command of twenty-two living languages (Spanish, Italian, Piedmontese, English, Mandarin, French, Esperanto, Portuguese, Romanian, Quechua, Shawi, Aymara, German, Dutch, Catalan, Russian, Hakka Chinese, Japanese, Korean, Guarani, Farsi, and Serbian), thirteen of which he speaks fluently. He also knows six classical or endangered languages: Latin, Ancient Greek, Biblical Hebrew, Shiwilu, Muniche, and Selk’nam, an indigenous tongue of Tierra del Fuego, which was the subject of his master’s thesis."

We read in the article a reference to Giuseppe Gasparo Mezzofanti (17 September 1774 – 15 March 1849), who was famed for his ability to speak more than 30 different languages.  We read of "Corentin Bourdeau, a young French linguist whose eleven languages include Wolof, Farsi, and Finnish; and Emanuele Marini, a shy Italian in his forties, who runs an export-import business and speaks almost every Slavic and Romance language, plus Arabic, Turkish, and Greek, for a total of nearly thirty."

A scientific paper says this about hyperpolyglots:

"There are many multilingual talented language geniuses in ancient and modern China and abroad (see Erard, 2012; Hyltenstam 2016, 2018, 2021; Adriana & Birdsong, 2019). Some famous examples include Popes John Paul II and Benedict XVI, as well as writers James Joyce, Tolkien, and Anthony Burgess, and also professional linguists such as Rasmus Kristian Rask, who is believed to speak 25 languages and can read in 35 languages. Griffiths & Soruç (2020) noted that Professor Andrew Cohen, an expert on learning strategies in the field of second language acquisition (SLA), is also an authentic hyperpolyglot who is proficient in 13 foreign languages including Chinese through self-study. Cohen has also presented and published related articles at international conferences about his multilingual talents (Cohen & Li, 2013). In addition, there are many polyglots who are diplomats, the most famous being Emil Krebs who mastered 68 languages in speech and writing and studied 120 other languages (Wikipedia)....Tim Keeley from the School of Intercultural Management, Kyushu Sangyo University in Japan is proficient in more than 30 languages, making him a real hyper-polyglot by all measures."

You can make a generalization about most of these cases of extraordinary human mental abilities. The generalization is that there are certain rare humans who have special mental abilities in which the average ability of a human is exceeded by more than ten-fold. Specifically:

• The ability of the best hyperpolyglots to speak languages is not merely twice as good as that of the average person, but more than ten times as good; for instead of being able to speak only 1 language, they can speak more than ten. 
• The ability of the best mental calculation aces to do math calculations or calendar calculations without aid of electronic devices, paper, pencils or blackboards is not merely twice as good as that of the average person, but more than ten times as good. Mental calculation aces such as Jacques Inaudi and Zerah Colburn could outperform average people by a factor of 1000% or more. 
• The ability of the best memorization marvels to memorize large bodes of text is not merely twice as good as that of the average person, but more than ten times as good. 
• The ability of those with Highly Superior Autobiographical Memory to remember events from their past is not merely twice as good as that of the average person, but more than ten times as good. A modern experiment showed those with Highly Superior Autobiographical Memory scoring 25 times higher on a random dates test. 
• The ability of the best ESP test subjects to perform well on tests of telepathy (subjects such as Hubert Pearce and the woman tested in the Riess ESP test) is not merely twice as good as that of the average person, but more than ten times as good. 

None of these realities is expected under the claim that the brain makes the mind. The largest human brains are only slightly larger than average-sized brains. There are no humans with exceptional abilities and brains twice as large or three times as large as average. In fact, in none of the cases discussed above is there any very substantial brain difference that can account for the huge difference in ability. For example, people with Highly Superior Autobiographical Memory do not have much bigger or faster brains; people who can memorize long books do not have bigger brains; hyperpolyglots do not have bigger brains; and mental math marvels do not have larger or faster brains. In fact, in many cases we see brain damage that corresponds to the exceptional ability. For example, Kim Peek was a memory and mental math marvel who could instantly tell the day of week of any day in his life, and who could recall each of 7000 books he had read. But the same man was born without the corpus callosum that connects the two hemispheres of the brain. 

Hopfield Networks Do Nothing to Explain How a Human Could Remember or Recognize Anything

 Humans have astonishing capabilities for recognizing many different types of things: faces, individual words, quotations, places, musical compositions, and so forth. There is no credible neural explanation for how recognition occurs. There is no robust evidence for any neural correlate of recognition. Brains do not look or act any different when you are recognizing something. For example:

• The year 2000 study "Dissociating State and Item Components
  of Recognition Memory Using fMRI" found no difference in brain signals of more than 1 part in 100, with almost all of the charted differences being only about 1 part in 500. 
• The study "Remembrance of Odors Past: Human Olfactory Cortex in Cross-Modal Recognition Memory" found no difference in brain signals of more than 1 part in 200.
• The study "Neural correlates of auditory recognition under full and divided attention in younger and older adults" found no difference in brain signals of more than 1 part in 500.
• The study "Neural Correlates of True Memory, False Memory, and Deception" asked people to make a judgment of whether they recognized words, some of which they had been asked to study. The study found no difference in brain signals of more than about 1 part in 300.
• The study "The Neural Correlates of Recollection: Hippocampal Activation Declines as Episodic Memory Fades" was one in which "participants performed a recognition task at both a short (10-min) and long (1-week) study-test delay." The study found no difference in brain signals of more than about 1 part in 300.
• The study "The neural correlates of everyday recognition memory" found no difference in brain signals of more than about 1 part in 500.
• The study "Neural correlates of audio‐visual object recognition: Effects of implicit spatial congruency" was one in which participants attempted a recognition task. The study found no difference in brain signals of more than about 1 part in 200.

Some have claimed that there is something in the brain called a "fusiform face area" that is more active when you are recognizing faces. Such a claim is not well-founded, for reasons I discuss in my post here. 

But some claim there is some theoretical basis for a little understanding of how a brain could recognize something. For example, the recent paper "Computational models of learning and synaptic plasticity" by neuroscientist Danil Tyulmankov is one of numerous pieces attempting to claim that computer science work provides models shedding insight on how a brain might learn. Such claims are unfounded because of the vast physical differences between what is going on in brains and what goes on inside computers. 

On page 7 of his paper Danil Tyulmankov gives us a typical example of someone trying to trick us into thinking that some computer software technique has some relevance to explaining how a brain could recognize something. Under a heading of "Memory paradigms" and subheadings of "Recall" and "Associative Memory" he states this:

"The colloquial use of 'memory' commonly refers to declarative memory (also called explicit memory) – the storage of facts (semantic memory) or experiences (episodic memory) – which requires intentional conscious recall. One of the most influential models of recall is the associative memory network (Figure 1a), also known as the Hopfield network (Hopfield, 1982). The model’s objective is to store a set of items ... such that when a perturbed version ... of one of the items is presented, the network retrieves the stored item that is most similar to it. For example, given a series of images, as well as a prompt where one of the images is partially obscured, the network would be able to reconstruct the full image. More abstractly, given a series of lived experiences, this may correspond to a verbal prompt to recall a piece of semantic or autobiographical information." 

We have here the typical shenanigans of one of the persons trying to conflate human memory and computer memory, something made rather easy by the fortunate happenstance that the same word ("memory") is used for two completely different things (human memory and computer memory).  Tyulmankov has given us above a paragraph that starts out with a sentence referring to human memory; he then refers to a purely computer software method with no relevance to human memory; and he then ends the paragraph with another sentence referring only to human memory.  It's kind of like someone trying to make you get the impression that the president of the USA is a dog, by having the first sentence of his paragraph referring to dogs, having the second and third sentence of his paragraph referring to the president of the USA, and then having the last sentence of his paragraph again referring to dogs. 

Let me explain some reasons why Hopfield networks do nothing to explain how a human could remember or recognize anything. Hopfield networks are groups of nodes in which each node has a connection to each of the other nodes in the group. The diagram below illustrates a very simple Hopfield network. Each of the circles is called a node. A Hopfield network might have any number of nodes. In the Hopfield network, the different connections between the nodes might have different numerical values called "strengths." 

Now, if you search on the Internet, you can find various examples of 

programming code that uses Hopfield networks to store and retrieve information. Sometimes while giving such examples, it is claimed that the code has some relevance to explaining how a brain could remember something. We are sometimes told that Hopfield networks have some relevance to the brain, because just as individual neurons in the brain can each be connected to many other neurons because of synaptic connections, each node in a Hopfield network is connected to each node in the network. To play up the similarity, the nodes of a Hopfield network are sometimes called "neurons," even though such a term is profoundly misleading, because of reasons I will explain below. 

There are, however, very strong reasons why Hopfield networks have no relevance to explaining how a brain could remember something. They are listed in my visual above. I will explain each. 

Reason #1: Neurons do not have any capacity for storing some learned piece of information such as an image, a number or a word. 

In a Hopfield network particular nodes of the network may store some item of information. But a neuron does not have any capacity that we know of for storing some item of learned information. No one has ever found an item of learned information by examining a neuron. Very much tissue has been extracted from the brains of living people, and no one ever found in a neuron something like the letter "A" or the word "cat" or the number "1776."  No one has ever found even a single number such as 0 or 1 stored within a neuron. 

Neurons also have no ability to function as binary switches similar to the light switches controlling whether a light is on or off.  A neuron fires at a varying rate, with very much variation from one minute to the next. There is nothing in a neuron that flips between a permanent "off" state and a permanent "on" state.  So even attempts to depict individual neurons as storing a value of 0 or 1 are invalid. Neurons are not like binary switches. 

The page here provides code for a Hopfield network, using the term "neuron" to describe the nodes of the network. It states, "Each neuron in the network represents a binary unit that can have a state of either +1 (active) or −1 (inactive)."  That does not correspond to the physical reality of neurons over any long time scale.  Over the course of a few seconds, a neuron can switch between between being active and inactive. But over a time span such as days, neurons do not switch between some active state and an inactive state. All neurons are electrically active over a time span of 24 hours. So it is not accurate to imagine some situation persisting over a long time in which one neuron corresponds to a 0, and another neuron corresponds to a 1. Neurons fire at a rate between 1 time per second and 200 times per second, and such firing rates vary unpredictably. 

So as simple a storage task as the storage of the word "dog" cannot occur through some method like that imagined above.  The word "DOG" corresponds to the ASCII numbers 68, 79 and 71, and those three digits correspond to the binary sequence 10100111111101100011.  But we can imagine no group of about 20 neurons storing the binary sequence 0100111111101100011 over a long period such as months, because there can be no situation in which some neurons are inactive over a period of months (corresponding to 0) while other neurons are active over months (corresponding to 1).  All neurons are continually active, and neurons do not have any switch-like feature that could enable binary information storage. Plus there's the fact that the brain has no such thing as an ASCII chart allowing a conversion between letters of the English alphabet and decimal numbers. 

Reason #2: Unlike Hopfield networks in computer software, the connections between neurons are noisy and unreliable

Some programming code using Hopfield networks will typically rely on a simple retrieval procedure in which information is extracted across the network with 100% reliability. That does not correspond to the situation in the brain. Almost all connections in the brain require signals passing across chemical synapses. But chemical synapses do not reliably transmit signals across synapses. 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." 

What this means is that computer programs using a Hopfield network to retrieve information are not realistically simulating the brain. Were you to modify such programs to realistically simulate the unreliable synaptic transmission in the brain, such programs would no longer be able to achieve their functions of information retrieval or recognition.

Reason #3: A group of neurons is a "fuzzy boundary" thing that does not make a closed network that can be traversed from beginning to end

To understand this reason, let us look at how neurons are arranged in the brain. A typical neuron has very many synapses that connect it to other neurons.  It has been estimated that the brain has about 100 billion neurons, and about 100 trillion synapses. This means the average neuron has about 1000 synapses, each of which is a connection between that neuron and other neurons. All those synapses lock a neuron in place at a particular location, just as the roots of a tree in a dense forest lock that tree into a particular location in the forest.  

The visual below (from the site here) shows some neurons in the brain.  The colors are artificial, supplied to show individual neurons. 

When I search for information on the average distance between neurons, compared to the average size of a neuron, I am told (a) that the average size of the soma at the center of a neuron is about 10-25 micrometers (millions of a meter), and that the average distance between neurons is also about 25 micrometers. So neurons are densely packed in the brain, rather like in the artistic depiction below. 

Now, there is a great problem with any spherical volume of neurons looking like the neurons above.  The problem is that such a volume has no particular spot or neuron that is its beginning, and no particular spot or neuron that is its end. So the volume of neurons cannot be traversed from its beginning to end. For any particular neuron connected to about 1000 other neurons, there is no such thing as a "next neuron" and no such thing as a "previous neuron." 

But a traversal from a beginning to an end is a crucial part of all programming that utilizes Hopfield networks. Traversal from a beginning to an end is crucial to the very idea of a Hopfield network. A Hopfield network does not correspond to a group of neurons, which has a fuzzy boundary and is not like a closed network with a beginning and an end. 

Reason #4: Because of high levels of synaptic remodeling and the short lifetimes of synapse proteins ( < 4 weeks), the strength of connections between neurons rapidly vary randomly.

Hopfield networks include a "weight matrix" that is touted as something similar to the connection between neurons. But in such networks this "weight matrix" is a stable thing. That does not correspond to the connections between neurons, which are ever-varying in a random way. 

Below is a quote from a scientific paper:

"A quantitative value has been attached to the synaptic turnover rate by Stettler et al (2006), who examined the appearance and disappearance of axonal boutons in the intact visual cortex in monkeys.. and found the turnover rate to be 7% per week which would give the average synapse a lifetime of a little over 3 months."

You can read Stettler's paper here. A 2019 paper documents a 16-day examination of synapses, finding "the dataset contained n = 320 stable synapses, n = 163 eliminated synapses and n = 134 formed synapses."  That's about a 33% disappearance rate over a course of 16 days, suggesting an average synapse lifetime of less than three months.

You can google for “synaptic turnover rate” for more information. Synapses typically protrude out of bump-like structures on dendrites called dendritic spines. But those spines have lifetimes of less than 2 years.  Dendritic spines last no more than about a month in the hippocampus, and less than two years in the cortex. This study found that dendritic spines in the hippocampus last for only about 30 days. This study found that dendritic spines in the hippocampus have a turnover of about 40% each 4 days. This 2002 study found that a subgroup of dendritic spines in the cortex of mice brains (the more long-lasting subgroup) have a half-life of only 120 days. A paper on dendritic spines in the neocortex says, "Spines that appear and persist are rare." While a 2009 paper tried to insinuate a link between dendritic spines and memory, its data showed how unstable dendritic spines are.  Speaking of dendritic spines in the cortex, the paper found that "most daily formed spines have an average lifetime of ~1.5 days and a small fraction have an average lifetime of ~1–2 months," and told us that the fraction of dendritic spines lasting for more than a year was less than 1 percent. A 2018 paper has a graph showing a 5-day "survival fraction" of only about 30% for dendritic spines in the cortex.  A 2014 paper found that only 3% of new spines in the cortex persist for more than 22 days. Speaking of dendritic spines, a 2007 paper says, "Most spines that appear in adult animals are transient, and the addition of stable spines and synapses is rare." A 2016 paper found a dendritic spine turnover rate in the neocortex of 4% every 2 days. A 2018 paper found only about 30% of new and existing dendritic spines in the cortex remaining after 16 days (Figure 4 in the paper). 

Furthermore, it is known that the proteins existing between the two knobs of the synapse (the very proteins involved in synapse strengthening) are very short-lived, having average lifetimes of no more than a few days. A graduate student studying memory states it like this:

"It’s long been thought that memories are maintained by the strengthening of synapses, but we know that the proteins involved in that strengthening are very unstable. They turn over on the scale of hours to, at most, a few days."

A scientific paper states the same thing:

Experience-dependent behavioral memories can last a lifetime, whereas even a long-lived protein or mRNA molecule has a half-life of around 24 hrs. Thus, the constituent molecules that subserve the maintenance of a memory will have completely turned over, i.e. have been broken down and resynthesized, over the course of about 1 week.

The paper cited above also states this (page 6):

"The mutually opposing effects of LTP and LTD further add to the eventual disappearance of the memory maintained in the form of synaptic strengths. Successive events of LTP and LTD, occurring in diverse and unrelated contexts, counteract and overwrite each other and will, as time goes by, tend to obliterate old patterns of synaptic weights, covering them with layers of new ones. Once again, we are led to the conclusion that the pattern of synaptic strengths cannot be relied upon to preserve, for instance, childhood memories."

A paper on the lifetime of synapse proteins is the June 2018 paper “Local and global influences on protein turnover in neurons and glia.” The paper starts out by noting that one earlier 2010 study found that the average half-life of brain proteins was about 9 days, and that a 2013 study found that the average half-life of brain proteins was about 5 days. The study then notes in Figure 3 that the average half-life of a synapse protein is only about 5 days, and that all of the main types of brain proteins (such as nucleus, mitochondrion, etc.) have half-lives of 15 days or less.  The 2018 study here precisely measured the lifetimes of more than 3000 brain proteins from all over the brain, and found not a single one with a lifetime of more than 75 days (figure 2 shows the average protein lifetime was only 11 days). 

The paper here states, "Experiments indicate in absence of activity average life times ranging from minutes for immature synapses to two months for mature ones with large weights."

When you think about synapses, visualize the edge of a seashore. Just as writing in the sand is a completely unstable way to store information, long-term information cannot be held in synapses. The proteins that make up the synapses are turning over very rapidly (lasting no longer than a few weeks), and the entire synapse is replaced every few months or every several months.  Conversely, humans can reliably remember things they learned or experienced 50 or 60 years ago; and humans can recognize songs, faces, names and quotes that they have not been exposed to in 50 years. For example, lying in bed the other day, there strangely popped into my mind the name "Tobie Tyler." I recognized the name as that of a circus movie involving a boy, one I had not seen or heard mentioned in well over half a century. A Google search confirmed this (I saw the movie around 1960).

Reason #5: There is no ability in the brain to read the strength of the synaptic connections between neurons. 

In a Hopfield network as implemented in computer software code, there is an ability to read the strength of all of the connections between nodes. But the brain has no corresponding ability. The brain has nothing like a synapse strength reader. 

Computer programmers take for granted certain conveniences. Every programmer knows that if he has a data structure named DS, he can run a loop something like the code below, to sum up  the numbers stored in each part of such a data structure:

int nTotal = 0;

int i =0;

for (i = 0; i < DS.length; i++)

    nTotal = nTotal + DS[i];

But while this type of thing is a basic convenience available in the world of programming, it does not correspond to anything possible in the brain. Physically, brains have no way to run loops performing some mathematical or summation operation on each neuron or synapse in a set of neurons or synapses.  A brain cannot sum up the strengths of a set of synapses, nor can a brain even read the exact strength of some particular synapse. Similarly, your muscular system has muscles of various strengths; but there is in your body no such thing as a muscle strength reader; and there never occurs in your body anything like a loop that sums up all the strengths of the muscles in some part of your body. 

In short, while having a small amount of superficial resemblance to the arrangement of neurons and synapses, Hopfield networks and the programing code that use them do not realistically simulate the realities of neurons and synapses.  The ability of Hopfield networks to do certain tasks does nothing to show that the brain is capable of doing such tasks. 

Below is a revealing confession by a neuroscientist named Slotine: "While neuroscience initially inspired key ideas in AI, the last 50 years of neuroscience research have had little influence on the field, and many modern AI algorithms have drifted away from neural analogies." 

NSF Funding Search Suggests Neuroscientists May Scarcely Believe in Engrams

 How can you determine how seriously scientists believe in something? There are several ways. One way is to look for how much a particular thing is mentioned in articles and papers written by scientists. But that method may not be very reliable, because of sociological effects involving conformity. Within some scientific community, it may become a speech custom to assert the existence of something, even though scientists may not believe very strongly in such a thing. 

Another way to try to judge how seriously scientists believe in something is to look for opinion polls taken of scientists.  But scientists are very bad about reliably polling themselves about what they think. Opinion polls of what scientists believe are not very often done. When such polls are done, they are usually done poorly. Often the polls will be biased polls that do not offer a fair selection of choices, but offer a choice between some "orthodox" position and a negatively worded "straw man" version of an alternative position. For example, a scientist polled about evolution may be given a choice between believing in the least objectionable statement of evolution ("change over time") versus the least defensible contrarian position. So, for example, the question may ask:

Which do you believe

(A) That mankind evolved over time, or 

(B) That mankind was created about 6000 years ago as described in the Bible?

A more fair way to ask such a question would be to pose the question like this:

Please choose one of these answers:

(1) The human species arose by unguided natural processes.

(2) The human species arose because some higher power wanted humanity to exist. 

(3) I don't know how the human species originated. 

Another problem with polls of scientists is that they are rarely secret ballot polls.  If a poll is not a secret ballot poll, a scientist may be unlikely to answer it in any way that he thinks is against the majority opinion of scientists, for fear that he may "get into trouble" by answering in such a way. 

Then there is an entirely different way to judge what scientists believe and how strongly they believe in it. That way is to search for what is being funded. Scientists largely control their own funding. Federal agencies such as the National Science Foundation are given budgets, and committees of scientists decide whether particular requests for research funding are approved. If scientists believe strongly in some thing that can be scientifically investigated, they will tend to approve funding to either prove or further investigate that thing. As a general rule, the more funding they approve, the more strongly they believe in such a thing. 

The web page here allows you to search grants that have been approved by the National Science Foundation:

If you type in "cancer" as the search string, and press the Search button, you will get about 740 results.  By multiplying the part of the page showing results per page by the part of the page showing how many pages of results were returned, you can figure out the total number of results. For example, in the search result below, we have 30 results per page, and 25 pages of results. So apparently there are about 750 National Science Foundation projects that have some involvement with cancer:

Now, let's try a different search. We will look for funded research projects relating to dark matter, a hypothetical type of matter that has never been directly observed. Below is what the search term "dark matter" produces:

We get 59 pages of results, with about 30 results per page. The listed number of results is 1769. So apparently the National Science Foundation is funding about 1770 projects involving dark matter. I could write a separate post complaining about all of the money that is being wasted on such a search. But here I use this example simply to show that even when something has never been directly observed, scientists can believe in it very strongly. It seems from these results that many scientists really do believe strongly in the existence of dark matter. 

Now, let's try a different search. We will look for funded research projects trying to look for proof or evidence that memories are stored in the human brain. The term scientists use to mean a hypothetical spot in the brain where a memory is stored (or some set of brain components believed to be storing a memory) is the term "engram." When that term is used in the NSF grant search tool, we get the result shown below. 

There are only 11 results returned by the query, and they are all shown above. Unlike the query about research projects involving dark matter, which produced 59 pages of result, the query about research projects involving engrams produces only a single page of results, consisting of the 11 rows shown above. 

Four of these projects are not actually neuroscience projects, but instead computer science projects. Four of the rows refer to different project grants for a project called "Understanding memory in neuronal networks through a brain-inspired spin-based artificial intelligence." One of the projects ("Ice Regime Shifts of Arctic Lakes Drive Interactions and Feedbacks with Permafrost and Climate") only appears in the search results because it mentions someone with a last name of "Engram." So in terms of neuroscience projects involving the brain and attempts to find evidence for engrams, there are only six  funded projects. 

This is a very low level of funding for the concept of engrams. We may reasonably suspect from such results that perhaps neuroscientists do not even strongly believe in the idea of engrams. Maybe when neuroscientists refer to engrams or claim that memories are stored in brains, they are mainly "paying lip service" to some old idea they do not very strongly believe in. Or maybe neuroscientists have very little confidence in the idea that there can ever occur any discovery of memories stored in brains.

Let's look at the six neuroscience projects that came up in this query. 

• Project #2422939: Building a Conceptual Ecology of the Engram. This is a project allocated $208,090. The abstract of the project is laughable, because there are question marks spread all over it, in appropriate places, as if the writer was ridiculously careless. For example, we read this: "Finding the engram ? the neural mechanism of memory retention ? has been a guiding project for neuroscience since its earliest days. But while it has long been assumed that there was an engram, only recently with the development of new tools and technologies have specific engrams been identified and activated." That is not at all correct -- there is no robust evidence that engrams have been identified or activated. The project calls itself a "project in the philosophy of neuroscience." We can classify this as some kind of philosophy project rather than a real neuroscience research project. 
• Project # 2337788: A Molecular Pursuit for the Engram: Microfluidic temporal transcriptomics for single cell learning  This is a project allocated $300,000. This project is a real neuroscience project, one that is trying to prove a hypothesis that has little support among neuroscientists -- the hypothesis that "RNA encodes memory and learning in single cells." The abstract claims that "studies have shown that RNA holds information that can transfer memories between organisms in multicellular species like C. elegans, Aplysia, flatworms, rats, and fish, challenging a purely synaptic view." We have no mention of specific scientific papers, and the claim is not well-established. It sounds like this project is not one that will involve human memory, and that the scientists will try to show some type of information transfer in animals, something that the scientists might describe as "memory transfer." The project was started in November, 2023, and it has an end date of October 31, 2025. A search for the recent papers of the principal investigator (Saad Bhamla) seems to show no hopeful signs that this project is producing important results. 
• Project 2143910:  Reward Learning Shapes the Fear Circuit. This is a project awarded about $504,000, with a "total intended award amount" of $1,250,939. The project started in 2022, and has an "estimated completion date" of mid-2024. The abstract starts out by claiming "neuroscience research tends to conceptualize particular brain regions as specialized to encode particular types of memories," but the truth is that neuroscientists lack any understanding of how any part of the brain could encode a memory. The project seemed to be something about challenging existing guesses about which part of the brain encodes a particular memory.  The project seems to be finished, and failed to show any evidence for engrams. Unlike the next project mentioned below, the page for this project lists no publications that resulted from the project. 
• Project 1845355: Opposing roles of cortical input to dorsal striatum.  We have a project awarded $900,000, spread over 2019 to 2023. The project specification makes no mention of the word "engram." The only reason this project has shown up in the search results is that it is supposedly related to a paper "FosGFP expression does not capture a sensory learning-related engram in superficial layers of mouse barrel cortex." which apparently reports a failure to find an engram. 
• Project 1743392: Dendritic spine mechano-biology and the process of memory formation. This project was awarded nearly a million dollars. It started in 2017 and ended in 2023. We read, "This research project quantitatively characterizes the relevant molecular processes involved in the dynamical 'tectonic' reorganization inside a dendritic spine involved in forming memories." There is no actual evidence that dendritic spines have anything to do with memory. Tiny bumps on dendrites, dendritic spines look nothing something that could store information. Also, dendritic spines are too unstable and short-lived to be a storage place for memories that can last for decades. We have a list of papers that resulted from the project. None of them sound like anything having much relevance to the topic of engrams or memory storage, except for the paper "Exploring the F-actin/CPEB3 interaction and its possible role in the molecular mechanism of long-term memory,"  which you can read here. Early on that paper states, "The growth and stabilization of dendritic spines is thought to be essential for maintaining long-term memory."  No, the tiny stubs that are dendritic spines bear no resemblance to an information storage device, and dendritic spines are too short-lived and unstable to be something that can explain memories that can last for decades. The paper gives us no observations supporting the claim that dendritic spines have anything to do with memory. Instead it merely provides a " computational structural model of the F-actin/CPEB3-ABD complex." The million dollars spent on this project did nothing to show any neural basis for memory, and did nothing to establish the existence of engrams in the brain. 
• "Project 8809208: Functional Dissociation Within the Hippocampal Formation: Learning and Memory."  This is a project completed in 1992. It was granted $163,070. We have no mention of any publications that resulted from the research. 

There is one other NSF-funded project I am aware of that is related to a search for engrams.  $600,000 has been allocated for the project described on this page:

https://www.nsf.gov/awardsearch/showAward?AWD_ID=2050850&HistoricalAwards=false

The project (NSF award # 2050850) is one entitled "Elucidation of RNA-Based Mechanisms of Long-Term Memory Storage." The idea of an RNA-based mechanism of long-term memory storage is an absurd one. RNA is a short-lived molecule. Referring to David Glanzman, the project incorrectly states, " the principal investigator has discovered that long-term memory (LTM) in the marine snail Aplysia appears to be stored in neurons by nuclear changes." No such thing has been discovered by Glanzman or anyone else. Glanzman's paper here received lots of press incorrectly talking about a "memory transfer" between marine snails.  The paper provided no robust evidence for any such thing, and involved study group sizes of only 7, way too small for a reliable result. A search for David Glanzman's recent papers on Google scholar shows that the NSF award # 2050850 has failed to produce any interesting papers backing up claims of RNA-based mechanisms of long-term memory storage. 

Then there is NIH Project # 1DP2MH129985-01 discussed on this page. Having funding of $1,434,188, the project had a title of "The Epigenetic Encoding of Learning and Memory." The project had an end date in 2024, but it did not produce any papers backing up the idea of memory storage in the epigenome, or anywhere else in the brain.. 

On the same official project page, there is a Publications section that lists 7 publications that resulted from this project (there is a double-listing for one of them). None of them do anything to establish the "epigenetic encoding of learning and memory" mentioned in the project title.  The papers are these:

• "Control of striatal circuit development by the chromatin regulator Zswim6" (link). This paper makes no mention of memory or learning. 
• "Histone variant H2BE enhances chromatin accessibility in neurons to promote synaptic gene expression and long-term memory" (link). The study provided no good evidence to back up its claim that H2BE has any relation to memory. To test the claim, the study produced "H2BE knockout" mice, whose performance was compared to normal test mice. The first test used was a "novel object recognition" test that is not an effective way of judging animal memory when a blinding protocol is not followed. In the test scientists attempted to judge how much time a mouse spends exploring a type of object it has already been exposed to, using manual scoring -- we are told "Time spent interacting with each object was manually analyzed." Such a test is not a reliable way of judging memory in rodents whenever there is a failure to follow a blinding protocol, and no mention is made that a blinding protocol was followed. The second test used was a test requiring a judgment of "freezing behavior," and such tests are utterly reliable in judging whether an animal recalled, for reasons discussed at length here. 
• "A nociceptive amygdala-striatal pathway for chronic pain aversion" (link). No mention is made of learning or memory in this paper. 
• "Loss of DOT1L function disrupts neuronal transcription, animal behavior, and leads to a novel neurodevelopmental disorder" (link). The authors first discuss 11 humans who had variations in something called DOT1L The paper claims that 2 of these 11 had "intellectual disability" without giving us any specifics. This does not constitute any evidence of a relation between this DOT1L and memory. The paper also claims that DOT1L modification in zebrafish had some effect on their cognitive performance. But the claim has no clear reference to memory, and the claim is not demonstrated, because the number of zebrafish tested is way too small, being only 3 zebrafish. There is then a claim that DOT1L modifications have some effect on mice. But no clear claim is made of an effect on memory performance. 
• "Histone variant H2BE controls activity-dependent gene expression and homeostatic scaling" (link). The research discussed does not involve learning or memory. 
• "SARS-CoV-2 disrupts host epigenetic regulation via histone mimicry" (link). The research discussed does not involve learning or memory. 
• "Identification of a transcriptional signature found in multiple models of ASD and related disorders" (link). The research discussed does not involve learning or memory. It merely makes a passing reference to memory, claiming (without providing any specifics) that a "histone code" plays a role in memory.

These are all the papers I am able to find searching for research on "engrams" funded by the National Science Foundation (I have added a couple of other projects I knew of that could have appeared in such a search if the word "engram" had appeared in their abstracts). Although adding up to a total funding of several million dollars, the funding is relatively little, compared to the money spent on other things scientists believe in, such as dark matter. The number of projects looking for proof of engrams is small, with only a tiny number of scientists doing such research. 

It's rather as if deep down inside, neuroscientists scarcely even believe in engrams, or as if deep down inside, neuroscientists know that any project looking for proof of engrams will be extremely unlikely to succeed.  Maybe some part of their minds have figured out that if it was really true that brains stored memories, microscopes would have discovered proof of that decades ago. 

The decisions scientists make about what to fund is a factor speaking in a louder voice than what scientists claim about what scientists believe. The weak funding scientists have given to searches for proof of engrams may suggest that neuroscientists do not really have high confidence in the idea that memories are stored in brains. The weak results of the small number of projects related to claims of brain storage of memories (engrams) suggest that research into this area is futile in terms of substantiating claims of a brain storage of memories. 

The CIA's Long-Running MK-Ultra Mind Control Program Failed, Because Brains Don't Make Minds

The story of the MK-Ultra project is one of the sickest stories in the history of abusive science. In the 1950's there began a CIA project called MK-Ultra. The project was all based on materialist notions of the mind. Making the erroneous assumption that the mind is merely the product of the brain and its chemical outputs, scientists attempted to find or produce chemicals that could control a person's mind. One ambition of the project was to find some chemical potion that could "break down a person's mind," so that, for example, a dedicated Communist might first have his mind "broken down," and then be converted into a capitalist or an anti-Communist. Another ambition of the project was to discover some "truth serum" that would cause a subject to confess any secrets he had sworn to keep. Another ambition of the project was to find some kind of amnesia drug that would cause someone to forget secret things he had recently learned, without destroying his memory entirely. 

The project was a dismal failure. None of its goals was achieved. While the project was operating, innumerable lives were disrupted or destroyed. The project is described in the Washington Post column below, written by the leading journalist Jack Anderson:

A page on the CIA web site tells us this about MK-Ultra:

"MK-ULTRA, or MKULTRA, was the code name for a covert CIA mind-control and chemical interrogation research program, run by the Office of Scientific Intelligence. This official U.S. government program began in the early 1950s, continuing at least through the late 1960s, and it supposedly used United States citizens as unwitting test subjects...The published evidence indicates that Project MK-ULTRA involved the surreptitious use of many types of drugs, as well as other methods, to manipulate individual mental states and to alter brain function. Project MK-ULTRA was first brought to wide public attention in 1975 by the U.S. Congress, through investigations by the Church Committee, and by a presidential commission known as the Rockefeller Commission. Investigative efforts were hampered by the fact that CIA Director Richard Helms ordered all MK-ULTRA files destroyed in 1973; the Church Committee and Rockefeller Commission investigations relied on the sworn testimony of direct participants and on the relatively small number of documents that survived Helms' destruction order.  Although the CIA insists that MK-ULTRA-type experiments have been abandoned, 14-year CIA veteran Victor Marchetti has stated in various interviews that the CIA routinely conducts disinformation campaigns and that CIA mind control research continued. In a 1977 interview, Marchetti specifically called the CIA claim that MK-ULTRA was abandoned a 'cover story.' On the Senate floor in 1977, Senator Ted Kennedy said: The Deputy Director of the CIA revealed that over thirty universities and institutions were involved in an 'extensive testing and experimentation' program which included covert drug tests on unwitting citizens at all social levels, high and low, native Americans and foreign'....At least one death, that of Dr. Frank Olson, resulted from these activities. The Agency itself acknowledged that these tests made little scientific sense.' "

Later in the same document we get these tidbits:

• "In 1964, the project was renamed MK-SEARCII. The project attempted to produce a perfect truth drug for use in interrogating suspected Soviet spies during the Cold War, and generally to explore any other possibilities of mind control."
• The MK-ULTRA project was interested in finding "materials and physical methods which will produce amnesia for events preceding and during their use,"  "a material which will cause mental confusion of such a type that the individual under its influence will find it difficult to maintain a fabrication under questioning,"  "substances which will promote illogical thinking and impulsiveness to the point where the recipient would be discredited in public," "materials which will render the induction of hypnosis easier or otherwise enhance its usefulness," 
  and "substances which increase the efficiency of mentation and perception."
• "The MK-ULTRA director was granted six percent of the CIA 'operating budget in 1953, without oversight or accounting." This presumably resulted in many millions of dollars of funding. 
• "LSD and other drugs were usually administered without the subject's knowledge or informed consent."
• "Volunteers were given LSD for 77 consecutive days."
• " CIA recruited Scottish psychiatrist Donald Owen Cameron did experiments that "consisted of putting subjects into drug-induced coma for weeks at a time (up to three months in one case) while playing tape loops of noise or simple repetitive statements. His experiments were typically carried out on patients who had entered the institute for minor problems such as anxiety disorders and postpartum depression, many of whom suffered permanently from his actions." 
• " Run by TSS chief Dr. Sidney Gottlieb, the program came to include 149 separate animal and human behavior modification projects, some conducted by Agency and Army researchers, but most involving one of 80 participating American and Canadian universities, hospitals, and research institutions operating under contracts that did not reveal Agency funding or associations."

The wikipedia.org article on Donald Owen Cameron is a portrait of a man who sunk into very dark depths of evil, after serving for two years as the president of the American Psychiatric Association.  Cameron devised sinister experimental programs of long-term mental torture, which had no useful results. The biography of Sidney Gottlieb is a portrait of a biochemist who sunk into depths of evil.  That biography of Gottlieb says, "Gottlieb retired from the CIA in 1973, saying he did not believe his work had been effective." 

Nothing useful came out of all the many years of reckless highly-funded experiments performed as part of the MK-Ultra project. No one found any chemical way to control a mind, nor did anyone find any chemical way to induce amnesia or produce a truth serum.  The dismal failure of the project makes sense after you have studied the very many powerful reasons (discussed in the posts of this blog) for thinking the human mind cannot be the product of the brain, and that brains cannot be a storage place for human memories. Also, the very deep involvement of US universities in this sinister project (over many years) is another reason why we should question the credibility of biology pronouncements coming from such universities. 

Physically Unrealistic NEPTUNE "Model" of Near-Death Experiences Is a Misleading Mishmash

I was previously asked by some of my readers for comments on the paper "A Neuroscientific Model of Near-Death Experiences." At that time I did not critique the paper because it was  behind a paywall, and the abstract gave no reason for suspecting that the paper was worth a 20 dollar payment.  The paper is now publicly available at the link here (alternate link here). We have a paper that claims to have a "model" of near-death experiences, but actually offers no physically realistic model of any such thing. What we get is a jargon-filled jumble that does nothing to explain any of the main features of near-death experiences. The abstract gives a clue of the hodgepodge farrago that the paper is, by saying that it will offer "a model for NDEs that encompasses a cascade of concomitant psychological and neurophysiological processes within an evolutionary framework." So the strategy is apparently something like: let's sprinkle some psychology talk with some brain chemistry talk and some Darwinist evolutionary biology talk, and see whether that adds up to an explanation for near-death experiences.  The result resembles someone wildly firing shots in all different directions. 

The co-authors start out by giving us a three-paragraph discussion entitled "Cerebral blood flow, blood gases and neuronal function." Here is the first paragraph:

"Just before and during cardiopulmonary arrest, cerebral blood flow is compromised, resulting in a swift decline in oxygen and glucose supplies and an accumulation of CO2. Oxygen deprivation (hypoxia) impairs cellular respiration and ATP production, thereby disrupting energy-dependent cellular processes. This deprivation also affects the function of enzymes such as monoamine oxidase (MAO), which is responsible for degrading monoamine neurotransmitters, including serotonin, dopamine, noradrenaline and histamine. In addition, elevated CO2 levels (hypercapnia) contribute to acid–base imbalance. CO2 combines with water to form carbonic acid (H2CO3), which dissociates into H+ and HCO3 – ions. During hypercapnia, the buffering capacity of HCO3 – is exceeded by an overabundance of H+ , leading to decreased pH43, disrupted ATP production, and cerebral acidosis. Reductions in brain pH activate acid-sensing ion channels (ASICs), leading to an influx of Na+ ions, which further contributes to neuronal depolarization and the triggering of action potentials."

We have lots of mention of chemistry details, a jargon-filled discussion that is meant to impress us. But it should not impress us in the least, because it has no relevance to explaining near-death experiences. There is one main relevant neuroscience-related fact here (which the paper fails to ever mention). It is that very soon after the heart stops beating during cardiac arrest, the brain shuts down electrically. This is shown in EEG readings, which show the brain flatlining within 10 to 20 seconds after cardiac arrest.  When this flatlining of brain signals occurs, the normal wavy appearance of brain waves become flat lines. 

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)."

For example, below is part of Figure S1A from the supplemental information of a scientific paper. We see the brain waves of a dying Patient One in blue (EEG readings), and we see in the last row a red ECG reading that is a  measure of heart activity.  

The text below this visual tells us this about these stages that are labeled S5, S6, S7, S8, S9 and S10, using the term "bradycardia" which means lower-than-normal heart rate: 

"The pacemaker was automatically turned off (S5) and restarted from S6. S7 starts when rapid heartrate drop was seen which ended when pacemaker was turned off by clinical staff. S8 denotes the bradycardia period where RR interval (RRI) is longer than 5s. In S9, RRI is below 5s (partial heartrate recovery). S10 saw the reappearance of the P-waves and further recovery of heartrate. S11 ends at the last recorded heartbeat with periodical PAC-like ECG pattern."

The evidence in this case is clear: there was virtually no brain activity at stage S10 (when there was "further recovery of heartrate") and no brain activity at all at stage S11, which ended with the "last recorded heartbeat." The lack of brain activity is shown in the blue flat lines we see under S10 and S11. 

The fact of the brain flatlining and becoming isoelectric within about 10 to 20 seconds of cardiac arrest is an all-important fact in any neuroscience attempt to explain near-death experiences. It means that all such attempts are doomed to failure.  There can be no brain explanation of some mental phenomenon if that phenomenon occurs when the brain is electrically inactive. Similarly, you can have no explanation of your computer performing some task if the task occurred while your computer was unplugged and your computer has no batteries. 

Does the paper "A Neuroscientific Model of Near-Death Experiences" ever tell us this all-important fact that brains become isoelectric (electrically inactive) within a few seconds after cardiac arrest? No, it does not. The paper does not use the word "isoelectric" and does not use the word "flatline." The paper makes no reference to EEG readings, and no reference to brain waves. The text of the paper fails to use the term "EEG" and fails to use the term "brain wave." So the paper's pretensions to be describing what goes on in a brain during cardiac arrest is a sham. The authors have ignored the most fundamental reality of what goes on in a brain during cardiac arrest. 

The vast majority of the paper "A Neuroscientific Model of Near-Death Experiences" is a discussion of brain chemicals. Before reviewing this discussion I can give some background information on that topic. The main chemicals the paper discusses are serotonin, glutamate, noradrenaline, acetylcholine, endorphins, dopamine and GABA. These chemicals are found in extremely tiny amounts such as 1 part per million in brain fluid.  Prior to the past few years, there did not exist any reliable method for accurately measuring increases in such chemicals occurring over a very short time span such as the few minutes following the beginning of cardiac arrest. There existed a technique called microdialysis, which involved inserting a needle or tube into the brain, and taking fluid from some tiny part of it. Such a technique was not suitable for reliably tracking changes in brain chemicals over a short period. Someone might try to insert such microdialysis needles three times in quick succession over a period such as ten minutes, and then analyze the extracted fluid. But any differences reported would be more likely to be due to region-to-region variations in such chemicals, or uncertainties in the attempted measurements themselves, rather than an actual increase over the short time span. The identification of chemicals existing in only extremely tiny trace amounts is an affair involving large chances for error, with uncertainties often spanning several orders of magnitude, between 10 and 1000 times. For example, the paper here lists studies that attempted to measure one brain chemical by using microdialysis, and the reported results vary between 1 nanomole and 2000 nanomoles. 

Whenever we hear any claims that some brain chemical was found to increase during ischemia (the blockage of blood to the brain), we should always ask questions such as these:

(1) How many studies reported such an effect, and were the study group sizes used sufficient to produce a high statistical power?

(2) What fraction of the brain was checked? Was it only a hundredth of the brain, such as only the striatum or the hippocampus?

(3) What was the time scale? Was it over hours or days (irrelevant for discussions of near-death experiences), or was it over some very short time scale that might be relevant to explaining something going during cardiac arrest or near-death experiences?

Almost always the answers to these questions will deflate any claims to have found a relevant surge in brain chemicals, showing that the claims are not well founded and not well replicated. 

Here are some of the sections in the paper "A Neuroscientific Model of Near-Death Experiences":

• The section entitled "the serotonergic system." We have eight paragraphs describing the role of serotonin in the brain. None of the discussion has any relevance to explaining any of the more interesting features of near-death experiences. Serotonin does not produce hallucinations. The paper "Serotonin and Human Cognitive Performance" discusses the results of "experimental studies involving healthy human volunteers," but makes no mention of hallucinations in these volunteers who had their serotonin levels artificially increased. Millions of people in the US take SSRI drugs that are specifically designed to increase serotonin levels; but such drugs do not produce hallucinations. The paper here (discussed in the appendix) involved experiments that increased by very many times (between 100 times and 1000 times, in other words 10000% to 100000%)  the serotonin levels in volunteers, by infusions of serotonin. No hallucinations were reported.  There is no robust evidence that serotonin surges in humans during near-death experiences or during cardiac arrest. The  paper "A Neuroscientific Model of Near-Death Experiences" makes the claim that "In rats undergoing asphyxia, a dramatic initial surge in brain serotonin levels was observed — up to 100–200 times higher than baseline." This is a reference to a 2015 paper that did not reliably observe any such thing, because at the time there was no reliable technology for measuring short-term spikes in serotonin levels, and the study group size was way too small (only 7 rats) for a reliable result to be claimed. The paper used a microdialysis and liquid chromatography-mass spectrometry (LC-MS) method that at the time was not very reliable because of reasons discussed in the appendix of this post. After giving us detail after detail about serotonin, none of which have any relevance to explaining near-death experiences, the section drifts off to a discussion of other topics such as DMT trips and speculations about evolution. The section has no relevance to explaining near-death experiences. 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." 
• The section entitled "the glutamatergic system." We have five paragraphs discussing the role of the neurotransmitter glutamate in the brain. None of it has any relevance to explaining near-death experiences. Senselessly the authors try to use this discussion as a launchpad for discussing ketamine, a hallucinogenic drug. This goes nowhere, because the authors confess that while someone "hypothesized that in life-threatening situations, an endogenous ketamine-like neurotoxin might be released," the fact is that "no empirical evidence has been found to support the existence of such a molecule." The authors attempt to insinuate that during cardiac arrest there may be a big increase in glutamate. There is no robust  evidence that this is true, and if it were true, it would be irrelevant, because glutamate is not any type of hallucinogen.  As I discuss in my post "The Groundless Myth That 'Floods'' or 'Surges' Help Explain Near-Death Experiences," there is no evidence that any type of relevant brain chemical surges during cardiac arrest or near-death experiences. Claims of such a surge is a deceptive element repeated again and again in articles or papers attempting to explain near-death experiences. There are two very strong reasons why such claims must be wrong or irrelevant. The first fact is that we know that neurotransmitters are synthesized at a very slow rate, making unbelievable all claims of a sudden surge in neurotransmitters at death. The second fact (supremely relevant but senselessly ignored by the co-authors of the paper "A Neuroscientific Model of Near-Death Experiences") is that brains become isoelectric (i.e. they flat-line) within 10 to 20 seconds of cardiac arrest, making all claims about neurotransmitter increases at such a time irrelevant or unbelievable. 
• The section entitled "the noradrenergic system."  We have three paragraphs giving an irrelevant discussion of a chemical called noradrenaline. The attempt to link this discussion to near-death experiences is feeble and laughable. We have the claim that "noradrenaline might also aid memory consolidation though its effect on the amygdala" and that "the ability of humans to recall vivid memories even on the verge of death could be explained by high  noradrenaline levels during asphyxia."  The statements are nonsensical. There is no evidence that memory recall is increased when people have higher levels of noradrenaline. The relevant fact here (completely ignored by the authors)  is that during cardiac arrest brain waves very quickly become isoelectric, and that brains shut down electrically and flatline, something that (under assumptions brains store memories) should completely prevent the formation of any new memories. Instead of there being a neuroscience reason why someone might form vivid memories during cardiac arrest, there is the strongest neuroscience reason why such a thing should be impossible under the assumptions of neuroscientists. 
• The section entitled "the cholinergic system."  We have two paragraphs discussing the neurotransmitter acetylcholine. We have the unfounded claim that acetylcholine enhances memory formation. Neuroscientists do not have any credible theory of memory formation, and there is no strong evidence that increased acetylcholine levels cause higher levels of memory formation.  The attempt in the paper to link acetylcholine to near-death experiences is a feeble one: merely something like insinuating that acetylcholine helps memory, and that acetylcholine might help someone remember a near-death experience.  The authors continue to be utterly oblivious to the most relevant fact here: that when a brain is isoelectric, in an EEG-flatline state and not generating any brain waves, the formation of memories should be impossible under "brains store memories" assumptions. 
• The section entitled "the endorphinergic system."  We have three paragraphs discussing endorphins, a type of brain chemical widely discussed as a "feel good" kind of chemical.  We have the incorrect claim that a study showed that endorphins increase in dogs undergoing sudden cardiac death. The reference is to a 1995 paper that should never be cited as credible evidence for such a claim.  In 1995 there did not exist any reliable technology for measuring very short-term spikes in brain chemicals in animals such as dogs. The paper does not mention any study group size, and we may assume that it was one of innumerable neuroscience experiments using a study group size way-too-small for a reliable result to be claimed. Here we must remember that if people had reliable evidence for the claim that endorphins increase during sudden cardiac death, they would be citing papers of recent decades, not papers from 30 years ago. The attempt to link endorphins to near-death experiences is a feeble one: merely the suggestion that endorphins might help explain mood elevation. 
• The section entitled "the dopaminergic system."  The brain chemical discussed is dopamine. We again have a dubious claim that such a chemical was found to have increased in dying rats. The claim is based on the 2015 paper here, the paper "Asphyxia-activated corticocardiac signaling accelerates onset of cardiac arrest."  At that time there did not exist any reliable methods for making real-time in vivo measurements of brain chemicals over short periods of time such as ten minutes. The technique used by the paper (microdialysis and liquid chromatography-mass spectrometry or LC-MS) was not suitable for accurately measuring real-time changes in neurotransmitters over a tiny time scale such as 10 minutes. (See the appendix for more on the problems with LC-MS.) The paper cited was not a robust science paper because of its use of way-too-small study group sizes such as only 7 rodents. One of the co-authors of the "A Neuroscientific Model of Near-Death Experiences" paper (Martial) makes a misstatement about a previous paper of hers, claiming, "Martial et al. found that coma survivors who reported NDEs exhibited suboptimal  source monitoring and an increased tendency to illusory recollection,  compared with those without NDEs." To the contrary, the paper in question (doing some memory test on 20 subjects reporting a near-death experience and 20 who did not) reported "we obtained equivalent proportions of correct and false recall performance in both groups." The section attempts to insinuate that dopamine causes hallucinations. There is no strong evidence that dopamine causes visual hallucinations. The paper "Effects of Dopamine in Man" reports on the effects of 13 subjects who were given a 1% infusion of dopamine, causing dopamine levels many times higher than naturally occur. The paper makes no mention of any hallucinatory effects or any mental effects. A similar experimental result (reporting no hallucinations) is reported in the paper here, which tested artificially produced dopamine spikes as high as 1000 times higher than normal. Attempts to claim dopamine levels have an association with the merely auditory hallucinations of schizophrenia are advanced by pharmaceutical companies and neuroscientists financially entangled with them, who are interested in selling pills that supposedly affect dopamine levels. The claim is irrelevant, because of the lack of robust evidence that dopamine sharply increases in humans during sudden cardiac arrest or near-death experiences (outside of perhaps one or two small areas in the middle of the brain like the striatum), the implausibility of the claim that it could very quickly increase during such rapid events (given the very slow production rate of all neurotransmitters), the fact that brains that quickly flatline a few seconds after cardiac arrest cannot be hallucinating brains, and the fact that very strong dopamine infusions in humans do not produce hallucinations. No one has ever caused someone to have a visual hallucination by giving him an injection or infusion of dopamine.  
• The section entitled "the gabaergic system."  We have two paragraphs discussing GABA, neither of which discuss any convincing link between such a chemical and near-death experiences. 

We then have a huge misstatement in the "A Neuroscientific Model of Near-Death Experiences" paper, this claim: "Anecdotal accounts of perceptions during NDEs are available, but no empirical research to date has used sufficiently rigorous methodology to objectively verify whether these perceptions corresponded to actual external stimuli."  This is not true at all. Researchers have very carefully attempted to discover whether reports of out-of-body experiences reported observations that an immobile observer should have been unable to make, and whether such observations could be verified. Very many times such observations were verified as correct. You can read very many examples in my post here. Because all such cases are totally unaccountable under a neuroscientific account of near-death experiences, I can understand why the paper authors would want to misinform us about the existence of such cases. 

We then have yet another example in the paper of a citation of a neuroscience paper that is almost certainly junk science. We read, "Interestingly, Britton and Bootzin demonstrated that NDE experiencers tend to have more temporal lobe epileptiform EEG activity and more temporal lobe epileptic symptoms than matched controls who never had an NDE." A look at the paper shows a paper behind a paywall, one that reports in its abstract no study group size. A very good rule of thumb regarding neuroscience experimental studies is that when the abstract reports no study group size, there is a very high likelihood that the experiment used some way-too-small study group size, a size that the authors were ashamed to mention in their abstract.  There is no good evidence that those having near-death experiences have different day-to-day EEG readings than those who do not. 

More bad citations follow. We have the claim that "intracranial stimulation of the right junction seems to elicit disembodiment resembling an OBE," and a reference is given to a paper that made no such claim. We have the claim that "electrical stimulation of the left junction can trigger an own-body illusion of another person in the extrapersonal space, resembling the encounter of entities reported in NDEs." The reference given is to another paper behind a paywall, one that does not make such a claim in its abstract, but instead merely claims that such electrical stimulation of the brain caused a single subject to report seeing a figure that "closely 'shadowed' changes in the patient's body position and posture," something not reported in near-death experiences. The claims are irrelevant, because they involve artificial electrode stimulations of the brain not matching what occurs during near-death experiences.

Having given us nothing at all in the way of a neuroscientific explanation for near-death experiences, the paper authors move on to some other parts of their muddled mishmash. The next part is a section entitled "Psychological Processes." We get nothing in the way of a credible psychological explanation for near-death experiences. The authors confess that "that most people who recall NDEs have no global cognitive functioning deficits or specific pathological disorders."  We have a claim that those who have near-death experiences daydream more often. Two papers are given for this claim, but neither of the papers make such a claim. 

Referring to near-death experiences, the authors then incorrectly claim, "Some related traits, such as fantasy proneness, have also been found in the NDE population." As the reference for this claim, the paper refers us to Martial's very poorly designed paper "Fantasy proneness correlates with the intensity of near-death experience." It's a very poor piece of work for several reasons. Subjects were given something called the Creative Experiences Questionnaire. That survey is described in the paper here. It is one of surveys in the psychiatric field that seems designed to gaslight and defame people who have had normal, healthy experiences with psychic phenomenon. Among the 25 questions are questions in which people are asked whether they agree with these statements:

• "I sometimes feel that I have had an out-of-body experience."
• "During my life I have had intense religious experiences which influenced me in a very strong manner."
• "I often have the experience of thinking of someone and soon afterwards that person calls or shows up."

Anyone having a near-death experience (in which out-of-body experiences are so common) would be likely to answer affirmatively to the first two of these questions. Anyone having the common experience of ESP would be likely to answer affirmatively to the last question. It is very bad circular reasoning to be including such questions in a survey given to those reporting near-death experiences, and using affirmative answers as evidence of higher "fantasy proneness." Answering affirmatively to such questions is not evidence of fantasy proneness. Neither near-death experiences nor ESP-type experiences occur through any process of fantasy. Martial's very poorly designed 2018 paper does not actually show any robust evidence that those having near-death experiences are more fantasy prone than those not reporting such experiences.  Excluding 3 of the questions, she gets an average score of  8 on this Creative Experiences Questionnaire for those having near-death experiences (Table 2); and she says that this is higher than the score of her 100 controls given the same survey. But the year 2001 paper introducing this Creative Experiences Questionnaire had given data for 332 normal subjects given the survey (not people having near-death experiences), and had reported that the average scores on the survey were 9.2 for men and 8.7 for women. So it would seem that instead of Martial's results showing greater fantasy proneness for those near-death experiences, her results actually show slightly less fantasy proneness. Very conveniently, Martial fails in the paper to make any mention of the survey data for the 332 normal subjects in the year 2001 paper, data which refutes her claim of greater fantasy proneness in those having near-death experiences. 

Near the end of the paper "A Neuroscientific Model of Near-Death Experiences" the authors claim to have a "model" of near-death experiences. They really have no such thing, because they have not addressed any of the main explanatory issues raised by such experiences. Their so-called model describes a set of events that does not match what happens physically to the body during cardiac arrest or during a near-death experience. They give the name NEPTUNE to this so-called model, with NEPTUNE standing for  Neurophysiological Evolutionary Psychological Theory Understanding Near-death Experience.  This acronym is an indication of what a mishmash mess we have. Evolution is something believed to occur over extremely long timespans such as millions of years or many thousands of years. It is nonsensical to use the term "evolutionary" to refer to brief events in a person's life. 

The paper's grand summary of the so-called "NEPTUNE model" consists of two paragraphs, both of which I quote below in italics. Here is the first paragraph:

"NEPTUNE assumes a cascade of concomitant psychological and neurophysiological processes, which might start with systemic hypotension, oxygen deprivation, elevated CO2 levels, disruption of ATP production, and a decreased pH, culminating in cerebral acidosis. Triggered by cellular energy deprivation, these intricate processes can set off a chain reaction of complex cellular responses, ultimately leading to increased neuronal excitability in cortical associative regions in the mesiotemporal lobe, occipital lobe, insular cortex and temporoparietal–occipital hot zone junction, permitting the perceptual content of the experience to become conscious. The neural mechanisms underlying NDEs tend to be similar to those underlying REM intrusions. Enhanced neuronal responsiveness, resulting in increased firing rates, ultimately leads to the massive release of neurotransmitters."

Comment: Near-death experiences typically occur during cardiac arrest, and the authors claim that "the model focuses

specifically on the prototypical scenario cardiac arrest, which seems to

be the most common triggering aetiology for NDEs."  Cardiac arrest bears no resemblance to "REM intrusions," the latter not involving the heart stopping. During cardiac arrest, there is no "Enhanced neuronal responsiveness, resulting in increased firing rates." There is exactly the opposite. EEG readings show that very quickly (within 10 to 20 seconds) after the heart stops in cardiac arrest, neuron firing rates die down to nothing, resulting in a flatlining of brain waves, something called an isoelectric state that is the exact opposite of "increased firing rates."  The scenario described in the quote above is a fantasy that is the exact opposite of what happens during cardiac arrest. We have here no "model" of what happens in cardiac arrest, but a description that is the exact opposite of what happens. It is rather like someone claiming to have a "model" of plant growth, one that claims that plants die when you water them, something that is the opposite of what is observed. When I do a Google search for "what are neuron firing rates when the brain is isoelectric," its latest AI gives this: "During an isoelectric state of the brain, which is often detected by a flatline or extremely low-amplitude EEG, the firing rates of neurons are significantly reduced and may be completely suppressed, particularly in the cortex." 

There is no sound  observational basis whatsoever for the claim that there is some "massive release of neurotransmitters."  Since the claim that such a thing happens is based on the exact-opposite-of-the-truth claim that there are "increased firing rates" in the brain during cardiac arrest, we should have no confidence in such a claim. Everything we know about the very slow synthesis and transmission of neurotransmitters in the brain argues against the possibility that there could be any such "massive release of neurotransmitters."

"In tandem with other neurochemical mechanisms, we hypothesize the following key neurochemical events in NDEs. We propose that calming effects are induced by increased 5-HT1A receptor availability, as well as by transient increases in endorphin and GABA levels, potentially leading to a feeling of deep peace, whereas vivid visual hallucinations are triggered by hyperactivation of 5-HT2A receptors and dopamine (Fig. 2). The profound feelings of hyper-reality associated with these hallucinations could be explained by increased release of dopamine specifically. Determining the precise role of glutamate in NDEs remains challenging, but we tentatively suggest that it could be involved in cognitive dissociation. Memory encoding of this phenomenology would be promoted by release of noradrenaline, acetylcholine and glutamate, triggered by the stressful or life-threatening situation, to enhance coping. Individual predisposition to dissociation might facilitate this neurophysiological cascade, and the dissociation process can be seen as a defence mechanism to cope with the stressful or life-threatening situation, consistent with an evolutionary role."

Comment: There seems to be nothing of any credibility or substance here. There is no robust evidence that endorphin levels or GABA levels increase very strongly in humans during cardiac arrest. Because the brain electrically shuts down very quickly during cardiac arrest (within 10 or 20 seconds after the heart stops), it cannot be that during such a time " vivid visual hallucinations are triggered by hyperactivation of 5-HT2A receptors and dopamine," and dopamine is not a cause of visual hallucinations.  Contrary to a "hyperactivation" of any part of the brain during cardiac arrest, there is the exact opposite: an electrical shutting down of the brain which would make impossible any such thing as brain-caused hallucinations.  There is no robust evidence of greatly increased dopamine levels in humans during cardiac arrest or near-death experiences, and it is not true that some surge in dopamine will produce a visual hallucination. No one has ever done an experiment in which injecting or infusing someone with dopamine produced a visual hallucination. In 1952 they did do an experiment in which 13 subjects were infused with 1% dopamine (causing dopamine levels very many times larger than naturally occur); and such an experiment produced no hallucinations and no mental effects. A similar infusion experiment increasing dopamine levels in humans a thousandfold is reported here; it also reports no hallucinations resulting. The comment about a defense mechanism is simply the thinnest of psychology hand-waving, using the old term "defense mechanism" that was popular with Freudian psychologists.  This is just a little psychology sprinkling, to dress up a tiny bit the physiology fantasy, which is a description that is the exact opposite of what happens in a brain during cardiac arrest. 

To clarify:

• There is no robust evidence that serotonin very sharply increases in the human brain during cardiac arrest or near-death experiences, and if it were to increase, that would do nothing to explain near-death experiences, because serotonin is not a hallucinogen, and brains are electrically shut down during cardiac arrest. The paper here (discussed in the appendix) involved experiments that increased by very many times (between 100 times and 1000 times, in other words 10000% to 100000%)  the serotonin levels in volunteers, by infusions of serotonin. No hallucinations were reported.
• There is no robust evidence that glutamate increases in the brain during cardiac arrest or near-death experiences, and if it were to increase, that would do nothing to explain near-death experiences, because glutamate is not a hallucinogen, and brains are electrically shut down during cardiac arrest. One paper says, "Many preclinical studies revealed decreased glutamate whole tissue content after ischemia." 
• Because adrenaline is often injected into people undergoing cardiac arrest to try and stop such an arrest, there may be noradrenaline increases in the brain during some cardiac arrest cases and near-death experiences. But that does nothing to explain near-death experiences, because noradrenaline is not a hallucinogen, and brains are electrically shut down during cardiac arrest. 
• There is no good evidence that acetylcholine increases in the brain during cardiac arrest and near-death experiences, and if it were to increase, that would do nothing to explain near-death experiences, because acetylcholine is not a hallucinogen, and brains are electrically shut down during cardiac arrest. 
• There is no strong evidence that endorphins increases in the brain during cardiac arrest and near-death experiences, and if endorphins were to increase during such events, that would do nothing to explain near-death experiences, because endorphins are not a hallucinogen.
• Discounting some not-very-convincing studies (with too-small study group sizes) that may suggest an increase in dopamine in two tiny regions of the brain (the striatum and the hippocampus) of rats during ischemia, there is no robust evidence that dopamine very sharply increases in the human brain during cardiac arrest and near-death experiences; and if it were to increase, that would do nothing to explain near-death experiences, because while hypothesized (without strong evidence) to be more common in some who have auditory hallucinations, dopamine is not a cause of suddenly appearing visual hallucinations, because very strong infusions of dopamine in humans do not produce any hallucinations or mental effects, and  because brains are electrically shut down during cardiac arrest. 
• There is no robust evidence that GABA increases in the brain during cardiac arrest and near-death experiences, and if it were to increase, that would do nothing to explain near-death experiences, because GABA is not a hallucinogen, and  because brains are electrically shut down during cardiac arrest.

Given the very extreme difference between what actually happens in the brain during cardiac arrest (a very quick flatlining and a shutting-down of electrical activity) and the fictional or fantasy "hyperactivation" description of the two paragraphs quoted above, no one should be describing the NEPTUNE scenario as a model of near-death experiences, unless they use model in quotation marks as I do in my title.  You do not model something when you give a physical description of that thing radically different from the observed physical reality. 

All attempts to dismiss near-death experiences as hallucinations lack credibility for several reasons:

(1) The lack of any robust evidence that any chemical capable of  causing sudden visual hallucinations is released at the time of a cardiac arrest. 

(2) The impossibility of brain-caused hallucinations during cardiac arrest, because of the reality of the brain very quickly shutting down electrically during cardiac arrest, which should prevent any conscious experience under "brains make minds" assumptions, whether involving hallucinations or not involving hallucinations. 

(3) The very high similarity of observational reports during near-death experiences, involving a very strong recurrence and repetition of descriptions of viewing the body from about two meters away or from the ceiling, descriptions of passing through a tunnel, descriptions of encountering some mysterious numinous light, descriptions of encountering some mystical realm, descriptions of life-reviews, and descriptions of encountering dead relatives.  Hallucinations could be of millions of possible things, and we would expect hallucinations to produce random content. The very strong observation repetition in near-death experiences argues very strongly against any hallucination explanation. Similarly, if three people on my block keep reporting the appearance of a bright blue van at 9:00 PM, it is very unlikely that such reports are occurring by hallucinations, as it would be very, very unlikely that hallucinations in different people would be so similar. 

(4) The many cases in which out-of-body experiences involve an observer claiming to see something that was not observable by his body, with the observation being subsequently verified as matching physical reality. Many such cases are described in my post here. 

What went on in the two previous italicized paragraphs quoted above is the same type of thing that goes on again and again when neuroscientists attempt to explain things utterly beyond their understanding.  We should remember that neuroscientists have no real understanding of ordinary mental phenomena such as insight, mathematical calculation, imagination, recognition, self-hood, memory formation, idea creation,  lifelong memory persistence, empathy, or the instant recall of lots of detailed relevant information upon hearing a name or seeing a face. Neuroscientists no more understand such common phenomena than they understand uncommon phenomena such as near-death experiences. When asked to explain such common things (which are actually beyond any neural explanation), neuroscientists engage in vacuous jargon-decorated hand-waving that does not amount to any credible explanation. They typically attempt to sprinkle such vacuous attempted explanations with lots of references to different types of chemicals, to try to impress those who are easily impressed. The astute and diligent scholar of the philosophy of mind, neuroscience and psychology will look at such charades and say, "There's no there there."  

Appendix (which the average reader may want to skip): The 2015 paper mentioned above entitled "Asphyxia-activated corticocardiac signaling accelerates onset of cardiac arrest" claimed to use technologies called microdialysis and 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."

A similar paper discusses at great length many pitfalls and ways-to-go-wrong using this method, stating "We observed cases of false-positive results with the use of liquid chromatography coupled with tandem mass spectrometry (LC-MS/MS)."  Still another paper (on page 109 of the document here) refers to an "Achilles heel" of this liquid chromatography-mass spectrometry method (LC-MS), saying the problem can lead to "gross errors" when trying to measure the levels of some chemical in a sample. The same document tells us on page 120 that "it must be emphasized that the risk of gross errors is probably higher for LC-MS/MS compared to analyses run on standard clinical chemistry analyzers." 

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 very tiny levels 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 reliable results, you would need at least three things:

(1) A sufficient sample size, such as 20 animals per study group, rather than the mere 7 animals used in the paper "Asphyxia-activated corticocardiac signaling accelerates onset of cardiac arrest."

(2) A blinding protocol which would make sure that each person analyzing extracted brain fluid had no idea where in a time sequence the sample corresponded to, to avoid some effect in which analyst bias helped produced higher estimations in later samples, to fit in with some desired "increase of neurotransmitters" narrative. 

(3) An adequate replication of the results by other well-designed studies using adequate sample sizes. 

Nothing of the sort occurred here. The sample size used was too small for any decent statistical power: only 7 animals. No mention is made of a blinding protocol. And the study was never replicated by additional well-designed studies. 

The paper here describes experiments in which human  subjects were infused with serotonin. The serotonin levels of the patients were increased by very many times. When I do a Google search for "Amount of serotonin in the blood moles per liter," I get an answer saying, "the normal range of serotonin in the blood, expressed in moles per liter, is approximately 0.00000028 to 0.00000114 mol/L" (moles per liter).  The paper says that it increased serotonin levels to between .0000001 and .0001 moles per liter for 22 subjects, and that two of the subjects had their serotonin levels increased to .001 moles per liter. This was an experiment that was increasing serotonin levels in humans by a factor of between 100 times and 1000 times. No hallucinations were reported. Clearly speculations that serotonin increases during cardiac arrest might cause hallucinations are as groundless as claims that dopamine increases during cardiac arrest might cause hallucinations.

The paper here ("HUMAN BEHAVIOURAL  AROUSAL INDUCED BY DOPAMINE") discusses experiments in which human subjects received dopamine infusions that increased their dopamine levels to as high as 1000 nanomoles per milliliter, which is a level more than 1000 times higher than normal. The paper fails to mention any hallucinations resulting. This is more evidence that it is senseless to try to speculate that dopamine spikes during cardiac arrest might explain near-death experiences. 

One of the worst parts of the "A Neuroscientific Model of Near-Death Experiences" paper comes in a diagram in which there is a box marked "Evolutionary advantages," and we have a reference to "enabling the individual to cope with life-threatening or painful situations." Near-death experiences do nothing to increase the likelihood of surviving a life-threatening situation.  Of course, someone undergoing cardiac arrest will not be more likely to survive if he has some mental experience of leaving his body while his heart has stopped.  And if someone is drowning or freezing to death, it will not at all increase his chance of surviving if his life flashes before his eyes, or if he sees himself floating out of his body and encountering a mystical realm or a numinous mysterious light. Far from increasing survival rates during such events, a near-death experience would be a distraction that would lessen the chance that someone would focus on what he needs to do to save himself in such a situation. So all attempts to postulate some Darwinian "survival of the fittest" explanation for near-death experiences are nonsensical.