Friday, April 4, 2025

Writing About Brains, Egnor Gets Things Halfway Right

Michael Egnor is a professor of neurosurgery and pediatrics whose writings often appear at the Evolution News site. Egnor has written some good posts at that site, often presenting the kind of evidence I discuss on this site.  But in one post this year on that site, Egnor seems to indicate that he is still clinging to some of the moldy old dogmas of neuroscientists, including some dogmas I regard as untenable. 

It is not that Egnor is afraid to believe in a human soul. In the post he says "we have spiritual souls and physical bodies." In fact, Egnor is the author of a new book entitled The Immortal Mind: A Neurosurgeon's Case for the Existence of the Soul. The problem is that the soul Egnor believes in seems to be only half of what we need to postulate to have a credible theory of human minds.  Egnor seems to believe that you have a soul responsible for your selfhood and consciousness and thinking, but that such a soul does not involve human memory.  He apparently thinks that memory is a product of the brain. Teaching an unfounded triumphal legend, he states, "The pioneering neuroscientists of the 20th and 21st centuries — Wilder Penfield, Roger Sperry, Justine Sergent, Yair Pinto, Benjamin Libet, and many others — have shown that the brain is the source of five of these kinds of activities—physiological control (of heartbeat, breathing, etc.), locomotion, perception, memory, and emotion." 

No, such neuroscientists sure did not show that the brain is the source of perception or locomotion or memory or emotion.  There are brain chemicals that can influence emotions such as fear and anger; and brains help you achieve visual perception through the eyes and locomotion through your legs. But no one has ever shown any neural basis for the more elevated human emotions such as romantic love or parental love or wonder or awe. No one has an explanation for how a brain could produce a locomotion decision such as when you decide to get up and go for a walk. There is no neuroscience basis for claiming that the brain is the source of instant human recall, which occurs despite the nonexistence in the brain of the things that make instant information retrieval possible in products humans manufacture (things such as addressing, indexing and sorting). And there are the strongest reasons for thinking that the brain cannot be the storage place of human memories, things such as the fact that human memories can last 1000 times longer than the average lifetime of brain proteins. 

In that quote by Egnor, he has a link to other posts, one link for each of the people he mentions. Let me discuss those links.

The Wilder Penfield Link

The link Egnor gives regarding Penfield is a link to a post he wrote about Wilder Penfield. The post is guilty of propagating one of the "old wives' tales" of neuroscience lore, the claim that Wilder Penfield produced memory recall by zapping people's brains with electricity. Penfield did no such thing. He merely noted that sometimes people would recall things when their brain was being electrically zapped. Since memory recall occurs almost all the time, memory recall during brain zapping does nothing to show that brains store memories. Penfield failed to document any effect by which one particular memory would always be evoked when some particular brain region was zapped. 

Strangely Egnor quotes Penfield as saying "none of the actions we attribute to the mind has been initiated by electrode stimulation or epileptic discharge." Such a claim contradicts the idea that he did anything to produce recall by zapping a brain, because memory recall is certainly one "of the actions we attribute to the mind." 

At www.archive.org I was able to find and borrow a 1967 book by Wilder Penfield, the book "The Excitable Cortex in Conscious Man." In that book Penfield discusses his research electrically stimulating parts of human brains. He makes no claim that a specific memory could be reproduced multiple times by stimulating a particular part of the brain. Instead on page 23 he merely refers to "experiential hallucinations" being produced by such brain stimulation. 

In a future post discussing pages 23 to 32 of this book, I will document cases of how Penfield described imprecise statements from electrically stimulated patients (statements lacking the precision of exact recollections of real events), and how Penfield jumped to conclusions by making unwarranted characterizations of such statements, claiming that they were based on things the patients had experienced, without ever verifying that this was the case, while at the same time calling such statements descriptions of "hallucinations." 

A review of 80 years of experiments on electrical stimulation of the brain uses the word “reminiscences” for accounts that may or may not be memory retrievals. The review tells us, “This remains a rare phenomenon with from 0.3% to 0.59% EBS [electrical brain stimulation] inducing reminiscences.” The review states the following:

"We observed a surprisingly large variety of reminiscences covering all aspects of declarative memory. However, most were poorly detailed and only a few were episodic. This result does not support theories of a highly stable and detailed memory, as initially postulated, and still widely believed as true by the general public....Overall, only one patient reported what appeared to be a clearly detailed episodic memory for which he spontaneously specified that he had never thought about it....Overall, these results do not support Penfield's idea of a highly stable memory that can be replayed randomly by EBS. Hence, results of EBS should not, at this stage, be taken as evidence for long-term episodic memories that can sometimes be retrieved."

So Egnor is wrong about Penfield. He did not do anything to show memories are stored in brains.  In particular, he made no attempt to determine whether accounts he collected from people being brain-stimulated matched actual things they had experienced.  We don't even know whether such accounts were actual memories. 

In another post Egnor continues to suggest incorrect ideas about the research of Penfield. He claims that some reader said that 5 percent of Penfield's stimulation produced memories. As his only link to back up this claim, he gives a link to the paper quoted above, which does not support any such claim, but instead tells us that "This remains a rare phenomenon with from 0.3% to 0.59% EBS [electrical brain stimulation] inducing reminiscences.”  So the actual rate is that when you stimulate someone's brain, maybe 1 out of 200 times they will remember something. This does nothing to show that memories are stored in brains, and you could probably get a similar rate of memory recollection by scratching someone's elbow, simply because normal speech is rich in memory recollection. 

The Roger Sperry Link

The link Egnor gives when referring to Roger Sperry is a link to the post here. The post discusses patients that underwent a cutting of the fibers connecting their two hemispheres. Such patients retained a single unified self. Such evidence is important in establishing that the brain is not the source of the mind, as they showed people with essentially two severed brain halves retain a single self. But split-brain operations do nothing to substantiate Egnor's mostly incorrect claim that "The pioneering neuroscientists of the 20th and 21st centuries — Wilder Penfield, Roger Sperry, Justine Sergent, Yair Pinto, Benjamin Libet, and many others — have shown that the brain is the source of five of these kinds of activities—physiological control (of heartbeat, breathing, etc.), locomotion, perception, memory, and emotion."

The Justine Sergent Link

The link Egnor gives is to the post here, which also discusses split brain operations, and mentions how neuroscientist Justine Sergent did some work following up on the "split brain" research of Roger Sperry, showing that two disconnected halves of a split-brain patient do not form connections reconnecting them.  The discussion does nothing to substantiate Egnor's mostly untrue claim that "The pioneering neuroscientists of the 20th and 21st centuries — Wilder Penfield, Roger Sperry, Justine Sergent, Yair Pinto, Benjamin Libet, and many others — have shown that the brain is the source of five of these kinds of activities—physiological control (of heartbeat, breathing, etc.), locomotion, perception, memory, and emotion."

The Yair Pinto Link

The link Egnor gives is to the post here, entitled "Split-Brain Research Confirms Unity of the Human Mind."  We read about how neuroscientist Yair Pinto did research further showing that split-brain patients retain a single unified mind. The discussion does nothing to substantiate Egnor's mostly untrue claim that "The pioneering neuroscientists of the 20th and 21st centuries — Wilder Penfield, Roger Sperry, Justine Sergent, Yair Pinto, Benjamin Libet, and many others — have shown that the brain is the source of five of these kinds of activities—physiological control (of heartbeat, breathing, etc.), locomotion, perception, memory, and emotion."

The Benjamin Libet Link

The link Egnor gives is to the page here, which does nothing to back up the mostly untrue claim quoted above. 

Egnor's Other Attempts to Show Brains Handle Memory

Egnor makes two other attempts to suggest brains handle memory.  He mentions Alzheimer's patients, saying "Alzheimer’s patients are quite conscious; what they lack is memory." Under the more severe understanding of the word "lack," this is a very bad misstatement. Alzheimer's patients are properly described as people with memory problems. The average Alzheimer's patient does have memory of various types, but performs more poorly than average in recalling and remembering (see the end of this post where I describe how by one measure they perform about 80% as well on average as normal people). Alzheimer’s patients do not show that memory is a brain process, because of the low correlation between brain damage and dementia. As I discuss in my post here, there is no convincing evidence that the brains of Alzheimer’s patients are more damaged or shrunken than the brains of people with  normal memory performance. And the brain plaques called a hallmark of Alzheimer’s are found abundantly in many millions of people with normal memory performance. 

Here is a quote from a book on dementia (you can find the quote using the link here and going to page 35):

lack of correlation between Alzheimers and brain damage

In  the paper here entitled "A Population-Based Clinicopathological Study in the Oldest-Old: The 90+ Study." we read this:

"Half of all non-demented participants (49%) and just over half of demented participants (57%) met pathological criteria for AD [Alzheimer's Disease], ... The pathologies examined to date failed to explain all dementia in this cohort, as almost one quarter (22%) of all demented participants did not have significant AD or any other pathology to explain their cognitive loss."

We see below a diagram from that paper showing the low link between dementia and brain pathology:

cause of Alzheimer's Disease

Egnor also makes this claim: "Similarly, bilateral hippocampal destruction by injury to the temporal lobes causes a catastrophic loss of ability to form new memories, but such patients are fully conscious." The claim is a myth of neuroscientists.  The neuroscience literature documents no case of a person  with "bilateral hippocampal destruction" by either surgery by injury who had a "catastrophic loss of ability to form new memories."  Claims that patient H.M. had such an inability to form new memories are untrue, as I document in my post here, where I cite quite a few cases of that patient learning new things after his injury and surgery. In that post I cite much research showing that damage to the hippocampus has little effect on the ability to form new memories.  One of the examples I quote in that post is that while the claim was made in the 1950's that patient H.M. could form no new memories, when patient H.M. was shown a Kennedy half-dollar in 1968, he stated that the man shown on it was President Kennedy, and that he had been assassinated (referring to the death of Kennedy that occurred in 1963). This is only one of many similar examples given in the paper here

Karl Lashley spent years doing experiments testing the cognitive effects of removing parts of the brains of animals, and was unable to find any "magic spot" crucial to memory. The screen shot below is from this page of a book on Lashley's research. We see a table comparing test performance on animals with different degrees of hippocampus damage. The animals with the most hippocampus damage (having "deep bilateral damage") performed as well as the animals with the least hippocampus damage. 

hippocampus damage effect on memory

Why "Brains Do Memory" Is Untenable

 In the post I have quoted Egnor seems to claim that memory is handled by the brain. There are many reasons why that cannot be correct. 

  • As shown in the many examples given herehereherehere and here, contrary to the predictions of "brains make minds" and "brains store memories" thinkers, human minds can operate very well despite tremendous damage to the brain, caused by injury, disease or surgery. For example, removing half of a person's brain in the operation known as hemispherectomy produces little change in memory or cognitive abilities. There have been quite a few cases of people (such as Lorber's patients) who were able to think and speak very well despite having lost more than 60% of their brain due to disease. Such cases argue powerfully that the human mind is not actually a product of the brain or an aspect of the brain, and is not a storage place of human memories. 

  • Although it is claimed that memories are stored in the brain (specifically in synapses), there is no place in the brain that is a plausible storage site for human memories that can last for 50 years or longer. The proteins that make up both synapses and dendritic spines are quite short-lived, being subject to very high molecular turnover which gives them an average lifetime of only a few weeks 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).  Both synapses and dendritic spines are a “shifting sands” substrate absolutely unsuitable for storing memories that last reliably for decades. Synapses are connected to dendritic spines, which have short lifetimesA 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). 

  • It is claimed that memories are stored in brains, but humans are able to instantly recall accurately very obscure items of knowledge and memories learned or experienced decades ago; and the brain seems to have none of the characteristics that would allow such a thing. The recall of an obscure memory from a brain would require some ability to access the exact location in the brain where such a memory was stored (such as the neurons near neuron# 8,124,412,242). But given the lack of any neuron coordinate system or any neuron position notation system or anything like an indexing system or addressing system in the brain, it would seem impossible for a brain to perform anything like such an instantaneous lookup of stored information from some exact spot in the brain.

  • If humans were storing their memories in brains, there would have to be a fantastically complex translation system (almost infinitely more complicated than the ASCII code or the genetic code) by which mental concepts, words and images are translated into neural states. But no trace of any such system has ever been found, no one has given a credible detailed theory of how it could work, and if it existed it would be a “miracle of design” that would be naturally inexplicable.

  • If human brains actually stored conceptual and experiential memories, the human brain would have to have both a write mechanism by which exact information can be precisely written, and a read mechanism by which exact information can be precisely read. The brain seems to have neither of these things. There is nothing in the brain similar to the “read-write” heads found in computers.

  • We know from our experience with computers the type of things that an information storage and retrieval system uses and requires. The human brain seems to have nothing like any of these things

  • As discussed here, humans can form new memories instantly, at a speed much faster than would be possible if we were using our brains to store such memories. It is typically claimed that memories are stored by “synapse strengthening” and protein synthesis, but such things do not work fast enough to explain the formation of memories that can occur instantly.

  • Contrary to the idea that human memories are stored in synapses, the density of synapses sharply decreases between childhood and early adulthood. We see no neural effect matching the growth of learned memories in human.

  • There are many humans with either exceptional memory abilities (such as those with hyperthymesia who can recall every day of their adulthood) or exceptional thinking abilities (such as savants with blazing-fast calculation abilities). But such cases do not involve larger brains, very often involve completely ordinary brains, and quite often involve damaged brains, quite to the contrary of what we would expect from the “brains make minds” assumption and the "brains store memories" assumption. 

  • For decades microscopes have been powerful enough to detect memories in brains, if memories existed in brains. Very much brain tissue has been studied by the most powerful microscopes: both brain tissue extracting from living patients, and brain tissue extracted from someone very soon after he died. Very many thousands of brains have been examined soon after death.  Microscopes now allow us to see very clearly what is in the tiniest brain structures such as dendritic spines and synapse heads. But microscopic examination of brain tissue has failed to reveal any trace whatsoever of learned information in a brain.  No one has found a single letter of the alphabet stored in a brain; no has found a single number stored in a brain; and no one has ever found even a single pixel of something someone saw a day or more before.  If memories were stored in human brains, microscopes would have revealed decisive evidence of such a thing decades ago.  But no such evidence has appeared. 

  • There is nothing in the brain that looks like learned information stored according to some systematic format that humans understand or do not understand. Even when scientists cannot figure out a code used to store information, they often can detect hallmarks of encoded information. For example, long before Europeans were able to decipher how hieroglyphics worked, they were able to see a repetition of symbolic tokens that persuaded them that some type of coding system was being used. Nothing like that can be seen in the brain. We see zero signs that synapses or dendritic spines are any such things as encoded information. 
  • Many humans can remember with perfect accuracy very long bodies of text, such as hundreds of pages; but synapses in the brain do not reliably transmit information. An individual chemical synapse transmits an action potential with a reliability of only 50% or less, as little as 10%. A recall of long bodies of text would require a traversal of very many chemical synapses. A 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." Moreover, the brain lacks any physical structure consistent with an ability to store very long sequences of information, as I discuss here.
  • Humans often form vivid new memories while humans are having near-death experiences taking place during cardiac arrest, when the brain has shut down, showing only flatlines of electrical activity. That brain state is called asystole, and it occurs within about 10 to 20 seconds after the heart stops.  If memories are created by the brain, the formation of new memories should be impossible while the brain is electrically inactive. But we know that very vivid and detailed memories can form during such states of brain electrical inactivity. That would not be possible if memory formation is a brain activity. Moreover, during near-death experiences occurring asystole, people do not find themselves as minds without memories. They find themselves as the same selves with the same memories. There are endless accounts along the lines of this: "Suddenly I was floating outside of my body, and could see it beneath me. Later I saw my deceased mother." No such experiences would occur if a soul lacking memory powers were to persist after the heart stopped and brain waves stopped.  In that case there would be no memory recall, and no memory formation. 
Oddly in a 2024 post Egnor had sounded like someone on the verge of ditching the claim that memories are stored in the brain. But in the post I have quoted above he sounds more like someone who can't ditch the old "brains form memories" doctrine. He should read some of the posts on this blog to learn more about why the old "brains form memories" doctrine fails all over the place. Looking through a series of many posts Egnor has published on the Evolution News site, I find a thinker who has many intelligent things to say about minds and brains, but someone who apparently has not given the topic of memory the extremely thorough study and analysis that someone should give  before lecturing us on its source. 

Below we have an old newspaper account of a person named John Bly, whose "retention of memory was remarkable" even though he had almost no brain because of a five-inch brain abscess filled with pus. Along with the case of the French civil servant with almost no brain but apparently good memory, this case shows the untruth of claims that a hippocampus is necessary for memory. See the post here to find the original source. 

good memory with bad brain

Michael Egnor has made some notable progress in moving away from some of the brain dogmas he was indoctrinated in while studying for his qualifications. To make further progress, he should study and ponder the topic of memory much more carefully and deeply, paying particular attention to the very important topic of brain physical shortfalls (discussed here), the very important topic of particular people with vastly above average memory abilities (discussed in the post here and the series of posts here), and the topic of the preservation of memory after very bad brain damage (discussed in posts such as the one here).  Brain physical shortfalls (the physical shortcomings of all human brains) tell us just as strongly that brains do not handle memory storage and retrieval as they tell us that brains are not the source of our selves and thinking.  

The MMSE test seems to be the main test used for dementia or cognitive impairment. You can get a score between 0 and 30 on the test, and any score of 25 or higher is considered "normal." It must be remembered that every single time a person answers one of the questions on the test correctly, that is a demonstration of some memory ability -- because any ability to recognize or use language requires some memory skill, skills such as recognition (of words heard) or recall of the correct words you need to use to state a correct answer.   

The scientific paper "Word retrieval in connected speech in Alzheimer’s disease: a review with meta-analyses" has a Table 1 that shows the MMSE scores for more than 1100  Alzheimer’s disease patients, collected from more than 50 different studies. Page 10 of the paper tells us that the average MMSE score for those with Alzheimer's disease (AD) was 19.07, and that the median was also about 19 (18.95). 

Although definitely an indication that Alzheimer's involves some memory difficulty, this data shows what a glaring error it is to speak about such people by saying, "Alzheimer’s patients are quite conscious; what they lack is memory," as Egnor did.  To the contrary, every single score above 0 on the MMSE is an indication that some memory ability still exists;  and data showing that Alzheimer's patients score an average of about 19 on this test (which has a maximum score of 30) suggests that on average those with Alzheimer's have most of the memory skill that they had in their prime. 

Similar data is found in Table 1 of the paper here, entitled "Brain-age predicts subsequent dementia in memory clinic patients."  We have cognitive performance data on 664 patients classified as "non-dementia," and 476 patients classified with "dementia."  The average MMSE score for those with dementia (about 22 out of 30) is almost as high as the average MMSE score for those classified as "non-dementia," a score of about 24. It would be very wrong to say those classified with dementia were "lacking memory," as you need quite a lot of memory skills to score 22 out of 30 on the MMSE test. The table also gives us figures for brain volume for both groups, and the brain volume for those classified with "dementia" is only slightly less than those classified as "non-dementia." Figure 3 of the paper is the scatter plot below, which tells us no clear tale about any clear relation between "brain age" (largely how much of your brain was loss to atrophy) and whether or not you will have dementia.

brain age for those with dementia

Monday, March 31, 2025

Anomaly Aversion Greatly Hurts Mind Cause Analysis and Medicine Side Effect Analysis

"The past three decades have shown that psychiatry’s medical vision is neither scientifically credible nor morally sound." -- Justin Garson, professor of philosophy at Hunter College (link) 

The Mad in America site (www.madinamerica.com) is a good site for getting contrarian opinion and analysis on the topic of psychiatric treatment.  On the day I am writing this post I will schedule for later publication, there is an interesting article on the site, one entitled "The Iatrogenic Gaze: How We Forgot That Psychiatry Could Be Harmful." The article by Alex Conway is a troubling portrait of psychiatrists who fail to do their job properly because they are doing too much avoiding, downplaying and ignoring reports of anomalies. The anomalies are side effects reported by people using the medicines prescribed by the psychiatrists, reports of side effects that are not on official lists of possible side effects of a drug. 

Normally when a drug is approved by a regulatory group such as the FDA, there is published an official list of common side effects, along with a list of rare side effects. But what happens when someone prescribed that drug reports a side effect not on such a list? The authority receiving such a report may treat such a report as an anomaly to be shunned, ignored or explained away.  In the article we read this chilling report of someone subjected to the most harmful gaslighting after she reported a side effect of a medicine:

" The doctor diagnosed her with a delusional disorder. Her medical records state: 'Firm fixed delusional belief about medications causing side effects… Impression: delusional disorder with significant health anxiety and OCD with comorbid depressive symptoms.'  Rosie was then committed against her will to a psychiatric facility and forced to take medication for her 'delusions'. Four years later, Rosie still suffers the same symptoms."

We read this:

"Drug Injuries are a piece of a wider problem known as iatrogenesis (doctor-made illness). Although drug injuries are virtually absent from public discourse, available research considers them a leading health risk. A 2018 paper examined FDA data on adverse drug events (ADEs) and found a rate of over 100,000 serious injuries per year. That rate has been increasing rapidly: 'From 2006 to 2014, the number of serious ADEs reported to the FDA increased 2-fold… A previously published study… found that from 1998 to 2005, there was a 2.6-fold increase in the reports of serious ADEs and a 2.7-fold increase in the reports of fatal ADEs'. It seems that the rate of serious drug injury is doubling per decade."

The article is very long-winded, and it is hard to quote a few choice lines or a paragraph to give its main idea. I can try to summarize it like this:

(1)  Psychiatrists are taught a kind of dogma about effects of the drugs they prescribe, including the idea that they only have a certain number of things called "side effects." 

(2) Patients often report what they believe are bad effects from taking such drugs, describing negative effects that are not on such a list of "side effects." 

(3) Psychiatrists receiving such reports go into "explain it away" mode, which may consist of various techniques such as assuring the patient he is mistaken, or in the worst case, recording the patient as having a delusion or some type of mental disorder because he made a report contrary to the dogma the psychiatrist was taught. 

After reading the article, I thought to myself: "That rather rings a bell." The kind of dogmatism, gaslighting and anomaly aversion reported reminded me of what goes on when mainstream scientists receive reports of the paranormal, such as reports of apparitions, near-death experiences, telepathy, clairvoyance, and so forth.  

I can describe a type of anomaly aversion that occurs with neuroscientists and other types of scientists:

(1)  Scientists are taught a kind of dogma about what mental powers or mental experiences are possible, dogma that is based on the idea that all mental experiences come from the brain and the senses.  

(2) Humans often report experiences conflicting with such dogma, describing events such as apparition sightings, near-death experiences, out-of-body experiences, ESP, clairvoyance, and other phenomena that cannot be explained by brain explanations. 

(3) Scientists receiving such reports go into "explain it away" mode, which may consist of various techniques such as telling the person making the report that he is mistaken, or in worse cases, trying to  insinuate that the witness was hallucinating or lying. 

Below is a comparison of similar behavior in two types of professionals:

anomaly aversion

Anomaly aversion and ignoring reported anomalies greatly hurts the proper study of medicine side effects. Anomaly aversion and ignoring reported anomalies also greatly hurts the proper consideration of what causes the human mind. All reports of human experiences that cannot be explained by the "brains make minds" dogma should be studied with great care. Such reports should be collected, preserved, classified, pondered and analyzed.  Ignoring such reports is the opposite of good scientific practice. 

The AI art visual below depicts scientific censorship in a visually memorable way:


When mainstream scientists repress observations of the paranormal, they don't act in such a visually noticeable way. Instead, they act in just as repressive and suppressive a way, but in ways that are not visually noticeable:
  • They refuse to include in their textbooks and papers a discussion of important observations of the anomalous and inexplicable.
  • They refuse to include in their class lessons a discussion of important observations of the anomalous and inexplicable.
  • When acting as peer reviewers and editors, they act to suppress the publication of other scholars fairly reporting on observations of the paranormal. 
  • In the rare times they discuss the paranormal, they typically make inaccurate generalizations about the quality of evidence for some paranormal phenomena. 
  • They refuse to approve funding for the further investigation of types of paranormal phenomena that have been well-established as highly worthy of further investigation. 
  • In the rare times they discuss particular reports of the paranormal, mainstream scientists use gaslighting and unfair characterization to undermine witnesses of the paranormal, and use selective reporting and distortion to make very compelling evidence sound like it is weak evidence.
gaslighting

gaslighting
Examples of gaslighting

dumb professor and smart professor


dumb professor and smart professor

Thursday, March 27, 2025

Neuroscientists Offer Only the Most Hazy Hand-Waving When Trying to Explain Memory

"Scientific journals have reported cases of persons whose injuries have necessitated the removal of a large portion of the brain, and whose memory and power of thought were unimpaired by the loss of much cerebral matter, or by damage to centers which are supposed to be necessary to memory and consciousness. Dr. Troude writes:  'As M. Bergson foresaw in 1897, the hypothesis of the brain as conservative of memory images, must be renounced once and for all, and other ideas as to the nature of its role in the act of memory must be accepted. ' "

--- Helen C. Lambert, A General Survey of Psychical Phenomena, p. 49.

Dictionary.com defines "hand waving" as "insubstantial words, arguments, gestures, or actions used in an attempt to explain or persuade." When neuroscientists attempt to explain memory by referring to the brain, they offer only the most hazy hand-waving. Typically what occurs is the repetition of empty slogans and catchphrases.  

standard neuroscientist account

For example, a neuroscientist may claim that memories are formed by "synapse strengthening." There is no substance in this claim, which is mere hand-waving. We have many examples of the storage of knowledge in human-made things such as books, drawings, computer files, messages, handwritten notes and electronic data.  Such knowledge storage never occurs through strengthening.  Instead what typically happens when knowledge is stored in books, films, messages, notes and computer files is that there occurs a repetition of symbolic tokens by some kind of writing process, and the use of some encoding system in which certain combinations of symbolic tokens represent particular words, things or ideas.  That is not strengthening.  

To give another example of empty hazy hand-waving, a neuroscientist may vaguely claim that memories are formed by "the formation of synaptic patterns." There is no substance in this claim, which is mere hand-waving.  It is possible to store information by the use of pattern repetitions. For example, you might consider each word in the English language as a pixel pattern, and then say that each use of the word "dog" in a printed book is a pattern repetition. But synapses do not form any recognizable repeating patterns. And if synapses did form such patterns, there would need to exist some synapse pattern reader to read and recognize such patterns; but no such thing exists.  Instead of being anything that could consist of stable repeating patterns, synapses are unstable "shifting sands" kind of things. Synapses are built from proteins that have an average lifetime of only two weeks or less.  The maximum length of time that humans can remember things (more than 50 years) is 1000 times longer than the average lifetime of the proteins in a synapse. So synapses cannot be the storage place of memories that can last reliably for so long. 

Last year we had an example of the type of empty hazy hand-waving that occurs when neuroscientists attempt to explain memory. It was a paper entitled "Consciousness” as a Fusion of the Global Neuronal Network (GNW) Hypothesis and the Tripartite Mechanism of Memory." The paper made quite a few uses of the word "mechanism" but it described no memory mechanism at all. All we got was the most hazy hand-waving. 

I may note that biologists are notorious for abusing the term "mechanism," and often claim to be describing "mechanisms" when they are discussing no such things.  The term "mechanism" is only properly used for an exact description of material things working closely together in time and space. The pumping of blood by the heart and the circulation of blood in the body is an example of a mechanism. But when you are describing things that are not closely working together in a mechanical way, you have no business using the term "mechanism." It is a glaring abuse of language to refer to so-called "natural selection" as a mechanism of evolution, given that the main imagined things (random mutations scattered across vastly separated times and places) are not anything like a mechanism. 

We have in the paper a section entitled "Evolving Memory Mechanism" which fails to describe any mechanism, giving us only the most hazy hand-waving. Then we have a section entitled "Tripartite Mechanism of Emotive Memory" which states only this:

"For the neural emotive memory, we proposed that the cognitive unit of information (cuinfo) is realized materially (sic. chemically [13,28,29]. Thus, a chemically based code permits the achievement of an emotive state instigated by neurotransmitters (NTs) released by neurons/glial cells and the recall of such [1-11]. The proposed tripartite mechanism for encoding memory involves the interactions of neurons with their surrounding extracellular matrix (nECM/PNN). It has been experimentally verified that neurons are not 'naked', but are enshrouded in a web of glycoaminoglycans [44-49] which we propose serves as a 'memory material' [13,28,29]. Incoming perceptions are encoded with trace metals +neurotransmitters (NTs) to form metal-centered cognitive units of information (cuinfo). We have developed a chemographic notation for the tripartite mechanism which captures the essence of this regarding emotive memory (Figure 2)."

This is merely the most hazy hand-waving, decorated by some references to neural anatomy, along with the tiniest sprinkling of chemistry jargon. The Figure 2 referred to is utterly unimpressive. It merely shows a few circles that are labeled as "cations." We have a groundless reference to "addresses" that is not justified. The brain has no actual addresses anywhere in it. The lack of addresses in the brain is one of the major reasons why there can be no credible theory of instant recall occurring by brain activity. Addresses, sorting and indexes are some of the things used by devices human manufacture to allow them to instantly retrieve information. But brains have no addresses, no sorting and no indexes. References 13, 28 and 29 in the quote refers to papers here and here and here, which are not  papers referring to biological memory storage, but papers referring to some type of electronic memory storage in human-made devices. Our authors have vaguely referred to some type of chemical as being a "memory material," and have supplied only references to papers not referring to biology, giving us the incorrect impression that there is some biological foundation for their vague reference. 

We read this conceptually empty piece of hazy hand-waving:

"In a binary-formatted computer memory, the individual bits (or bytes) are stored in a matrix. But comprehensive memory results from the collective activity of a group of neurons, not only from the cuinfo of an individual neuron. Thus, a working model of how the brain generates emotive memory needs to meld physiologic effects with electro-biochemical processes. The GNW hypothesis suggests a 'brain cloud' that permits the neural net to consolidate the contribution of individual neurons in different anatomic compartments into comprehensive recall, effectively an integration of units of dispersed units of cognitive information [52]." 

This does not describe a mechanism, and does not contain any specifics. Next to this hand-waving paragraph, we are given a diagram that fails to depict any specific theory of memory.  The diagram is below:

neuroscientist hand-waving

There is no substance here. The gray circles merely represent regions of the brain. The little "c" squares represent memories that the authors claim are stored in the brain. This isn't a depiction of a memory, nor is it a depiction of any real theory of neural storage of memories. All that we have represented is the vague idea of a brain storing memories. 

In their Conclusion section, we have nothing that summarizes any actual theory of brain memory storage or brain memory recall or brain memory preservation.  Three times in the section the authors claim to have described a mechanism, but no such mechanism was described. All that has gone on is a claim of memory storage, and some references to different parts of the brain, sprinkled with the tiniest bit of chemistry jargon (by use of the word cation).  Nothing but the haziest hand-waving has gone on here. 

And so it is throughout neuroscience literature. You will never find a single paper that even attempts to give a precise description of how a brain could store the simplest bit of knowledge such as "my dog has fleas." Another example of the empty hand-waving of neuroscientists in regard to memory can be found in the paper here, entitled "Why not connectomics?" We have this example of conceptually empty hand-waving about memory storage:

"Brains can encode experiences and learned skills in a form that persists for decades or longer. The physical instantiation of such stable traces of activity is not known, but it seems likely to us that they are embodied in the same way intrinsic behaviors (such as reflexes) are: that is, in the specific pattern of connections between nerve cells. In this view, experience alters connections between nerve cells to record a memory for later recall. Both the sensory experience that lays down a memory and its later recall are indeed trains of action potentials, but in-between, and persisting for long periods, is a stable physical structural entity that holds that memory. In this sense, a map of all the things the brain has put to memory is found in the structure—the connectional map."

The first sentence is groundless dogma. There is no evidence that brains "can encode experiences and learned skills in a form that persists for decades or longer."  There is merely the fact that humans can have experiences and learn skills that they remember for decades.  The second sentence is a confession that there is no understanding of how such a brain storage of memories can happen. The authors confess that "the physical instantiation of such stable traces of activity is not known,"  The claim that memories are stored by "the specific pattern of connections between nerve cells" is empty hand-waving, and the speculation stated is unbelievable. No one who has ever studied the connections between nerve cells (neurons) has ever seen anything like some symbolic pattern that could encode a record of human experiences or human learned skills or learned conceptual knowledge such as school learning.  The brain does not have any such thing as a connection pattern reader that could read and interpret such patterns if they existed. Moreover, the connections between brains are structural units too short-lived to explain human memories that reliably persist for decades. Synapses and the dendritic spines they connect to do not last for years, and the proteins they are made of have average lifetimes of only a few weeks. 

neuroscientist hand waving

Sunday, March 23, 2025

Y-Maze Memory Tests Are Almost as Unreliable as Freezing Behavior Tests

It cannot be said that the reliability of an experimental neuroscience paper is directly proportional to the reliability of measurement techniques it uses. There are various reasons why you might have an utterly unreliable neuroscience experiment that used reliable measurement techniques, such as the reason that the experiment may have used too-small a study group size to have produced a reliable result. But it can be said (roughly speaking) that the unreliability of an experimental neuroscience paper is directly proportional to the unreliability of any measurement techniques upon which the experiment depends. That is why when examining neuroscience experiments, we should always pay extremely close attention to whether the experiment used reliable measurement techniques. 

For decades very many neuroscience researchers have been senselessly using a ridiculously unreliable measurement technique: the case of "freezing behavior" estimations. "Freezing behavior" estimations occur in scientific experiments involving memory. "Freezing behavior" judgments work like this:

(1) A rodent is trained to fear some particular stimulus, such as a red-colored shock plate in his cage. 

(2)  At some later time (maybe days later) the same rodent is placed in a cage that has the stimulus that previously provoked fear (such as the shock plate). 

(3) Someone (or perhaps some software) attempts to judge what percent of a certain length of time (such as 30 seconds or 60 seconds or maybe even four minutes) the rodent is immobile after being placed in the cage. Immobility of the rodent is interpreted as "freezing behavior" in which the rodent is "frozen in fear" because it remembered the fear-causing stimulus such as the shock plate. The percentage of time the rodent is immobile is interpreted as a measurement of how strongly the rodent remembers the fear stimulus. 

This is a ridiculously subjective and inaccurate way of measuring whether a rodent remembers the fear stimulus. There are numerous problems with this technique, which I explain in my post " All Papers Relying on Rodent 'Freezing Behavior' Estimations Are Junk Science." The technique is so unreliable that all experimental neuroscience studies relying on such a technique should be dismissed as worthless. 

There are other techniques used in neuroscience experiments. There are various types of maze techniques used.  A mouse may be trained to find some food that requires traversing a particular maze. It is easy to time exactly how long the mouse takes to find the food, after a series of training trials.  Then some modification might be made to the mouse (such as giving it an injection or removing part of its brain). The mouse can be put again in the maze, and a measurement can be made of how long it takes to find the food. It if took much longer to find the food, this might be evidence of a reduction in memory or learned knowledge. 

mouse and maze

This seems like a pretty reliable technique. But there's another much less reliable technique called the "free exploratory paradigm." When this technique is used, a mouse is given some compartments to explore. The mouse is first only allowed to explore half or two-thirds of the compartments.  Then later the mouse is given the freedom to explore all of the compartments, including previously unexplored compartments.  Some attempt is made to measure what percent of the time the mouse spends in the never-previously-explored compartments compared to the previously explored compartments. 

A figure in the paper "The free-exploratory paradigm as a model of trait anxiety in rats: Test–retest reliability" shows how this method might be used.  First the mouse is allowed to explore only the three compartments on the right, with access to the left compartments blocked. Then the mouse is allowed to access all of the compartments, and some attempt is made to judge whether the mouse spent more time in the left compartments than the right. 

The assumption is made that this can be some kind of test of memory. The experiment designers seem to have assumed that when a mouse goes to compartments already visited, the mouse will kind of recognize those compartments, and be less likely to explore them, perhaps having some kind of "I need not explore something I've already explored" experience. This is a very dubious assumption. 

It's as if the designers of this apparatus were assuming that a mouse is thinking something like this:

"My, my, these experimenter guys have given me six compartments to explore!  Well, there's no point in exploring any of the three compartments I already explored.  Been there, done that. So I guess I'll spend more time exploring the compartments I have not been to. I'm sure there will just be exactly the same stuff in the three compartments I've already explored, and that I need not spend any time re-exploring them to check whether there's something new in them." 

The assumptions behind this experimental design seem very dubious. It is not at all clear that a mouse would have any such tendency to recognize previous compartments the mouse had been in, and to think that such previously visited compartments were less worthy of exploration. 

The best way to test whether such assumptions are correct is by experimentation. Without doing anything to modify a mouse's memory, you can simply test normal mice, and see whether they are less likely to spend time in compartments they previously visited. Figure 2 of the paper "The free-exploratory paradigm as a model of trait anxiety in rats: Test–retest reliability" gives us a good graph testing how reliable this "free-exploratory paradigm" is, using a 10-minute observation period. The test involved 30 mice:

The figure suggests that this "free-exploratory paradigm" is not a very reliable technique for judging whether mice remembered something. In the first test, there was no tendency of the mice to spend more time exploring the unexplored compartments. In the second test there was only a slightly greater tendency of the mice to explore the previously unexplored compartments. Overall the mice spent only 55 percent of their time in the previously unexplored compartments, versus 45 percent of their time in the previously explored compartments. 

What is the relevance of this? It means that any neuroscience experiment that is based on this "free-exploratory paradigm" and fails to use a very large study group size is worthless.  An example of a worthless study based on such a technique is the study hailed by a press release this year, one with a headline of "Boosting brain’s waste removal system improves memory in old mice." No good evidence for any such thing was produced. 

The press release is promoting a study called "Meningeal lymphatics-microglia axis regulates synaptic physiology" which you can read here. That study all hinges upon an attempt to measure recall or recognition by mice, using something called a Y-maze, which consists of 3 compartments, the overall structure being shaped like the letter Y. The Y-maze (not actually a maze) is an implementation of the unreliable "free-exploratory paradigm"  measurement technique described above.  The study used a study group size of only 17 mice. But since the "free-exploratory paradigm" requires study group sizes much larger than 17 to provide any compelling evidence for anything, the study utterly fails as reliable evidence. 

Using a binomial probability calculator, we can compute the chance of getting a false alarm, using a measurement technique like the  "free-exploratory paradigm." Figure 1C of the paper "Meningeal lymphatics-microglia axis regulates synaptic physiology" shows only a very slight difference between the "free-exploratory paradigm" performance for the modified mice and the unmodified mice:

Given this "free-exploratory paradigm" that is something like only 55% effective in measuring recognition memory, the probability of getting results like this by chance (even if the experimental intervention has no real effect) is roughly the same as what we see in the calculation below:

Produced using the calculator here

The chance of getting purely by chance a result like the result reported in the paper is roughly the 1 in 3 shown in the bottom line above. When we consider publication bias and the "file drawer" effect, getting a result like the reported result means nothing. Why? Because it would be merely necessary to try the experiment a few times before you could report a success, even if the experimental intervention had no effectiveness whatsoever. 

We should never be persuaded by results like this, because what could easily be happening is something like this:

  • Team 1 at some college tries this intervention, seeing no effect. Realizing null results are hard to get published, Team 1 files its results in its file drawer. 
  • Team 2 at some other college tries this intervention, seeing no effect. Realizing null results are hard to get published, Team 2 files its results in its file drawer. 
  • Team 3 tries this intervention, seeing a "statistically significant" effect of a type you would get in maybe 1 time in three tries. Team 3 submits its positive result for publication, and gets a paper published. 
In a scenario like the one above, there is no real evidence for the effect. All that is happening is a result like what we would expect to get by chance, even if the effect does not exist. 

What we must also consider is that any researcher wanting to tilt the scales a bit can do so when using this free-exploratory paradigm. When these type of experiments are done, the compartments are not empty. Instead some items are put in the compartments.  There is no standard protocol about what is put in the compartments. A researcher can put in the compartments anything he wants. Each compartment is supposed to have a few items, but there is no standard number or size of items to use. So imagine you are trying to show what looks like a loss of memory recognition in some experiment using this free-exploratory paradigm.  All you need to do is put some less interesting items or fewer items in the unexplored compartments. And if you want to show what looks like an improvement in memory, you need merely put some more interesting items or more items in the  unexplored compartments. Since there is no standard protocol used using this free-exploratory paradigm, an experimenter can get whatever result he wants, by varying conditions in the compartments. 

At the top I give a graph from the the paper "The free-exploratory paradigm as a model of trait anxiety in rats: Test–retest reliability," which showed a mere 55% reliability using this free-exploratory paradigm in ten minute tests, but a greater reliability with 15 minute tests. How long a time length does the paper "Meningeal lymphatics-microglia axis regulates synaptic physiology" use? Only 2 or 3 minutes. I doubt very much that there is any evidence that such tests have much more than 50% reliability with such a short time span. This is a common defect of both the free-exploratory paradigm and the "freezing behavior" approach: they can produce wildly different results depending on the time interval used. And since there is no standard for a time interval used, an experimenter can use any time interval, including some interval that has not been verified as having any decent reliability. This is all the more reason to think that such methods are "see whatever you are hoping to see" affairs that have no validity as solid measurement techniques for measuring recall or recognition in rodents. I can imagine how things might work: an animal may be tested for 10 minutes using either technique; and if the experimenter doesn't like the result in the full ten minutes, he can simply report in his paper on the first 5 minutes; and if he does not like that result, he can report in his paper on only the first three minutes; and so on and so forth. If the paper is not a pre-registered paper committing itself to an exact detailed observational protocol, an experimenter can get away with that; and few neuroscience experiments these days follow such a pre-registered approach. Today's experimental neuroscience is such a standard-weak freewheeling farce of loose and bad methods that it is probably considered permissible to gather a particular type of data for ten minutes, and then report on only the results gathered in any arbitrary fraction of those minutes, as long as you start from the beginning. 

In the paper here, it says, "In the Y-maze
continuous procedure, the rat or mouse is placed in the maze for a
defined period (typically 5 min) and the sequence of arm choices
is recorded." But in the paper "Meningeal lymphatics-microglia axis regulates synaptic physiology" discussed above, the Y-maze test time was only 3 minutes; so we have a deviation from the typical procedure with this device. The same paper tells us "Hippocampectomized animals notoriously adopt side preferences, e.g., always turning right on a T-maze," something we can suspect may also be true in a Y-maze, giving another reason for doubting the suitability of such tests (both examples of the free exploratory paradigm) for testing memory modifications such as hippocampus lesions. 

The sad truth is that experiments done with this free-exploratory paradigm (such as a Y-maze experiment or a T-maze experiment) are worthless unless they use large study group sizes of at least 30 subjects per study group, and also an exact protocol that has been proven to be a reliable method of measuring recall or recognition in rodents. So we can have no confidence in the results reported by the  study referred to above, the one called "Meningeal lymphatics-microglia axis regulates synaptic physiology" which you can read here. That study all hinges upon an attempt to measure recall or recognition using the free exploratory paradigm, but does not use a large enough study group size to produce a reliable result using that paradigm. And we have no evidence of exactly following a precise protocol proven to be a reliable measure of rodent recall. 

Neither the free-exploratory paradigm (such as Y-maze experiments) nor "freezing behavior" experiments produce reliable results when anyone uses study group sizes smaller than 30. Both are poor, unreliable ways of measuring recall or recognition in rodents, allowing so much flexibility and opportunity for bias that it's just a "see whatever you want to see" type of affair. But what kind of methods tend to produce good, reliable results in measuring recall in rodents? I can think of four:

(1) A "find the food reward" maze technique like the one described above, in which you measure how many seconds a rodent takes to find a food reward, using a maze the rodent had been previously trained on to find a food reward. 
(2) The Morris water maze test, a widely used test that is not really a maze test, but a test of how well a rodent will remember to find a submerged platform after previously being trained to find that platform in a water tank. However a scientific paper cautions that the Morris water maze test may not work well with many strain of mice, saying this: "Neuroscientists have been warned that many strains [of mice] perform poorly on the submerged-platform water escape test task, which is better suited to rats than to mice, yet it is used widely for the study of memory in mice."  Another paper gives  a similar reason for thinking that the Morris water maze test (MWM) may only be suitable for rats, stating this: "Interestingly, when MWM data were analyzed in a large dataset of 1500 mice by factor analysis, the principle factors
affecting MWM performance in mice were noncognitive
(Lipp and Wolfer 1998).... It is important to note
that this is not the case in rats, but the fact that performance
factors are salient in mice provides an important cautionary
note when interpreting mouse MWM data." 
(3) A fear recall technique, measuring spikes in heart rate. The heart rate of a mouse will very dramatically spike when the mouse is afraid. So a mouse can be trained to fear some painful stimulus such as a shock plate. Then the mouse can be placed in a cage that has the fear-inducing stimulus. If the mouse's heart rate speeds up very much, that is good evidence that the mouse has remembered the fear-inducing stimulus such as the shock plate. 
(4) The Fear Stimulus Avoidance technique depicted below, which does not require heart-rate measurement. After being trained to fear some fearful stimulus such as a shock plate, the mouse can be placed in a cage that offers two paths to a food reward: one path that requires going through the fearful stimulus such as a shock plate, and another other path to the food reward that is physically much harder to traverse, such as a path requiring climbing steep stairs. If a rodent takes the much harder path to get to the food reward, that is good evidence that it remembered the pain caused by the fearful stimulus such as the shock plate. 

good way to measure recall in rodents

The mere use of a more reliable measurement technique does not guarantee a reliable result. While the Morris water maze test seems to be a reliable test when used with rats, it must be used with a big enough study group size, and very many neuroscience experimenters fail to do that. A paper notes the problem, stating this about the Morris Water Maze test (MWM):

"Many MWM experiments are reported with small group sizes. In our experience with the MWM and other water mazes, group sizes less than 10 can be unreliable and we use 15 to 20 animals per group, especially for mice, whose performance in learning and memory tests tends to be more variable than for rats. It is noteworthy that regulatory authorities require that safety studies have 20 or 25 animals per group. This number is for each of at least four groups (control and three dose levels) (Food and Drug Administration 2007; Gad 2009; Tyl and Marr 2012). Such group sizes are used by the US Environmental Protection Agency, the US Food and Drug Administration, the Organization for Economic Cooperation and Development, and Japanese and European Union regulatory agencies. Although the 3 Rs (reduce, refine, and replace) are worthwhile goals in the use of animals in research, it is not a justification to underpower experiments and run the risk of false positives, which, in the long run, cost more time, more animals, and more money to prove or disprove."

Postscript:  The term "spontaneous alternation behavior" is used to describe a case in which a rodent that has explored one arm of a T-maze or Y-maze is exposed to the maze again, and switches to a different arm. The higher the average "spontaneous alternation percentage" is (the higher above 50%) in control rodents, the more reliable such a T-maze or Y-maze is as a test of memory; and a well-established average "spontaneous alternation percentage" of maybe 75% would indicate a pretty good test. The graph here shows female controls showing such behavior only 55% of the time, and male controls showing such behavior 60% of the time; but the sample size is only 5.  Figure 4 of the paper here shows control rats using such "spontaneous alternation behavior" only 50% of the time in a Y-maze. The sample size is only 6. The graph here shows only about 60% "spontaneous alternation behavior" for 9 control rodents tested with a Y-maze. Figure 3 of the paper here shows male control rodents showing such "spontaneous alternation behavior" only about 50% of the time.  Figure 1 of the paper here shows a "spontaneous alternation percentage" of only about 57% for 6 control mice. In Figure 1 of the paper here, the "spontaneous alternation percentage" is only 35% in control rodents. These results are consistent with my claim above that such tests are not-very-reliable tests requiring large study group sizes to produce even borderline, modest evidence of a memory effect. 

The problem with a measurement technique that only gives you the right answer about 60% of the time is that when using such a technique it is really easy to get false alarms, particularly with small study group sizes. So you have no basis for strong confidence in some study testing only about 15 rats using a T-maze or a Y-maze.