Once Again, the Nobel Prize Organization Blunders

 My 2018 post "'Nobel's Razor' as a Rule of Thumb for Judging Science Claims" rather naively suggested a "rule of thumb" for judging whether something is top-notch well-established science, a rule based on whether some scientific claim or research has won a Nobel Prize. At the time I wrote that post in 2018, I was not aware of some cases of the Nobel Prize committee bungling in its granting of awards, and bungling in its statements announcing awards, cases I have since learned about, some of which I describe in my 2024 post here and my 2025 post here. I have now added at the end of that 2018 post a statement retracting my claim that we should trust any research that has won a Nobel Prize, and modifying my recommendation, suggesting that such a "Nobel's Razor" principle works as only a very rough rule of thumb, with there  being notable exceptions. 

I now regard the awarding the Nobel Prizes with significantly greater skepticism than I had in 2018. I have come to realize that the awarding of a Nobel Prize (along with the announcements of such prizes) may often be part of the social construction of some unfounded triumphal legend that serves the misguided agenda of materialists. Let us look at some Nobel Prize awards that should not have been awarded, or that were accompanied by incorrect statements by a Nobel Prize committee when the award was made. 

• In 2014 a Nobel Prize committee made the big mistake of awarding a Nobel Prize in Medicine and Physiology to John O'Keefe, May-Britt Moser and Edvard I. Moser "for their discoveries of cells that constitute a positioning system in the brain."  There is no robust evidence that any such positioning system exists in the brain. The reference to cells is a reference to cells that are wrongly referred to as "place cells" (a catchy cell nickname that went viral).  My post here discusses how the research of these three failed to provide any good evidence for place cells or a navigation system in the brain. The original "place cell" papers of John O'Keefe are badly guilty of Questionable Research Practices such as the use of way-too-small study group sizes. For example, a 1993 paper co-authored by O'Keefe was entitled "Phase Relationship Between Hippocampal Place Units and the EEG Theta Rhythm." The paper used way-too-small study group sizes of only three rats and two rats.  No blinding protocol was used, and the paper was not a pre-registered study. We have some wavy-line analysis that seems extremely subjective and arbitrary. To give another example, a 2008 paper co-authored by O'Keefe was entitled "The boundary vector cell model of place cell firing and spatial memory." The paper used a way-too-small study group size of only two rats. No blinding protocol was used, and the paper was not a pre-registered study. Scientists claiming "place cells" in the brain are guilty of "see what you hoped to see" pareidolia that is a kind of "seeing Jesus in the toast" affair. 
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• A Nobel Prize organization made the big mistake of giving Christian Anfinsen the Nobel Prize in Chemistry in 1972.  The 2022 paper "The Anfinsen Dogma: Intriguing Details Sixty-Five Years Later" tried to reproduce Anfinsen's experiment that got him that prize, but was unable to reproduce them.  That paper tells us about some of the false claims made about Anfinsen's work. We read, "The statement reported in many textbooks that Anfinsen removed denaturing and reducing agents by means of dialysis has no confirmation in the literature."  The authors state flatly that the main research result claimed by Anfinsen (a claim that got him the Nobel Prize) -- the result that "RNase refolds spontaneously into correct secondary and tertiary structures" is a result that "must be completely refused" (in other words, a result that is dead wrong). 
• In 1999 a Nobel Prize committee bungled by awarding a Nobel Prize to Gunter Blobel, "for the discovery that proteins have intrinsic signals that govern their transport and localization in the cell." We do not know how protein molecules end up in the right places in a cell, and do not know how the right type of cells end up in the right positions in a body. No one has ever discovered signals that "govern" such a transportation. The verbs "govern," "regulate" and "guide" are words that are enormously misused in the fields of biochemistry and biology, to try to suggest that little things such as genes have powers of control or guidance or construction that they do not have. Engaging in "give me an inch, and I'll take a mile" nonsense, a page on the Nobel Prize web site makes this untrue claim: "In 1975 Günter Blobel showed that in certain cases amino acids in a protein serve as an address label that determines where a protein is to be delivered." Cells have no addressing system, and proteins do not have any addresses or address labels. Claims to the contrary based on very limited studies of yeast cells are "give me an inch and I'll take a mile" examples of pareidolia and wishful-thinking speculation. 

• In 1995 a Nobel Prize committee made an inappropriate award to Edward B. Lewis, Christiane Nüsslein-Volhard and Eric F. Wieschaus “for their discoveries concerning the genetic control of early embryonic development." A gene merely specifies low-level chemical information such as which amino acids make up a protein. Genes do not have any specification of anything larger than a protein molecule, and it was incorrect to claim "a genetic control of early embryonic development." 

On the website of the Nobel Prize organization, there is a list of prize winners in each category. The list has prize descriptions that tend to be very concise, consisting of a single sentence. Such descriptions are mostly unobjectionable. But if you click near the description of an award for a particular year, you will go to other pages on the site that contain incorrect information, which may be in either a press release or some biography of one of the prize winners. 

So, for example, the entry for the Nobel Prize for Medicine or Physiology for the year 2000 has the sparse claim that the prize was awarded to Arvid Carlsson, Paul Greengard and Eric Kandel “for their discoveries concerning signal transduction in the nervous system.” That's a modest claim. But each of these names has a link to a biography, and clicking on the link for Eric Kandel takes you to a dogma-infected page on the Nobel Prize site. We have the untrue claim that brain signals "control our bodies and behavior." That's wrong; we control our bodies and behavior. We have the false claim that "short-term and long-term memories are formed by different signals," and the assurance that this is true "in all animals that learn, from molluscs to man." Scientists do not have any understanding of how a brain could cause a human to learn, and they do not at all understand how a signal could cause memory storage in a brain.

Kandel's work on snails did nothing to prove that learning occurs by the modification or strengthening of synapses. Synapses randomly change in strength and size and number, partially because they are made of proteins with average lifetimes of only a few weeks and are attached to dendritic spines that tend not to last for months. So it is always possible to examine a few synapses and claim that they strengthened when learning occurred; but such claims are never robust evidence that the learning caused the change in some synapses. And the tiny size of a synaptic cleft (about 1000 times smaller than a neuron soma width) makes it all-but-impossible to reliably measure the strength of synapses. 

Now let me finally explain why this post has the title "Once Again, the Nobel Prize Organization Blunders." The latest blunder I am referring to is mainly the awarding of the year 2026 Nobel Prize in Medicine or Physiology. That award went to Peter Hegemann, Georg Nagel and Karl Deisseroth for some research that used a light-zapping technique called optogenetics.  The choice was a poor one. The research of these figures was not very important research; and although widely used these days, optogenetics has done very little to substantially increase our understanding of brains or minds. 

I can give some background information. Optogenetics is some technique in which a tiny wire is inserted into an organism, to send light to some part of an organism (often an organism that has been genetically modified to be more sensitive to such light manipulation). The technique has been used for a wide variety of research, much of it very low-quality research guilty of procedural sins such as the use of way-too-small study group sizes. 

In their press release on the latest Nobel Prize in Medicine and Physiology, the Nobel Prize organization has made the very bad mistake of failing to distinguish between good research using optogenetics and bad research using optogenetics. The very first sentence of the press release is this bogus boast: "The Nobel Prize in Physiology or Medicine 2026 is awarded for optogenetics — a method that makes it possible to show how nerve cells shape memories, feelings and behaviours in the living brain." No robust research using optogenetics did anything to show that "nerve cells shape memories, feelings and behaviors in the living brain."

Neuroscience research using optogenetics has tended to be very low-quality research. Some examples of such poorly-designed experiments are discussed in my posts here and here. The Nobel Prize press release makes this groundless claim: "Using optogenetics, researchers have been able to reveal neural circuits governing specific memories, feelings, and behaviours relevant for neurological and psychiatric disorders." No such thing occurred. The Nobel Prize press release fails to link to any scientific papers that back up such a claim  A Google search or Google Scholar search will reveal various memory-related papers using optogenetics, but such papers tend to be low in quality. 

I can give a sketch of a typical optogenetics experiment. A small number of mice fewer than 20 (sometimes genetically modified to be more sensitive to light zapping) will be trained to fear a shock plate. A little optogenetic wire will be inserted into the brains of these mice, with the scientists guessing about where the memory of the shock plate was stored.  Then these mice will be put in a cage. and some energy will be sent down the optogenetic wire. The mobility of the mice (how often they move during some arbitrary time unit) will be measured, and compared to the mobility of mice in a similar cage, who were not brain-zapped using optogenetics. If lesser mobility is seen in the brain-zapped mice, this will be claimed as evidence that the optogenetic stimulation caused the mice to remember the shock they received, so that they "froze in fear."  This is the idea of artificial memory reactivation. An example of a very low-quality paper using a method like this can be found here. The study group sizes are 5 and 12, way-too-small for any strong evidence to be claimed. The paper fails to report any sample size calculation, a failure typical in junk science experimental studies. 

This research design is nonsensical. First of all, you would have no good evidence of an artificial elicitation of a memory unless the experiment used at least 15 or 20 rodents per study group; but experiments of this type usually use only a way-too-small study group size maybe half as large as that (with the expense of optogenetics used as an excuse for the tiny study group size). Second, you do not show that a fearful memory is being recalled by showing that some group of mice getting optogenetic stimulation was less mobile than some other group not getting such stimulation. This "freezing behavior" technique is a worthless technique for judging whether a rodent remembered something, for reasons I explain at length in my post here. Third, it is unreliable to a particularly strong degree to be combining the unreliable "freezing behavior" method with optogenetic stimulation, as the very act of stimulation may itself be causing an increase in "freezing behavior," because mice being brain-zapped may be more likely to be immobile (i.e. "freeze"), regardless of what they are recalling. 

What often goes on is that optogenetics is being used as a kind of hi-tech gloss, a "glamor spray" to give an aura of respectability to crappy-design studies that we should not respect because they are guilty of multiple forms of Questionable Research Practices, such as the use of way-too-small study groups, and the use of unreliable techniques for measuring fear or recall in rodents. 

What the Nobel Prize organization has done this year is to issue the Nobel Prize in Medicine or Physiology for a method of research (optogenetics) that is by now thoroughly entangled with junk science research and very highly associated with bad methods, Questionable Research Practices and poor design in experiments. That does not make sense, because in the fields of medicine and physiology there are so many researchers who follow good practices, researchers who produced important results so much better than almost anything that has come from the soggy swampland that is optogenetics research, which is a kind of "play around by zapping cells" sandbox or playground that is fun for zapping-fixated neuroscientists, but of little clear value to the advancement of medicine or physiology. 

There are hundreds of types of things scientists should be doing that are far more useful in understanding brains and minds than zapping parts of the brain with optogenetics or zapping particular cells with optogenetics. One of those things is adequately studying medical case histories that contradict "brains make minds" dogma and "brains store memories" dogma. Another of those things is adequately studying cases of exceptional human mental performance (discussed here, here, here and here), and pondering whether such cases are compatible with "brains make minds" dogma and "brain store memories" claims, given all of the many physical shortfalls in all brains, which neuroscientists fail to adequately study and pay attention to. 

This year the Nobel Prize in Physics went to Francis Halzen  "for decisive contributions to the IceCube Neutrino Observatory and the discovery of high-energy neutrinos of astrophysical origin." This was another poor choice by the Nobel Prize organization. No very important discovery has come from such an observatory. Neutrinos are particles of no significance to the current existence of life or Earth's habitability, in the sense that all of us would get along just fine without neutrinos. We have long known that neutrinos constantly flow very abundantly from the sun, and the IceCube Neutrino Observatory discovered a few dozen cases of neutrinos coming from high-energy sources outside of the solar system. Such a not-at-all-surprising discovery is of no great significance. It has been known for several decades that there are rare places beyond our solar system that are high-energy sources of intense radiation, so being able to detect some neutrinos from a few sources beyond the solar system is a "just what we expected" type of thing. Most of these claimed neutrino detections from outside the solar system are mere "statistical significance" things that are not solid proof, and apparently only a handful of these detections are "solid proof" type of things.  

There were hopes that much grander things than run-of-the-mill neutrinos would be discovered by the IceCube Neutrino Observatory, things such as "sterile neutrinos" or the direct detection of dark matter of maybe some evidence for string theory. But such hopes have not been realized. Given such a shortfall  and given "count on the fingers of your hands" observational results (counting only the firmly established observations), it is puzzling that  Halzen got a Nobel Prize. 

Postscript: I will give another example of a low-quality research paper that uses optogenetics. The paper is "Labelling and optical erasure of synaptic memory traces in the motor cortex," a paper that (like so many neuroscience papers) has a title that makes a groundless boast of doing something that was not done. Examining mice, the authors claim to have identified some dendritic spines that changed during a learning activity. Because mice have billions of dendritic spines, and because most such dendritic spines have short lifetimes and are constantly changing in size, there is zero reason to believe that the few dendritic spines the authors chose are any such things as "synaptic memory traces" or memory traces of any kind. The authors used optogenetics to zap their selected spines, and claim that following this, there was a weakened memory performance. There is no reason to assume any causal relation between such an activity and the claimed decrease in memory performance, particularly since the number of cells and dendrites involved was very small (less than 20).  The number of mice used is never clearly specified in the paper, and when that occurs there is typically a high probability that the study group sizes were some way-too-small number such as less than 10 mice. My best guess looking at the figures was that the study groups had an average size of only about six mice (way too small for the author's claims to be taken seriously). No claims of a sample size calculation is made. No use was made of a blinding protocol, and no use is made of a control group. The graphs provide no clear evidence of a significant change in memory produced by the optogenetic zapping. This is very low-quality science.