Header 1

Our future, our universe, and other weighty topics


Tuesday, April 7, 2026

Very Many Types of Protein Complexes Each Require 10,000+ Specially Arranged Parts

 Let us look at a scientific paper which sheds light on the very high functional thresholds of protein complexes.  The concept of a functional threshold is a supremely important topic for anyone seriously studying biological organization and biological complexity.  A functional threshold is the minimum number of parts and arrangement of those parts for some particular biological function to be met. Enormously complex organisms such as human beings have innumerable functions, most of which have very high functional thresholds. 

Most of the scientific papers in biology literature do a very bad job of shedding light on just how high functional thresholds are. But the paper "A high-accuracy consensus map of yeast protein complexes reveals modular nature of gene essentiality" by G Traver Hart, Insuk Lee and Edward R Marcotte (which you can read here) has a table that helps to show how high such functional thresholds are. 

The scientists studied protein complexes in yeast, a one-celled organism sometimes called simple. But even the simplest one-celled organism is really a marvel of organization and fine-tuned complexity.  Early in the paper the scientists begin to give us a clue about the underlying complexity, stating this:

"The molecular machines that carry out basic cellular processes are typically not individual proteins but protein complexes. Even in the relatively simple model organism Saccharomyces cerevisiae, most machines that process and store biological information are in fact large protein complexes comprised of many subunits.."

For those unfamiliar with the hierarchical organization of the human body, I can give a sentence that describes it. The sentence is: a human body consists of a skeletal system and organ systems; organ systems  are made up of one or more organs and other components; organs are made up of tissues; tissues are made up of cells; cells are made up of many organelles of many types; organelles are made up of protein complexes and proteins; protein complexes are made up of many different types of proteins;  proteins consist of special well-arranged sequences of hundreds or thousands of amino acids, folded into 3D shapes; amino acids consist of atoms; and atoms consist of protons, neutrons and electrons.

Let's look at these units called protein complexes.  Typically a protein is of no use by itself, and the protein only becomes useful when it becomes part of a protein complex. A protein complex is a group of proteins connected together to perform a particular function.  How many amino acids do you have to have  specially arranged for you to have a useful protein complex? The answer is: many thousands.  Similarly, it takes a special arrangement of thousands of letters or characters for you to get a page full of text in a technical manual using fine print. 

An example of one of many types of super-complex protein complexes in the human body is thapoptosome protein complex involved in programmed cell death. Below is a visual of the complex. 

apoptosme

(Image credit:  Wikipedia Commons, derived from Yuan et al. 2010, Structure of an apoptosome-procaspase-9 CARD complex)

We can start to realize what the answer to that question (" How many amino acids do you have to have  specially arranged for you to have a useful protein complex?") by examining Table 1 in the paper mentioned above. Below is an annotated photo of the beginning of that table. 

protein complex examples


The text in blue gives my comments elaborating on some of the data in the table. The table lists various protein complexes used by yeast.  The "Size" column in the table lists the number of  types of proteins used in the protein complex.  The "% Essential" column lists what percent of these proteins are needed for the protein complex to function. The numbers shown under the "% Essential" column are high. 

So, for example, when we see a number of 74% as the "% Essential" entry for the C1 complex, what that means is that this protein complex needs 74% of its proteins to do its job. And when when we see a number of 93% as the "% Essential" entry for the C4 complex, what that means is that this C4 protein complex needs 93% of its proteins to do its job.

No one should be very surprised to be reading the type of numbers we see under the "% Essential" column. It is a very common characteristic of complex functional things that they need most of their parts to be functional.  Consider an object such as a bicycle. It requires most of its parts to be functional, but not all of them.  You can actually ride a bicycle without its seat, although it is very uncomfortable to do so.  I once discovered this fact after I rode home in a bicycle without a seat, after a thief had stolen my bicycle's seat. 

Or consider an object like an automobile. It requires most of its parts to be functional, but not all of them. You can remove the windshield and tear out most of the seats and tear out the radio, and the automobile will still be useful as a vehicle for travel. But  the automobile requires most of its parts to function, and its engine requires a special arrangement of very many parts. 

Now, an important question is: how many parts have to be assembled just right for one of these protein complexes to be functional? We can make a rough estimate using the data in the table. Let's start with the C1 protein complex. 

According to the table, that complex consists of 35 types of proteins. One of those proteins is the RPA135 protein, which has a special sequence of 1203 amino acids, as you can see on the page here. Another of those proteins is the RPA190 protein, which has a special sequence of 1644 amino acids, as you can see on the page here. Another of those proteins is the RP031 protein, which has a special sequence of 1460 amino acids, as you can see on the page here

The proteins I just mentioned are some of the most complex proteins that make up this C1 protein complex, and most of the proteins are less complex than the ones I've mentioned. But even most of the less complex proteins each require a special sequence of hundreds of amino acids. 

The main facts here are:

(1) This C1 protein complex requires 35 types of protein molecules, 74% of which are "essential" for its function. 

(2) Several of these proteins each require a special amino acid sequence consisting of well over a thousand amino acids. 

(3) Almost all of these proteins require a special amino acid sequence consisting of at least hundreds of amino acids. 

From these facts, we can roughly estimate that all in all this C1 protein complex requires the special arrangement of more than 10,000 amino acids.  The functional threshold here is roughly as high as the amount of arrangement of letters you need to produce a blog post or essay of about five pages or about 2000 words, consisting of about 10,000 well-arranged characters. Just as a five-page essay does not need all of its words and all of its sentences to be functional, this C1 protein complex apparently does not need all of its proteins. Just as it is impossible that chance (such as a monkey typing for an hour) might produce a readable, functional five-page essay or a coherent useful readable 2000-word blog post, it is impossible that chance or random mutations or random combinations might produce a special arrangement of 10,000 amino acids needed to produce this protein complex. 

It is very appropriate to compare the difficulty of getting just-right arrangements of amino acids and the difficulty of getting just-right arrangements of characters in the English alphabet, partially because in both cases the likelihood of chance combinations being functional is similar. Just as there are 26 characters used in the English alphabet, there are 20 amino acids used by living things; and a random permutation in a gene may produce nucleotide base pairs corresponding to any of 20 amino acids. 

We have a similar situation in regard to the second protein complex mentioned in the image above. The protein complex is named as the C4 protein complex, and the paper says it uses 27 types of proteins,  and that 93% of them are "essential." One of those proteins is the BMS1 protein, which has a special sequence of 1183 amino acids, as you can see on the page here. Another of those proteins is the ECM16 protein, which has a special sequence of 1267 amino acids, as you can see on the page here 

The main facts here are:

(1) This C4 protein complex requires 27 types of protein molecules, 93% of which are "essential" for its function. 

(2) Several of these proteins each require a special amino acid sequence consisting of well over a thousand amino acids. 

(3) Almost all of these proteins require a special amino acid sequence consisting of at least hundreds of amino acids. 

From these facts, we can roughly estimate that all in all this C4 protein complex requires the special arrangement of more than 10,000 amino acids.  The functional threshold here is roughly as high as the amount of arrangement of letters you need to produce a blog post or essay of about five pages or about 2000 words, consisting of about 10,000 well-arranged characters. Just as it is impossible that chance (such as a monkey typing for an hour) might produce a readable, functional, useful five-page essay or coherent 2000-word blog post, it is impossible that chance or random mutations or random combinations might produce a special arrangement of 10,000 amino acids needed to produce this protein complex. 

My image above shows only the first two protein complexes listed in Table 1 of the scientific paper.  There are other protein complexes listed with similar levels of complexity and similar functional thresholds.  All of this accidentally unachievable complexity is involved in a mere microscopic yeast.

 In the human body there are thousands of types of protein complexes that are mysteriously assembling every day. Their assembly is not explained by DNA. DNA and its genes specify which amino acids make up a particular protein. But DNA and its genes do not specify the structure of any protein complex.  The visual below shows what is and is not specified by DNA. 

pyramid of biological complexity

There are six main reasons why we must regard the protein complexes in the human body as as accidentally unachievable, things that cannot be explained by unguided natural processes. 

Reason #1: Chance processes such as Darwinian evolution could never produce the genes needed to make the proteins that make up such protein  complexes (the gene origination problem)To perform the task a particular protein molecule performs, a type of protein molecule typically requires some specific fine-tuned gene, an amino acid sequence with most or nearly all of the protein's actual amino acid sequence, a chain of hundreds or thousands of amino acids specially arranged to produce a functional effect. Evolutionary biologist Richard Lewontin stated"It seems clear that even the smallest change in the sequence of amino acids of proteins usually has a deleterious effect on the physiology and metabolism of organisms." A biology textbook tells us, "Proteins are so precisely built that the change of even a few atoms in one amino acid can sometimes disrupt the structure of the whole molecule so severely that all function is lost." And we read on a science site, "Folded proteins are actually fragile structures, which can easily denature, or unfold." Another science site tells us, "Proteins are fragile molecules that are remarkably sensitive to changes in structure." paper describing a database of protein mutations tells us that "two thirds of mutations within the database are destabilising."  Those who think that functional folded protein molecules could gradually arise (getting longer and longer from a small size) will be dismayed to read this statement in a 900+ page textbook on protein chemistry: "Polypeptides less than about 70 amino acids in length should not fold because they should not be able to bury a large enough number of hydrophobic amino acids to overcome the configurational entropy of their random coils." Folding is required for most functional protein molecules. 

Accordingly, we cannot explain the origin of genes through some gradualism approach that imagines that first there was one tenth of the gene that was useful for one purpose, and then there was two tenths of the gene that were useful for some other purpose, and then finally we got the version of the gene that humans now have.  Human genes with only half of their base pairs or a third of their base pairs are not useful, and their corresponding protein molecules are not useful with half of their amino acids. 

But how hard would it be to get by chance or random mutations an amino acid sequence that would be the core of a useful protein molecule? That depends on the number of amino acids in the protein. Here we run into a simple principle that is the bane of all theories of accidental biological origins: the principle that a simple linear increase in the number of parts that must be well-arranged results in an exponential or geometric increase in the unlikelihood of such an arrangement occurring by chance. A small increase in the number of parts quickly results in what is called a combinatorial explosion, in which the number of possible combinations skyrockets. This is why computer security experts often tell you to use at at least 14-characters for the password of any financial account.  If you change your password from 7-characters to 14 characters, that doesn't make it merely twice as hard for a hacker trying all combinations to break into your account; instead it is is roughly 10,000,000,000 times harder. 

The chart below shows some of the relevant mathematics. If you doubt these numbers, you can verify them using the Large Exponents Calculator here. Since there are 20 different amino acids used in protein, you use 20 in the first row of such a calculator. Numbers such as E+6 refer to powers of ten. So 3.2 E+6 means 3,200,000; 1.024 E+13 means 10,240,000,000,000; and E+26 means 1 followed by 26 zeros. The bottom of the chart is a number of combinations equal to about 1 followed by more than 2600 zeros. 


Number of amino acids in a molecule

Number of possible combinations of the molecule's amino acids

5

3.2 E+6

10

1.024 E+13

20

1.048576 E+26

40

1.099511627 E+52

80

1.208925819 E+104

160

1.461501637 E+208

320

2.135987035 E+416

640

4.562440617 E+832

1280

2.081586438 E+1665

2000

1.148130695 E+2602


We can see from the chart above that the odds become utterly prohibitive once you start to get amino acid lengths much longer than about 160. Even if you very generously assume that a particular protein molecule only needs to have half of its amino acid sequence matching its actual sequence (an assumption too generous because of what we know about the sensitivity of protein molecules to small changes), you still have a case where we should never expect chance processes to produce successful amino acid sequences (corresponding to functional protein molecules) as long as 320 amino acids. 

In innumerable protein complexes in the human body, we have some very complex proteins consisting of very long amino acids chains that we should never expect to have arisen by chance or Darwinian processes, never in the entire visible universe even given billions of years. I will give some numbers (you can find the specifics in my post here which names which proteins I am talking about):

  • One of the protein complexes (the spliceosome) has a protein consisting of 2335 well-arranged amino acids.
  • Another of the complexes (the apoptosome) had a protein consisting of 1248 well-arranged amino acids. 
  • The nuclear pore protein complex has one protein requiring 2090 well-arranged amino acids, and another protein requiring 2012 well-arranged amino acids, along with three other types of proteins each requiring more than 1000 well-arranged amino acids.
  • The origin recognition complex/replicative helicase complex requires 7 types of proteins that each required more than 700 well-arranged amino acids. 
  • The RNA polymerase II protein complex  has five types of proteins each requiring more than 2000 well-arranged amino acids, and three other types of proteins each  requiring more than 1000 well-arranged amino acids.
I could say much more about why proteins with amino acid sequences as long as this are not explicable by Darwinian processes, but that would involve repeating too many of the points in a previous post. See my previous post here for quite a long discussion on why it is not credible to suppose that fine-tuned amino acid sequences of this length ever could have arisen through any type of natural selection.  

Reason #2: we lack any explanation as to why very complex proteins would fold correctly. To be functional, proteins have to fold in just the right way, to achieve very complex three-dimensional shapes. But we don't understand how this folding occurs. DNA specifies only the linear sequence of the amino acids that make up a protein, not the complex 3D shape of a protein. Don't be fooled by press accounts claiming that the AlphaFold2 software did something to solve the protein folding problem. Such software did not produce any progress in solving the protein folding problem (the problem of how proteins are able to fold into the complex 3D shapes needed for their function). Such software merely produced progress in a different problem: the protein folding prediction problem, which is the problem of predicting the 3D shape of a protein from its amino acid sequence. 

One maneuver is an appeal to what is called Anfinsen's Dogma, a claim that the 3D shape of a protein is entirely a function of its amino acid sequence. Such an appeal is futile because it is a "rob Peter to pay Paul" affair rather like "solving" your college tuition burden by charging your tuition on your credit card.  If Anfinsen's Dogma were true, then genes would all-the-more-enormously have to be "just right" to allow for a properly folded 3D protein molecule; and in that case the gene origination problem becomes exponentially worsened.  The person who appeals to Anfinsen's Dogma lessens the protein folding problem at the expense of exponentially worsening the gene origination problem  (the problem of how 20,000+ suitable genes ended up in human DNA).    Appealing to Anfinsen's Dogma seems to make Reason #2 of these six reasons seem less convincing, at the expense of making Reason #1 seem enormously and exponentially more convincing. Such an appeal produces no net progress in making molecular machines like those above seem accidentally achievable. 

I may note that there are very good reasons for rejecting Anfinsen's Dogma, such as the very massive reliance of protein folding on helper molecules called chaperone proteins, which show that the 3D shapes of proteins are not a simple function of their amino acids sequences as Anfinsen's Dogma claims. 

Reason #3: we have no credible physical explanation for how  a transcription event could promptly find the right gene to make a particular protein (a "needle from the haystack" type of event). Cells are constantly creating new proteins to replace proteins that disappeared because of the short lifetimes of proteins. The page here has a chart showing the lifetimes of human proteins, and we see a bar graph showing most of the proteins have a half-life between about 10 hours and 70 hours. A muscle protein might live for three weeks, but a liver protein might live for only a few days. To create new proteins, a cell uses a process called gene transcription. In this process a particular gene in DNA will be converted to a messenger RNA molecule that helps to build the new protein. 

Cell transcription occurs quickly. The source here lists a time of ten minutes for a gene to be transcribed by a mammal, but another source lists a speed of only about a minute. The great majority of that is used up by the reading of base pairs from the gene, with typically more than 1000 base pairs being read each time a gene is transcribed. The finding of the correct gene to read in DNA seems to occur in only seconds, not minutes, or at most a few minutes. 

Descriptions of DNA transcription fail to explain a huge issue: how does a cell find the right gene in DNA so quickly? Human DNA contains more than 20,000 genes, each of which is just a section of the DNA. The DNA is like an extremely long necklace of many thousands of beads, and a typical gene is like a group of several hundred of those beads. We should actually imagine multiple such necklaces, because DNA is scattered across 23 different chromosome pairs. Now if genes had gene numbers, and DNA was a set of numbered genes in numerical order, it might be easy to find a particular gene. So if a cell knew that it was trying to find gene number 4,233, it could use a binary search method that would allow it to find that gene pretty quickly. 

But no such method can be used within the human body. Genes do not have gene numbers that can be accessed within the human body, and DNA is not numerically sorted. DNA has no indexes that might allow a cell to find some particular gene that it was trying to find within DNA.  So we have an explanatory "needle in a haystack" problem.  Or we might call it a "needle in the haystacks" problem, because human DNA is scattered across 23 different chromosome pairs, as shown in the diagram below:


scientific text tells us some information that makes this explanatory problem seem more pressing:

"One might have predicted that the information present in genomes would be arranged in an orderly fashion, resembling a dictionary or a telephone directory. Although the genomes of some bacteria seem fairly well organized, the genomes of most multicellular organisms, such as our Drosophila example, are surprisingly disorderly. Small bits of coding  (that is, DNA that codes for ) are interspersed with large blocks of seemingly meaningless DNA. Some sections of the  contain many genes and others lack genes altogether. Proteins that work closely with one another in the cell often have their genes located on different chromosomesand adjacent genes typically encode proteins that have little to do with each other in the cell. Decoding genomes is therefore no simple matter. Even with the aid of powerful computers, it is still difficult for researchers to locate definitively the beginning and end of genes in the DNA sequences of  genomes, much less to predict when each  is expressed in the life of the organism. Although the DNA sequence of the human genome is known, it will probably take at least a decade for humans to identify every gene and determine the precise  sequence of the protein it produces. Yet the cells in our body do this thousands of times a second."

We have here a very severe navigation problem. A cell is somehow able to find the right gene in only seconds or a few minutes when a new protein is made, even though DNA and chromosomes seem to have no physical organization that could allow for such blazing fast  access to the right information. In an article on Chemistry World, we read this:

"How does the machinery that turns genes into proteins know which part of the genome to read in any given cell type? ‘To me that is one of the most fundamental questions in biology,’ says biochemist Robert Tjian of the University of California at Berkeley in the US: ‘How does a cell know what it is supposed to be?"

Biochemist Tjian has spoken just as if he had no idea how it is that a cell is able to navigate to the right place to read a particular gene in DNA. Later in the article we read this:

"For one thing, the regulatory machinery ‘is unbelievably complex’, says Tjian, comprising perhaps 60–100 proteins – mostly of a class called transcription factors (TFs) – that have to interact before anything happens. ....As well as promoters, mammalian genes are controlled by DNA segments called enhancers. Some proteins bind to the promoter site, others bind to the enhancer, and they have to communicate. ‘This is where things get bizarre, because the enhancer can sit miles away from the promoter,’ says Tjian – meaning, perhaps, millions of base pairs away, maybe with a whole gene or two in between. And the transcription machinery can’t just track along the DNA until it hits the enhancer, because the track is blocked. In eukaryotes, almost all of the genome is, at any given moment, packaged away by being wrapped around disk-shaped proteins called histones. These, says Tjian, ‘are like big boulders on the track’: you can’t get past them easily.... ‘Even after 40 years of studying this stuff, I don’t think we have a clear idea of how that looping happens,’ says Tjian. Until recently, the general idea was that the TFs and other components all fit together into a kind of jigsaw, via molecular recognition, that will bridge and bind a loop in place while transcription happens. ‘We molecular biologists love to draw nice model schemes of how TFs find their target genes and how enhancers can regulate promoters located millions of base pairs away,’ says Ralph Stadhouders of the Erasmus University Medical Centre in Rotterdam, the Netherlands. ‘But exactly how this is achieved in a timely and highly specific manner is still very much a mystery.’ "

Later in the article Tjian says he was shocked by the speed at which some of the process occurs. He expected it would take hours, but found something much different:

"The residence times of these proteins in vivo was not minutes or hours, but about six seconds!’, he says. ‘I was so shocked that it took me months to come to grips with my own data. How could a low-concentration protein ever get together with all its partners to trigger expression of a gene, when everything is moving at this unbelievably rapid pace?’ "

The rest of the article is just some speculation, which Tjian mostly knocks down, and the article itself calls "hand-wavy." We are left with the impression that no one understands how cells are able to instantly find the right gene.

Reason #4: chance processes would never produce the arrangements of proteins like those found in the protein complexes listed above. What we must never forget is that a protein complex involves three types of organization:
  • The one-dimensional organization of amino acids found in the sequence of amino acids that makes up a protein;
  • the three-dimensional organization of such a sequence to make a complex folded three-dimensional shape needed for a particular protein molecule to function properly;
  • the entirely different three-dimensional organization needed for the proteins of a protein complex to fit together in the right way to make a physical arrangement so complex that it may be called a "molecular machine."
How is it that protein molecules form into protein complexes consisting of multiple protein molecules? Some may guess that DNA is read to determine which type of proteins should team up with other proteins to make particular protein complexes.  But that does not happen. DNA does not specify which proteins belong to particular protein complexes. In fact, the tables in my post here show that the genes corresponding to the proteins that make up the protein complexes are typically found in widely scattered chromosomes. That would seem to be the opposite of what would happen if DNA was specifying that particular protein molecules should team up with other types of protein molecules to make particular kind of protein complexes. 

So what explanation do biologists give for how protein complexes form? Their attempts at explanations consist of little more than hand-waving.  They mainly appeal to chance collisions of molecules floating around in the human body. This is no more credible  than claiming that tornadoes passing through junkyards can create automobiles out of the spare parts that are lying around the junkyards. 

A very important point here is that vast wonders of molecular assembly are happening continuously in the human body. Every week very many of the molecular machines described above (and countless others not described) are being assembled in your body. And as I have shown above, such molecular machines are built using amino acid sequences from very scattered chromosomes So we have an effect no more explainable by chance collisions than tornadoes building cars out of junk scattered in diverse places of a junk yard. And such an effect is constantly occurring in your body, in massive numbers. 

There is no way to explain this by trotting out some Darwinist phrase such as "very lucky things can happen given a million years of chance events."  We are not talking here about some miracle of genetic luck that occurred once in an eon. We are talking about miracles of complex purposeful assembly that are occurring in massive numbers every single day in your body. Darwin doesn't do anything to get the materialist out of this jam. 

The statements below are indications that scientists simply have no credible explanation as to how very complex protein complexes (like those discussed above) can form from their constituent protein parts:

  • "The majority of cellular proteins function as subunits in larger protein complexes. However, very little is known about how protein complexes form in vivo." Duncan and Mata, "Widespread Cotranslational Formation of Protein Complexes," 2011.
  • "While the occurrence of multiprotein assemblies is ubiquitous, the understanding of pathways that dictate the formation of quaternary structure remains enigmatic." -- Two scientists (link). 
  • "A general theoretical framework to understand protein complex formation and usage is still lacking." -- Two scientists, 2019 (link). 
  • "Protein assemblies are at the basis of numerous biological machines by performing actions that none of the individual proteins would be able to do. There are thousands, perhaps millions of different types and states of proteins in a living organism, and the number of possible interactions between them is enormous...The strong synergy within the protein complex makes it irreducible to an incremental process. They are rather to be acknowledged as fine-tuned initial conditions of the constituting protein sequences. These structures are biological examples of nano-engineering that surpass anything human engineers have created. Such systems pose a serious challenge to a Darwinian account of evolution, since irreducibly complex systems have no direct series of selectable intermediates, and in addition, as we saw in Section 4.1, each module (protein) is of low probability by itself." -- Steinar Thorvaldsen and Ola Hössjerm, "Using statistical methods to model the fine-tuning of molecular machines and systems,"  Journal of Theoretical Biology. 

Reason #5: once assembled, such molecular machines act as if they knew where to go, which would not happen by accident. It is not merely the assembly of such molecular machines that defies anything we should expect to occur accidentally. It is also the behavior of such molecular machines, in the sense that they always seem to act exactly as if they knew where to go to. For example, the nuclear pore complex molecular machines go to just where they are needed (the nuclear membrane), and the spliceosome and RNA polymerase II complex go to appropriate places in the cell.  To have an analogy for the whole storyline of the construction and target reaching of such molecular machines occurring accidentally, we would have to imagine something like tornadoes passing through junkyards, constructing many cars, and also blowing the cars to just the right places to pick up a million scattered people who needed rides.  How accidentally unachievable would that be? 

Reason #6: such molecular machinery behavior occurs massively every day.  If something occurs only very rarely, we might regard is as accident. For example, if you come to your door with a friend, and realize you lost your  key, and your friend suggests he tries his key on your door, and his key opens your door, you may regard this as a lucky coincidence, having seen such a thing only once in your life. But when some type of lucky thing occurs all the time in massive numbers, in some way you cannot account for, chance and coincidence are no longer reasonable explanations. 

How often does there occur in your body the assembly and correct positional targeting of the molecular machines I have listed above? Billions or trillions of times every day. For example, very many  instances of the nuclear pore complex discussed above are needed in the construction of a new cell, and it has been estimated that the human body makes 300 billion new cells every day. What would be the chance of the totality of such daily feats of construction occurring accidentally? Something like the chance of a winter ice storm constructing a thousand-mile-high ice arch stretching all the way from Europe to North America. 

The infographic below shows some of the most impressive protein complexes in the human body, which act like molecular machines. 

protein complexes as molecular machines

Sufficiently pondering and studying the weighty facts above, and the nine-month progression from a speck-sized zygote containing no anatomy specification or cell specifications to the vast organization of a full human body, an objective mind may start to draw towards one of the weightiest philosophical conclusions: that both the physical origin and lifelong continuation of every human body is a miracle of teleological fine-tuned organization and preservation utterly beyond the explanation of materialist science and mechanistic theory, something that can only be credited to mysterious purposeful agency of unfathomable power and intelligence. The origin of any human mind is as mechanistically inexplicable as the origin of any human body. 

Saturday, April 4, 2026

Looking Back at My Blogging Activity, Part 3: The Year 2015

This is the third in a series of rarely-appearing posts in which I will look back at particular years of my blogging activity (see here and here for parts 1 and 2). In this post I will look at my blogging activity in the year 2015. 

In early 2015 I wrote a four-part series of posts entitled "50 Things Science Cannot Explain" which you can read here, here, here and here.  The image below mentions some of the things discussed in the post. 

Things Science Cannot Explain

The third of these posts was one of the first posts in which I discussed the failure of scientists to develop any credible theory of human memory. I wrote this:

"We know exactly how the memory of our computers and digital devices work. On the lowest level, all information is stored as binary bits, sequences such as 01100111010101; and such bits are stored magnetically on surfaces such as hard drives. But we have no such understanding at all of how our own memory works. Try looking up human memory on the Internet. You will get a lot of discussion that makes quite a few points that don't add up to a substantive answer. We have no idea whether memory is stored chemically, electrically, through neuron connections, through some combination of the three, or through some entirely different means. Nor do we have the slightest idea about what kind of code or alphabet the brain might use to store memory. A modern neuroscientist can say quite a few things about memory, but he can't really explain it."

This paragraph stands up very well after ten years. During that time my studies on the topic of memory greatly deepened, and I became aware of specific reasons why we should reject the doctrine that human memories are stored in brains. Such reasons are discussed in the posts of my blog site here, and in my free online book "Why Mind and Memory Cannot Be Brain Effects," which you can read here

My March 2015 post "The Top 6 Problems With Using a Multiverse To Explain Cosmic Fitness" was a good explanation of why speculations about other universes do nothing to explain the fine-tuned habitability of our universe.  In the same month I wrote my post "If You Had Always Lived in a Random Universe," which involved a big  leap of imagination. Because human bodies require a universe with very special conditions, you cannot credibly imagine a body such as yours existing in a truly random universe.  But you can imagine yourself as a very different type of entity (such as a formless gas) existing in a very random universe with no special conditions. It was just such a leap of imagination that I took in this post. 

My post "Trying to Explain Things, Naturalism Offers a Jumbled Mishmash" did a good job of discussing how materialists rely on the most scrambled hodgepodge of attempted explanations, rather than anything with coherence. My August 2015 post "Does Darwinism Plausibly Explain the Origin of Human Intelligence?" offered an answer of "no, it does not," which was the same answer given by Alfred Russel Wallace (the co-founder of the theory of natural selection) in the 19th century. 

I wrote this:

"Comments such as these by leading Darwinists strongly suggest that Darwinism does not offer a plausible account of the origin of human intelligence. Generally speaking, you only offer a plausible explanation of something when you offer some explanation under which such a thing is likely....Similarly, if Darwinists cannot give us a situation under which the evolution of intelligence is likely under Darwinist principles, they have not provided a plausible explanation of the origin of human intelligence. You do not give a plausible explanation of something if you describe it as being a strange rare fluke under your theoretical framework, something we would be unlikely to see again on any of millions of other planets....We need to start pondering explanations of the origin of human intelligence which describe a situation under which the appearance of human intelligence is a likely event rather than some incredibly improbable fluke. No theory that describes the origin of human intelligence as some strange improbable fluke can claim to have offered a plausible account of the origin of human intelligence."

My November 2015 post "Can Natural Selection Explain the Human Mind?" asked a similar question, and reached a similar answer of "no."

My September 2015 post "The Ocean Deniers of Centralia" is one of my favorites of the stories I have wrote. It is a portrait of the stubbornness of authorities who refuse to believe evidence conflicting with their worldview. I've written other stories with a similar theme, including "The Sun Seers of Planet Evercloudy"  and "Planet of the Blind.

In my December 2015 post "The Difficulties in Explaining the Big Leaps in Life's History" I criticized the sophistry and misstatements in Bill Nye's book trying to sell us on Darwinism. After making a list of biological wonders (mostly great leaps of physical organization), I stated this:

"Overall, the ability of natural selection and mutations to explain these things is poor. If scientists think otherwise, it's partly because they have long had a habit of underestimating requirements...The very clannish and dogmatic community of evolutionary biologists will probably continue for quite a while to push the Official Party Line that natural selection explains the origin of biological complexity, in a way rather similar to the way that Marxist dogmas (an Official Party Line) would be handed down authoritatively from Moscow in the years of the Soviet Union."

In January 2015 I started my Orb Pro blog, devoted to publishing photos I had taken of mysterious orbs.  By January 2015 I already had the most extraordinary backlog of photos of the mysterious that I had taken during 2014. And the year 2015 was one of my most successful years in getting photos of the mysterious. So I was able to start the blog "full blast," and was able to keep it running "full blast" throughout 2015. I look back on years such  as 2015 as my peak period as an orb photographer. I still get astonishing orb photos, but not as frequently as I got around the year 2015. 

An example of one my year 2015 orb photos was the photo below taken in Grand Central Terminal in New York, one of the most dramatic moving orb photos I have ever taken. We seem to see five position states of a mysterious pink orb moving very fast. 

moving orb

Below is a photo from December 9, 2014 showing a large orb in Grand Central Terminal, one I published in January 2015. 

Grand Central Station mysterious orb


Wednesday, April 1, 2026

Origin-of-Life Researchers Pile Up Groundless Boasts

 For 70 years the mainstream science literature has presented enormously misleading coverage about origin-of-life research.  There has been a huge amount of bunk and baloney in the press coverage of origin-of-life research, and the statements made on this topic by scientists themselves have very often been wildly  inaccurate. Many examples of such misstatements can be found here and here and here and here and here and here and here.

Never has more boasting and hype been written when the results were so minimal and meager.  It is not merely that no experiments have ever produced life from non-life. The reality is that no experiments realistically simulating the early Earth have ever produced any of the main building components of single-celled life, and that no experiments realistically simulating the early Earth have ever produced any of the building components of the building components of single-celled life. 

empty boasts of origin-of-life researcher

The research output: "peanuts" (i.e. "chickenfeed") 

The main building components of one-celled life are functional protein molecules, which have never been produced in any experiment realistically simulating the early Earth. The building components of such building components are amino acids, which have never been produced in any experiment realistically simulating the early Earth.  The widely-discussed Miller-Urey experiment (which did produce some amino acids) was not anything like a realistic simulation of early Earth conditions, requiring a very specially constructed glass gizmo unlike anything that would have existed on the early Earth, and requiring a degree of electricity exposure unlike any part of the early Earth would have experienced. 

Let us look at a recent example of groundlessly boasting origin-of-life research. Some scientists created a very fancy chamber device which they claim simulates interstellar space. Inside the device they put some glycine, which is the simplest amino acid. They zapped the chamber with some energy that they claim was simulating cosmic rays, and got the most meager result: a mere peptide molecule. The peptide molecule they got was what you can get from combining two glycine molecules. The result was as simple as 1 +1 = 2 or "a + a = aa." 

The result is passed off as a simulation of what could happen in interstellar space. But is that claim accurate? No, it is not, because there is no robust evidence that glycine exists in interstellar space.  Recent claims to have found glycine after a soil sample retrieval from an asteroid in the solar system do not count as such robust evidence, both because such an asteroid is not in interstellar space, and because the amounts supposedly detected are so minute they can credibly be accounted for by assuming terrestrial contamination (as I discuss here). 

In the 2006 paper here we read about an apparent false alarm regarding the detection of the amino acid glycine in interstellar space:

"The early searches for glycine were all negative, but two years ago  reported detection of a number of glycine lines, some 27 in several astronomical sources. Unfortunately, this claim has not been confirmed. The amount of glycine claimed by Kuan et al. is in conflict with previously published upper limits (e.g. ; ), and glycine lines which should have appeared were not found. In a detailed analysis of the evidence,  recently concluded that few, if any, of the lines attributed by Kuan et al. to interstellar glycine were actually from that molecule. The spectroscopic data on which the claim of Kuan et al. was based have not been published or made available to other workers, and there is now a fairly wide consensus among radio astronomers and laboratory spectroscopists that glycine has not yet been found in space."

A more recent 2022 paper tells us this: "The simplest amino acid, glycine (NH2CH2COOH), has been searched for a long time in the interstellar medium, but all surveys of glycine have failed." 

So,  you are not realistically simulating interstellar space by putting glycine in a chamber and zapping it with energy.  The glycine-zapping experiment does nothing to make it seem more likely that extraterrestrial life exists, or that life could form naturally.  But our clickbait-loving "science news" press fell for the story "hook, line and sinker."

And so we have an article at the clickbait-heavy phys.org, an article with the extremely misleading headline shown below. At least the article has a visual which shows that all that is going on is "one plus one equals two" stuff. I added the bottom row as commentary to what is shown above. 


We have a quote from the main researcher, Sergio Ioppolo making this untrue claim: "We already know from earlier experiments that simple amino acids, like glycine, form in interstellar space." Experiments could never show that glycine forms in interstellar space. Only observations could show that, and no robust observations show that. 

Ioppolo makes this false claim: "But research like ours shows that many of the complex molecules necessary for life are created naturally in space." No, it does not show any such thing. All it shows is that when you stick in a chamber two simple glycine molecules and zap them with energy, you might get a molecule looking like two glycine molecules joined together, which is a result as unimpressive as the deduction that one plus one equals two. 

Sunday, March 29, 2026

Physicists Try to "Big-Mystery-Glamorize" Their Pigeonhole Pet Projects

 Scientists believe that when two very high-energy photons collide, they produce equal amounts of matter and antimatter, and that when matter collides with antimatter, it is converted into high-energy photons. Such a belief is based on what scientists have observed in particle accelerators such as the Large Hadron Collider, where particles are accelerated to near the speed of light before they collide with each other. But such conclusions about matter, antimatter and photons lead to a great mystery as to why there is any matter at all in the universe.

Let us imagine the early minutes of the Big Bang about 13 billion years ago, when the density of the universe was incredibly great. At that time the universe should have consisted of energy, matter and antimatter. The energy should have been in the form of very high-energy photons that were frequently colliding with each other. All such collisions should have produced equal amounts of matter and antimatter. For example, a collision of high energy particles with sufficient energy creates a matter proton and an antimatter particle called an antiproton. So the amount of antimatter shortly after the Big Bang should have been exactly the same as the amount of matter. As a CERN page on this topic says, "The Big Bang should have created equal amounts of matter and antimatter in the early universe." 

But whenever a matter particle touched an antimatter particle, both would have been converted into photons. The eventual result should have been a universe consisting either of nothing but photons, or some matter but an equal amount of antimatter. But only trace amounts of antimatter are observed in the universe. A universe with equal amounts of matter and antimatter would have been uninhabitable, because of the vast amount of lethal energy released when even a tiny bit of matter comes in contact with a tiny bit of antimatter.

The mystery of why we live in a universe that is almost all matter (rather than antimatter) is called the baryon asymmetry problem or the matter-antimatter asymmetry problem.  There is not much of a prospect that this problem will be solved in our lifetimes.  It's like the problem of "why is there something rather than nothing?" That's not a problem we can expect to solve in our lifetimes. The infographic below explains this matter-antimatter asymmetry problem. 

matter-antimatter asymmetry


But sometimes when scientists have embarked on a boondoggle costing billions, they may evoke the matter-antimatter asymmetry problem to try to sanctify their misguided schemes.  That is what is going on with various boondoggle projects researching neutrinos. They include these projects:
  • An ongoing T2K experiment in Japan that beams neutrinos over a distance of 295 kilometers. 
  • An ongoing 280-million-dollar NOVA experiment in the USA that beams neutrinos 804 kilometers (500 miles), from the Fermi National Accelerator Laboratory in Illinois to a 14,000-ton detector in Ash River, Minnesota.
  • An under-construction 3-billion-dollar DUNE experiment in the USA that will attempt to beam neutrinos 1300 kilometers (800 miles), from the Fermi National Accelerator Laboratory in Illinois to a very-deep-underground facility in Lead, South Dakota. 
The first two experiments have been running for years, and there was recently released a paper announcing a kind of combined results from the projects. Nothing of any importance was found.  But you might think otherwise from some of the press coverage, some of which attempts to make this "found nothing" result sound like something worthwhile. 

Scientists were hoping to find evidence of something called "mass ordering" or something else called "inverted ordering," but the paper says, "The data show no strong preference for either mass ordering."  We read, "There is no statistically significant preference obtained for either of the mass orderings." We also read, "We do not see a significant preference at present for either mass ordering."  

The only thing the paper authors say on the question of the matter-antimatter asymmetry is, " It is unknown whether neutrinos—and thus leptons—violate charge-parity (CP) symmetry and thereby provide a source of matter–antimatter asymmetry in nature, which is of great interest given the connection between CP violation and the unexplained matter dominance in the Universe." Since the paper says nothing else on the topic of matter-antimatter asymmetry other than this "say nothing" sentence,  the results obtained utterly fail to shed any light on the mystery of matter–antimatter asymmetry, contrary to the sales pitches for these very expensive projects, which tried to suggest that they would give important insight on this topic. 

The Reuters article on this paper describes it without exaggeration, and does not claim that the work shed any light at all on the matter-antimatter asymmetry problem. We have a headline of only "Researchers in US and Japan offer insight into ghostly neutrinos."
A Caltech press release on the paper uses some scrambled reasoning to gin up some relevance to the results. It states this:

"The combined results of NOvA and T2K so far do not favor one mass ordering scenario over another. However, if future results show the neutrino mass ordering is inverted and not normal, NOvA's and T2K's results published today provide evidence that neutrinos do exhibit the suspected asymmetry, potentially explaining why the universe is dominated by matter instead of antimatter. "

This is  kind of like someone saying, "My photo published today of triangular marks in the mud provides no evidence of extraterrestrial creatures; however if it is proven in the future that there are extraterrestrial visitors with triangle-shaped feet, then my photo published today potentially provides evidence of such creatures." 

In the article here, a Professor Yu speaks in a bungling way. We read,  "Professor Yu said, 'Given these results, we expect that next-generation neutrino research facilities such as Japan’s Hyper-Kamiokande or America’s DUNE will discover matter–antimatter asymmetry,' adding, 'We anticipate being able to understand why matter exists in overwhelmingly greater amounts than antimatter in the universe.' ”  But we already know that matter-asymmetry exists, so it makes no sense for Yu to be claiming that it will be discovered by the still-under-construction DUNE project. That's as silly as saying that you anticipate that some new project will discover that the sun exists. There is no basis whatsoever for the described "anticipation." The new paper describes 14 years of expensive neutrino search that failed to shed any light on why "matter exists in overwhelmingly greater amounts than antimatter in the universe."

We can describe the neutrino study projects listed above as "pigeonhole pet projects." That's because they are investigations of some topic of no interest to the general public, and only of interest to a very small number of physicists, such as neutrino specialists. If you are a scientist trying to get funding for one of these pigeonhole pet projects that are of no interest to 99% of the public, what sales strategy can you take? One strategy: try to make your little pigeonhole pet project sound like it has some relevance to some grand mystery that people are interested in. 

stumbling scientists