Fast Tree: A Science Fiction Story

In the year 2045 Nat Watkins should have been happy with his lot in life. His wife Matilda was a genetic engineer who had invented a product called Fast Trees that was a huge success. The success of the product had made the couple five million dollars.

When Matilda first discussed the idea of genetically engineered Fast Trees with Nat, he told her it would never work. People like natural things in their backyard, Nat argued, not a genetically engineered tree. But Matilda was insistent that the product would succeed. She said the main reason few people plant trees in their back yards is that the trees take years to reach a decent size. But, Matilda explained, a genetic engineer like her could remedy that defect, by using gene-splicing to create a tree that would grow two meters every month.

Matilda was right. After she got the genetic engineering right, Fast Trees became popular all over the country. People loved the idea that they could plant a tree in April and get a good shade tree by July or August.

Nat should have been happy with his clever wife and the financial bonanza she had produced. But there was only one problem. Matilda was middle-aged and plain-looking, and Nat had developed a big crush on a much younger and prettier woman named Vanessa who lived down the street. Slowly an evil idea began to grow in Nat's mind: that he could kill his wife, and be left with the family fortune to do anything he pleased, such as wooing the lovely Vanessa.

For weeks Nat thought about ways he could commit the crime of killing his wife. Then one day he came home and found his wife in the back yard planting a tree. 

“We've made so much money from Fast Trees, it's about time we had one in our own yard,” said Matilda. She had dug a large hole in which to plant the tree sapling. Next to the hole was a large pile of soil and the tree sapling. 

At this point a terrible thought entered Nat's mind. This is my golden opportunity, he thought to himself. Now that she's dug that hole, I'll just kill her with the shovel, and bury her in the hole.

BANG! Nat struck his wife's head with the shovel, and she fell to her knees. BANG! Nat hit his wife's head again with the shovel, and she fell to the ground, twitching. BANG! Nat hit his wife's head again with the shovel, and she died.

Nat then threw Matilda's body into the hole. He asked himself: what should I do with the Fast Tree sapling? He decided to throw that into the hole also. Then he filled up the hole, tossing all of the soil from the pile of soil into the hole. He then covered up the filled hole with a sprinkling of leaves. 

Nat then began to tell a story that his wife had ran away with another man. He began to spend some of the family fortune on fancy cars, gambling, and wild parties. Meanwhile, the Fast Tree planted in the back yard began to grow very quickly, just as genetically engineered Fast Trees always did.

One day Nat was having a wild party with several beautiful young women including Vanessa. There was loud music and much drinking. But suddenly the party was interrupted by a loud noise.

BANG! There was a sound of something rapping on the window. BANG! The loud sound was heard again. BANG! The third rapping sound caused Nat to wonder if this could be the police coming to investigate his wife's disappearance. Nat went to the window.

“Oh, it's only a branch rapping against the window,” said Nat. The branch was a branch of the Fast Tree, which in the two months since Matilda's murder had now grown to a height of four meters.

Nat felt a chill when he looked at the branch that was knocking on the window. The end of the branch had finger-like protruding twigs that made the branch resemble a human hand.

There was no further noise from the branch that day. The next day Nat was alone watching his holographic wall-screen. He was again disturbed by a rapping noise.

BANG! The tree branch knocked on the window. BANG! The loud sound was heard again. BANG! The third rapping sound caused Nat to notice that it had been three raps against the window, just like on the previous day.

There were no more knocks of the branch against the window. The next morning Nat had a troubling thought. He remembered he had killed his wife using three blows with a shovel. And each night the branch had rapped on the window, it had banged three times. Nat asked himself: was this just a coincidence?

Nat was troubled, and he tried to smother his worries with alcohol and partying. The next night he again entertained friends, including the young Vanessa. There was more loud music and laughing conversation. But then the sounds returned.

BANG! The tree branch knocked on the window. BANG! The loud sound was heard again. BANG! The third rapping sound caused Nat to lose his composure.

“Bang, bang, bang!” hollered Nat. “BANG, BANG, BANG! Have you noticed that the accursed tree branch always bangs the window three times? It's like the branch was trying to remind me of the three blows I struck to my wife's head!”

“What's that?” said Vanessa. “You told me your wife had left you, not that you hit her three times on the head. I'd better leave, and let you work this out in your own mind.”

Vanessa left, and drove immediately to the police. She told about what Nat had said. The next day the police arrived at Nat's house with a search warrant. Using one of the new portable X-ray scanners, they scanned the back yard, and quickly found the shape of a buried body. They dug up the Fast Tree that was two months old. They found that the roots of the tree had become completely entwined with the heart of a decaying corpse. It was the corpse of Nat's murdered wife Matilda.

Presented with the evidence, Nat confessed the murder. He was sentenced to life in prison.

After his imprisonment, there was debate about the strange case. Some said that the banging of the strange branch with a hand-like end must have been somehow caused by the spirit of Nat's wife Matilda, who may have haunted the tree entwined with her corpse. Others said it was all just a coincidence.

Which of these was right? The answer will never be known in this mortal life.

The Poor Design of Online Heart Risk Calculators

A few days ago the Washington Post published an article criticizing the reliability of online heart risk calculators. But the article failed to discuss the main reasons why such calculators are poorly designed. Let's look at some of the reasons why the average heart risk calculator is likely to do a poor job of alerting you if you have a relatively high risk of a heart attack over the next ten years.

Reason #1: The calculators ask for inputs on current cholesterol levels rather than asking about your lifetime eating habits.

All of about 8 or 9 online heart risk calculators I've looked at ask for your current total cholesterol level and the level of your HDL or “good” cholesterol. There are some big problems with doing that. The first is that a large fraction of all people don't remember what their latest HDL reading was. If you are like most people over 50, you probably remember whether your latest cholesterol reading was above 200, but don't remember what your HDL reading was. In such a case you will be unable to proceed when you come to a calculator such as the calculator here.

Another problem is that your latest cholesterol reading may not be a very good indicator of your current eating habits. Many people alter their eating habits in the weeks before taking a scheduled blood test, in hopes of getting a better cholesterol reading.

A third reason is that your heart attack risk depends relatively little on your current cholesterol level, and more on your lifetime eating habits. A heart attack can occur when plaque builds up in your arteries. The likelihood of that happening depends on your eating habits over the past few decades. Let's imagine two people, Ed and Sam, both age 60. Ed has been eating tons of red meat for four decades, but in the past year has reformed his eating habits, and brought his total cholesterol down to 200. Sam for the past 40 years has been eating little food high in bad cholesterol, and lots of food high in good cholesterol. But in the past year he's slipped a little, and his total cholesterol is now 220. Which has a higher chance of heart attack? It's Ed, not Sam, despite Ed's current lower cholesterol – because your lifetime eating habits determines how much plaque is in your arteries.

It would seem that rather than asking about your latest cholesterol reading (requiring an HDL number you probably don't know), our heart risk calculators should instead be asking about your lifetime eating habits.

Reason #2: None of the calculators has an input for resting heart rate.

There have been many scientific studies indicating that a person's resting heart rate has a large effect on a person's chance of having a heart attack or suffering sudden cardiac death. In the large Framingham heart study, the average resting heart rate for a male was 64 beats per minute. A much larger FitBit data set (derived from millions of users of FitBit devices) suggests that the average heart rate for male 60-year-olds in the US was about 62 beats per minute. But what if your resting heart rate is 70 beats per minutes or 80 beats per minute or 87 beats per minutes? According to numerous studies such as this one, your risk of heart failure or sudden cardiac death is much higher – perhaps as much as 300% higher for someone with a heart rate greater than 85 beats per minute.

Given the significance of heart rate, and the ease in which anyone can get their own resting heart rate by holding their wrist and using a clock, there would seem to be no excuse for not having a heart rate input slot on every online heart risk calculator. But how many such calculators have such a thing? None of them do.

Reason #3: Most of the calculators don't allow you to specify whether you have a family history of heart disease.

Most of the online risk calculators use what is called the ASCVD algorithm, and such calculators do not ask you whether you have any family history of heart disease. For example, the first calculator I get when I do a Google search for “heart risk calculator” is a calculator that does not ask me for whether anyone in my family had a heart attack.

But there is one online heart risk calculator that uses the “Reynolds risk” formula for computing heart risk, and that calculator does ask me “Did your mother or father have a heart attack before age 60?” When I choose “Yes,” my calculated 10-year heart attack or stroke risk jumps from 8% to 13%. So evidently whether your father or mother had a heart attack before 60 is a big factor that can affect your heart risk by as much as 40%. So why do the vast majority of online heart risk calculators not allow you to specify whether your mother or father had a heart attack before the age of 60?

Reason #4: None of the calculators allow you to specify whether you have a diagonal earlobe crease.

A diagonal earlobe crease is a line that some people have going across their earlobes. It looks like this:

Quite a few scientific studies have shown that if you have a diagonal earlobe crease on both ears (called a “bilateral” earlobe crease), the chance of you having cardiovascular disease is much higher. For example, this 1982 study was based on exact measurements of the artery health of 340 people, using coronary arteriography. The study found that having a diagonal earlobe crease has a positive predictive value of 91% for coronary artery disease, meaning if you have the diagonal earlobe crease you are 91% likely to have coronary artery disease. A similar 2004 study of 415 people (also using exact artery measurements though angiography) found that having the diagonal earlobe crease had a positive predictive value of 89% for coronary artery disease.

Clearly all of our heart attack risk calculators should have an input allowing you to specify whether you have an earlobe crease. But none of these calculators has such an input.

Reason #5: None of the calculators has an input asking about your exercise levels.

How much a person exercises can affect his risk of having a heart attack. It will come as little surprise that not exercising at all will increase your risk of a heart attack. But what is surprising is that a major study found that those who exercise very heavily may have a much higher risk of heart attack. Such is the finding of the very large CARDIA study. The Science Daily site reports this finding with the headline, “Physically active white men at high risk for plaque buildup in arteries.” The site states, “White men who exercise at high levels are 86 percent more likely than people who exercise at low levels to experience a buildup of plaque in the heart arteries by middle age, a new study suggests.”

Clearly, a decent heart attack risk calculator should have an input for how much you exercise. But none of the online calculators has such a thing.

Reason #6: None of the calculators has an input asking about how much time you spend sitting. 

It is sometimes said, "Sitting is the new smoking," because too much sitting can cause an increased chance of heart attack.  A 2015 meta-analysis on the association between heart risk and sitting found an association, but a pretty modest one, with a hazard ratio of 1.143, meaning lots of sitting might cause a 14% higher chance of a heart attack.   But a 2012 meta-analysis found a much larger risk, finding that those who sit the most can have "a 147% increase in the RR [relative risk] of cardiovascular events." Clearly a question on how long you spend sitting each day should be included in a heart risk calculator. None of them currently has such a thing. 

Reason #7: None of the calculators has an input asking about how much time you spend standing at work. 

Given the information just discussed, you will be surprised to read the following quotes from a scientist who summarizes a large study done by he and his colleagues:

We found that people who primarily stand on the job are twice as likely to develop heart disease as people who primarily sit....In fact, the incidence of heart disease among those respondents who stood a lot at work (6.6 per cent) was similar to the incidence of heart disease among workers who smoked on a daily basis (5.8 per cent) or those who were obese (6.9 per cent). 

What a decent heart attack risk calculator would look like

Based on all these considerations, I can show what a good heart attack risk calculator would look like. It would look like the page below, a page looking very different from all existing heart attack risk calculators. Unfortunately I can give you no URL for a page that implements such a design. I hope someone with expertise in this field will one day implement such a calculator. 

The Two Huge Asymmetry Mysteries Scientists Can't Solve

Among the many mysteries scientists cannot solve, two of them involve gigantic asymmetries that scientists cannot explain. The first such asymmetry is what is called the matter/antimatter asymmetry. 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 leads 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. So the amount of antimatter 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.

It would be incredibly inconvenient if matter and antimatter were equally distributed. So much energy is released when matter makes contact with antimatter that if there were trace amounts of antimatter lying about, you'd have “oops, someone blew up Europe because he stepped on a tiny piece of antimatter” situations all over the place.

The asymmetry of matter and antimatter (the fact that matter and antimatter do not exist in equal amounts) reminds us of the fact that the Big Bang theory is not quite a successful theory, in the sense of making only predictions that match reality. We read in the popular press triumphalist talk like the statement below by cosmologist Ethan Siegel:

This picture is part of what’s known as the hot Big Bang, and it makes a whole slew of predictions. Each one of these predictions, like a uniformly expanding Universe whose expansion rate was faster in the past, a solid prediction for the relative abundances of the light elements hydrogen, helium-4, deuterium, helium-3 and lithium, and most famously, the structure and properties of galaxy clusters and filaments on the largest scales, and the existence of the leftover glow from the Big Bang — the cosmic microwave background — has been borne out over time.

Siegel here fails to mention that the Big Bang theory predicts a universe with either equal amounts of matter and antimatter, or all energy and no matter (which is what would result from all the matter combining with antimatter). That is a gigantic prediction of the theory that does not match reality. We don't patch up this problem by adding the “cosmic inflation” speculation to the Big Bang theory, as that also predicts a universe with either no matter or equal amounts of matter and antimatter. So rather than engaging in such triumphalist talk, our cosmologists should be saying, “There must have been something far more going on at the beginning than we understand.”

Every several years we hear about some type of result (typically preliminary) which we are told may hold an answer to the mystery of matter/antimatter asymmetry. But such results don't hold up over time. The latest report of a promising preliminary result came in 2017, but by 2018 news stories were throwing cold water on such results, saying they did nothing to explain the mystery of matter/antimatter asymmetry.

There's another gigantic mystery involving asymmetry that scientists don't understand: the mystery of homochirality. Chemicals such as amino acids and sugars can be either left-handed or right handed. A left handed amino acid looks like a mirror image of the right-handed amino acid. Homochirality is the fact that in living things essentially all amino acids are left-handed, and all sugars are right-handed. But when such things are synthesized in a laboratory, or experimentally produced in experiments such as the Miller-Urey experiment, you see equal amounts of left-handed and right-handed amino acids or equal amounts of left-handed and right-handed sugars.

A left-handed amino acid and its right-handed counterpart

Based on the fact that it is just as easy for left-handed amino acids to form in the laboratory as right-handed amino acids, and just as easy for left-handed sugars to form in the laboratory as right-handed sugars, we would expect for there to be a symmetry in the handedness of amino acids, with an equal amount of left-handed and right-handed amino acids. We would also would expect a symmetry in the handedness of sugars, with equal amounts of left-handed sugars and right-handed sugars. But what we see is an asymmetry, with living things having only left-handed amino acids and right-handed sugars.

I can give an analogy for why homochirality is such a mystery. Let us imagine a stack of cards. On one side is a particular word.

And on the other side is the mirror image of that word.

Now, let us imagine someone tosses this stack of cards into the air, and the cards randomly arrange into a long, elaborate instruction. Let us also imagine that all of the cards show only one side: the side with the intelligible word, and not the side with the mirror image of that word.

We would have two great problems in explaining such a thing. The first would be that this elaborate set of instructions had formed randomly. The second problem would be explaining how all the cards had landed in a way so that all of the regular words had appeared, without any of the mirror image words appearing. A similar problem comes with explaining the origin of life. We have to explain not merely the “organization explosion” in which huge amounts of functional information appeared, but also the fact of all the amino acids being left-handed and all the sugars being right-handed. The fact of this homochirality greatly compounds the problem of explaining the origin of life.

There was in the news recently a goofy news story on this topic, which stated the following:

Homochirality, or one-handedness, plays a key role in cellular chemical reactions, and all living organisms (that we know of) contain the ‘left-handed’ molecules. Scientists aren’t sure why this is, but some believe the answer may have something to do with the molecules’ cosmic origin. In 2016, researchers found propylene oxide, a chiral molecule, in Sagittarius B2, which is a massive molecular gas cloud roughly 25,000 light years from Earth, near the center of our Milky Way Galaxy. The findings suggest that the chiral molecules necessary for life may have come from space, particularly from star-forming regions.

This is hardly helpful in explaining the mystery of homochirality. What we want to know is why sugars and amino acids display homochirality, and the fact of a “chiral molecule” of the biologically irrelevant propylene oxide modecule does nothing to explain that. The existence of a chiral molecule does not explain homochirality, just as the existence of a two-sided penny does not explain 300 consecutive coin flips that were all heads rather than tails. The problem isn't the existence of chiral molecules (molecules that can be left-handed or right-handed). The problem is why in living things we see only left-handedness in amino acids and right-handedness in sugars.

A much better article about homochirality is “The Origin of Homochirality” in the Chemistry World magazine. The article points out why homochirality is necessary for living things, saying, “No homochirality, no life.” The article says that according to a London chemist, “understanding homochirality is still completely unresolved.”

It would seem that once we consider homochirality, we need three miracles for life to appear from non-life. The first miracle is just for you to get all of the genetic information needed for life to begin, at least 160,000 DNA base pairs arranged in just the right way (with also the proteins that correspond to such a genome). The second miracle is for you to have homochirality, so that all of the amino acids have the same handedness, and all of the sugars have the same handedness. The third miracle is for the genetic code to originate, a complex symbolic system of representations in which particular combinations of nucleotides represent particular amino acids. Similarly, it would be a triple miracle if your 2-year-old in America were to start speed typing well-written how-to books in French. The first miracle would be that he could understand enough to write how-to-books, the second miracle would be that he could write in French, and the third miracle would be that he could do speed typing on a keyboard.

Memory Engram Theorists Vacillate All Over the Map

In a February post entitled "Turmoil of the Baffled Engram Theorists," I discussed a Science News article that showed the theoretical disarray of engram theorists, scientists who speculate about a physical brain basis for human memories. Three scientific papers in recent years suggest that claims that human memories are stored in brains do not have a solid theoretical basis well-substantiated by experiments.

One paper was entitled “The mysteries of remote memory,” and was published in the Philosophical Transactions of the Royal Society B. Speaking of long-lasting memories, the authors told us that “our current knowledge of how such memories are stored in the brain and retrieved, as well as the dynamics of the circuits involved, remains scarce.” Using the term “engrams” to mean the hypothesis that there are cells in the brain that store memories, the authors state “what and where engrams are implicated in remote memory storage and how they change over time have received little experimental attention thus far.” The authors also frankly tell us that “From engrams to spines surprisingly little evidence exists in the literature on the grounds of remote information processing, maintenance and storage to account for the lifelong and persistent nature of the mnemonic signal.” This type of candor is a refreshing contrast from the click-bait hype about memory research that we get in the science news, where dubious studies using insufficient experimental groups are often trumpeted as scientific breakthroughs.

One of the ideas about a brain storage of memory is that memories get stored in dendritic spines, little bumps on dendrites. But this study found that dendritic spines in the hippocampus last for only about 30 days. And this study found that dendritic spines in the cortex of mice brains have a half-life of only 120 days. So such dendritic spines don't last enough to store memories that last for years. The “Mysteries of remote memory” paper mentions a study that found that studied the persistence of dendritic spines, and found a “near full erasure of the synaptic connectivity pattern within 15 days post-learning.” The paper says “these incongruent findings point to the need for an alternative explanation to spine dynamics for remote memory stability.” In other words, we can't explain dendritic spines as some physical basis for long-term memory. Referring to the often stated speculations that memories start out in the hippocampus and are transferred to the cortex, the paper states “unequivocal experimental evidence in support of it is lacking.” The paper then spends some time talking about the very speculative possibility that DNA methylation has something to do with long-term memory, an idea for which there is no evidence. 

The overall impression we get from reading such a paper is one of uncertainty and disarray, as if no clear idea was emerging from brain studies on the long-term storage of memory. We get such an impression even more strongly from two other papers on this topic published in recent years. One is the 2016 paper “What Is Memory? The Present State of the Engram.” Very oddly for a scientific paper, the paper consists of ten sections, each written by a different author or authors. We get conflicting theories as to how a brain might store memories, with little agreement between the sections.

The 2017 paper here is entitled, "On the research of time past: the hunt for the substrate of memory." It is a portrait of memory theorists in disarray, presenting no one theory about how memory might be stored in a brain, and instead suggesting seven or more possibilities, none of which is plausible. The paper is all over the map in its speculations, like someone shooting a gun in all different directions.

The paper tells us on its sixth page that “Engram-labeling studies have shown that certain populations of neurons encode specific memories in mice.” This is not correct. The studies in question are typically small-sample studies with very low statistical power, in which there is a high chance of false alarms. In a typical such study, an experimenter will zap some small portion of a mouse's brain, and claim that he has elicited a fear memory stored in that part, producing a freezing effect in the mouse. But such freezing effects (which require subjective judgments) mean little, since it is known that there are many parts of a mouse's brain that can be stimulated to produce a freezing effect in a mouse.

The paper tells us on page 9 that “synaptic weight changes can now be excluded as a means of information storage.” But for many years neuroscientists have been pushing the very dubious dogma that memories are stored by changes in synaptic weights. As discussed here, this idea never made any sense, for there has never been a proven case of any information that was ever stored as changes in the weights of something, and also synapses are too volatile to store memories that last for decades, for reasons discussed later in this post. 

The authors then proceed to discuss a wide variety of possibilities for how memory might be stored in a brain.  These include the following (the quotes below in italics are from the paper):

Theory 1: “The particularly longlived proteins associated with DNA (i.e., nucleoporins and histones).” This is not a good option because a scientific paper tells us that the half-life of histones in the brain is only about 223 days, meaning that every 223 days half of the histone molecules will be replaced. So histones are not suitable for storing memories lasting decades.

Theory 2: “Some have suggested that DNA (or the epigenetic modifications on it) is the most suitable candidate for memory, being the cellular storage mechanism for other (lifelong) information.” For why this speculation is untenable, see the section entitled “Why Very Long-Term Memories Cannot Be Stored in the Cell Nucleus” in this post. Human DNA molecules have been exhaustively analyzed by multi-year projects such as the Human Genome Project and the ENCODE project, and no evidence has been found of human memories stored in DNA. See the "Why Long-Term Memories Cannot Be Stored in the DNA Methylome" section of this post for why DNA methylation is also an unsuitable possibility for memory storage. If DNA molecules stored memories, we would find that the DNA molecules in the brain of a dead person would vary a lot, with one DNA molecule in the brain being very different from another. Instead, all DNA molecules in the brain are basically the same, and are the same as DNA molecules in other parts of the body. 

Theory 3: “The late Roger Tsien recently proposed the notion that perineuronal nets, the extracellular matrices around neurons and synapses, provide the architecture for information.” Wikipedia tells us that these perineuronal nets are “composed of chondroitin sulfate proteoglycans,” but this paper tells us that the half-life of such molecules is only 10 days, making them unsuitable for a storage of memories lasting a lifetime. The idea behind this perneuronal nets speculation is that memory may be stored in a pattern of holes, like punch cards. The idea is absurd. IBM punchcards worked back in the 1960's because they worked with a punchcard reader which shined light through the punch cards. The brain has nothing like a punchcard reader to read information if it had information stored in such a way, and such a system only works with flat two-dimensional surfaces, not three-dimensional surfaces like that in the brain. There are two research papers that claim to have a result suggesting that perineuronal nets may be important in memory, but both do nothing to establish such a claim, because they both used fewer than 10 animals in some of their study groups (for a moderately reliable research result, 15 is the minimum number of animals per study group).

Theory 4: “Structures composed of short-lived components could constitute a long-term memory if the configurations were preserved by normal homeostatic replenishment.” To the contrary, there is certainly no “normal” bodily mechanism that might allow “structures composed of short-lived components” to store memories for decades.

Theory 5: “Other theories involve information storage or processing in microtubules, the long polarized helices of tubulin subunits that compose the cellular skeleton.” There is no evidence for such theories, and there is a good reason for rejecting them: the fact that there is high molecular turnover in microtubules. This paper tells us, “Neurons possess more stable microtubules compared to other cell types...These stable microtubules have half-lives of several hours and co-exist with dynamic microtubules with half-lives of several minutes.” So microtubules in the brain last less than a week, and are not any place that memories lasting decades could be stored.

Theory 6: “The physical connectivity within neural ensembles is a plausible new candidate substrate for memory information storage, with many merits, including robustness to insult, bioenergetic efficiency, stability of information storage in a potentially binary format, and a high capacity for informational content.” This is a completely different idea from all the previous things discussed, and the paper does not discuss it truthfully. Far from being a "plausible" idea having “many merits,” the idea has no merits. No one has any plausible idea as to how mere “physical connectivity” could be storing the complex things human remember. The paper refers us to the previously mentioned “What Is Memory? The Present State of the Engram” paper, but the sketch of the idea given in that paper does not present the idea in a coherent manner. We see a diagram showing what looks like a necklace of green beads as a representation of how "physical connectivity" could supposedly store information.  That's not a way to store complex information like humans learn. If there is “stability of information storage” in the connections between neurons, it is not the type of stability that would allow memories to be stored for years, let alone decades. The proteins in synapses have an average half-life of less than a week, and synapses themselves have a lifetime of less than a year. The research of Stettler suggests that synaptic connections do not last longer than about three months. In a paper he stated the following, referring to remodeling which would break any "connectivity pattern":

Depending on whether the population of boutons is homogeneous or not, the amount of bouton turnover (7% per week) has different implications for the stability of the synaptic connection network. If all boutons have the same replacement probability per unit time, synaptic connectivity would become largely remodeled after about 14 weeks.

A very important recent scientific paper is the paper “Synaptic Tenacity or Lack Thereof: Spontaneous Remodeling of Synapses.” The paper used the term “synaptic tenacity” for the idea that synapses (brain connections) are relatively stable. Making a devastating case against such a claim, the paper stated the following:

The aim of this Opinion is to discuss challenges to the notion of synaptic tenacity that come from general biological considerations and experimental findings. Such findings collectively suggest that synaptic tenacity is inherently limited, since synapses do change spontaneously and to a fairly large extent....It is probably unrealistic to expect that synapses maintain their particular contents and, by extension, their functional properties with pinpoint precision. This expectation is further challenged by the fact that synapses are not rigid structures but rather are dynamic assemblies of molecules (and organelles) that continuously migrate into, out of, and between neighboring assemblies through lateral diffusion, active trafficking, endocytosis, and exocytosis....Closer examination reveals, however, that properties of individual synapses, such as spine volume, presynaptic bouton volume, synaptic vesicle number, active zone (AZ) molecule content, and PSD protein content fluctuate considerably over these timescales....Imaging studies in primary culture indicate that synaptic configurations erode significantly over timescales of a few days....The findings summarized above indicate that synaptic tenacity is inherently limited or, using the terminology of Rumpel, Loewenstein, and others, that synapses are intrinsically ‘volatile’....When it comes to cognitive functions, long-term memory is one area where the notion of synaptic volatility raises perhaps some of the most challenging questions. In light of findings discussed in this Opinion article, and possibly others, age-old notions concerning relationships between histories of ‘elementary brain-processes’, connection strengths, and memory traces might need to be revisited; put differently (to paraphrase James, modern science might need to improve on this explanation.

The evidence presented by this “Spontaneous Remodeling of Synapses” paper is devastating evidence against the predominant theory of the brain storage of memories (that memories are stored by changes in synapse strength), and also Theory 6 mentioned above, that memories are stored by some “connectivity pattern” created by synaptic connections. Neither theory can be true if synapses have the kind of volatility described in the paper.

In a 2010 book two neuroscientists state that they are “profoundly skeptical” about the main theory of a physical storage of memory, but suggest that they have nothing like a substitute theory to offer:

We take up the question that will have been pressing on the minds of many readers ever since it became clear that we are profoundly skeptical about the hypothesis that the physical basis of memory is some form of synaptic plasticity, the only hypothesis that has ever been seriously considered by the neuroscience community. The obvious question is: Well, if it’s not synaptic plasticity, what is it? Here, we refuse to be drawn. We do not think we know what the mechanism of an addressable read/write memory is, and we have no faith in our ability to conjecture a correct answer.

I submit that the reason for such hesitancy is that there is no theory of a physical storage of memory that can stand up to careful scrutiny, no theory that can explain both memories that can form instantly and the fact that we can instantly retrieve memories of things learned or experienced long ago. Deprived of any credible neural explanation, we should conclude that human episodic and conceptual memory must be a spiritual or psychic or soul phenomenon, not a neural phenomenon.

One of the many reasons for rejecting claims that memories are stored in brains discussed at this site is the essentially instantaneous speed at which humans are able to remember very rarely recalled pieces of information. You say to me, “Dizzy Dean,” and I may in less than two seconds start saying, “eccentric St. Louis Cardinals pitcher, in the 1930's,” even though I haven't thought or read about Dizzy Dean in decades. How could a brain achieve this effect through reading just the right little spot where the information was stored, which would be like instantly finding a needle in a mountain-sized haystack, given a million little spots in the brain where a memory might be stored?

One major reason why it seems hard to believe that the brain could achieve instant recall is that neurons are slow. Information is passed around in a brain at the slow speed of about 100 meters per second, which is only the tiniest fraction of the speed at which electrical signals move about in a computer. Based on this fact we should consider a brain absolutely incapable of performing memory recall as quickly as humans do.

It is often claimed that the brain “makes up” for its slow speed of nerve transmission by being “massively parallel.” The claim that the brain is massively parallel is false. In the computer world, a computer system is massively parallel if it consists of multiple CPUs or central processing units, each of which is running a computer program. We know of nothing in the brain that acts like a computer CPU, nor do we know of anything like a program that the brain runs to compute. It is false to claim that each neuron is like its own CPU. Neurons do not run any program like a computer CPU does. So we cannot at all overcome the problem of low signal transmission speeds in the brain by claiming that the brain is “massively parallel.” It is true that the brain consists of many neurons working together, but that does not make the brain massively parallel. My television set has many transistors working together, but my television set is not massively parallel; and my arms have many cells working together, but that does not make my arms massively parallel. The brain does does not consist of multiple programs running together on multiple processors, and we don't even know of a single program running anywhere in the brain.

Let us imagine some weird group of conspiracy theorists who maintain that secret information from the World War II era is stored in the leaves lying about in modern Germany. If the theorists were to maintain that such information is written on individual leaves, you could easily show the absurdity of the theory by pointing out that leaves don't last much longer than a year. If the theorists were to maintain instead that it was the arrangements of the leaves that stored the information, with one type of leaf pile representing one thing and another type of leaf pile representing something else, you could also show the error of the theory by pointing out that leaf piles are unstable and ever-changing, being blown around by the wind. Similarly, the protein turnover, synaptic volatility and synaptic remodeling discussed in the "synaptic remodeling" paper above are constraining effects as powerful as the short lifetimes of leaves and the instability and impermanence of leaf piles. Anyone claiming that memories persist in synapses for 50 years is advancing a claim as unbelievable as the 50-year "leaf storage" claims of such conspiracy theorists.