Sunday, November 18, 2018

#45. The Denervation-supersensitivity Theory of Mental Illness [neuroscience, evolution, genetics]

NE     EV     GE     
Red, theory; black, fact.

People get mental illness but animals seemingly do not, or at least not outside of artificial laboratory models such as the unpredictable, mild-stress rodent model of depression. A simple theory to account for this cites the paleontological fact that the human brain has been expanding at breakneck speed over recent evolutionary time and postulates that this expansion is ongoing at the present time, and that mental illness is the price we are paying for all this brain progress.

In other words, the mentally ill carry the unfavorable mutations that have to be selected out during this progress, and the mutation rate in certain categories of mutation affecting human brain development is elevated in modern humans by some sort of "adaptive" hot-spot system. "Adaptive" is in scare quotes here to indicate that the adaptation inheres in changes in the standard deviation of traits, not the average, and is therefore not Lamarkian.

In brain evolution, the growth changes in the various parts very probably have to be coordinated somehow. I conjecture that there is no master program doing this coordination. Rather, I conceive of the human brain as comprising scores of tissue "parcels," each with its own gene to control the final size that parcel reaches in development. (This idea is consistent with the finding of about 400 genes in humans that participate in establishing body size.) All harmonious symmetry, even left-right symmetry, would have to be painstakingly created by brute-force selection, involving the early deaths of millions of asymmetrical individuals. This idea was outlined in post 10.

Assuming that left and right sides must functionally cooperate to produce a fitness improvement, mutations affecting parcel growth must occur in linked, left-right pairs to avoid irreducible-complexity paradoxes. I have previously conjectured in these pages that the crossing-over phenomenon of egg and sperm maturation serves to create these linked pairs of mutations, where the two mutations are identified with the two ends of the DNA segment that translocates. (See "Can Irreducible Complexity Evolve?")

Most of the evolutionary expansion of the human brain appears to be focused on association cortex, which I conjecture implements if-then rules, like those making up the knowledge bases familiar from the field of artificial intelligence. The "if" part of the rule would be evaluated in post-Rolandic cortex, i.e., in temporal and parietal association cortices, and the "then" part of the rule would be created by the pre-Rolandic association cortex, i.e., the prefrontal cortex. The white matter tracts running forward in the brain would connect the "if" part with the "then" part, and the backward running white-matter tracts would carry priming signals to get other rules ready to "fire" if they are commonly used after the rule in question.

Due to such tight coordination, I would expect that the ideal brain will have a fixed ratio of prefrontal cortex to post-Rolandic association cortex. However, the random nature of the growth-gene bi-mutations (perhaps at mutational hot-spots) permitting human brain evolution will routinely violate this ideal ratio, leading to the creation of individuals having either too much prefrontal cortex or too much temporal/parietal cortex. In the former case, you will have prefrontal cortex starved of sensory input. In the latter case, you will have sensory association cortex starved of priming signals feeding back from motoric areas.

Denervation supersensitivity occurs when the normal nerve supply to a muscle is interrupted, resulting in a rapid overexpression of acetylcholine receptors on the muscle. This can be seen as an attempt to compensate for weak nerve transmission with a tremendous re-amplification of the signal by the muscle. Analogous effects have been found in areas of the cerebral cortex deprived of their normal supply of sensory signals, so the effect seems to be quite general.

In cases of genetically-determined frontal-parietal/temporal imbalance, I conjecture that the input-starved side develops something like denervation supersensitivity, making it prone to autonomous, noise-driven nervous activity.

If the growth excess is in sensory association cortex, this autonomous activity will manifest as hallucinations, resulting in a person with schizophrenia. If the growth excess is in the prefrontal cortex, however, the result of the autonomous activity will be mania or a phobia. Depression may originally have been an adaptation to the presence of a man-eating predator in the neighborhood, but in civilized contexts, it can get activated by the unpredictable (to the sufferer) punishments resulting from manic activity. If the mania is sufficiently mild to co-exist with depression, as in type II bipolar disorder, then the overall effect of the depressive component may be like a band-aid on the mania.

The non-overgrown association cortex might even secondarily develop the opposite of denervation supersensitivity as the result of continual bombardment with autonomous activity from the other side of the Rolandic fissure. This could account for the common observation of hypoprefrontality in cases of schizophrenia.

#44. Sunshine in Covey's Gap [evolutionary psychology, neuroscience]

EP     NE     
Red, theory; black, fact.

Who has not felt frustration at the difficulty and seeming impossibility of making a disagreeable emotion go away before we weaken and act it out, to our detriment? Techniques of true emotional control, i.e., making the bad feelings disappear rather than white-knuckle, open-ended resistance to acting them out, are not impossible, just non obvious. You just have to persuade yourself that this bad is good and believe it.

For the modern person, that second part, the believing, is difficult to achieve robustly if one is using religious solutions to the problem, the domain of soteriology (being "saved"), easier with psychoanalytical solutions, and, I am here to say, easiest of all with scientific solutions. "Believing," for me, means being prepared to bet your life on the truth of a proposition.

Steven Covey writes in "The Seven Habits of Highly Effective People" that between stimulus and [emotional] response, humans have, somewhat metaphorically, a "gap" in the causal chain and animals do not. In the gap, you find such things as imagination, self-awareness, conscience, and self will. He correctly lays tremendous emphasis on this point. George Santayana seems to have grasped this truth when he wrote: "Our dignity is not in what we do but in what we understand. The whole world is doing things." [source, Wiki quotes, accessed 11-06-2018]

Neuroscientist Joseph LeDoux has even elucidated what could be the neural pathways that make Covey's gap possible. A direct pathway from the thalamus to the amygdala mediates the basic fear response but an indirect pathway that leads from thalamus to cerebral cortex to amygdala provides a more nuanced, intelligent amendment to the first response. Full cancellation of the direct pathway by the indirect would account for Covey's gap, and in principle, this could be done by a cortical relay through the inhibitory interstitial neurons of the amygdala that terminate on the amygdalar projection cells.

The doctrines of classical religion probably lead to such cancellation of emotions such as hate and fear by activating the same circuits that are used by a parent to reassure a needlessly fearful infant.

Apparently, classical religion is all about getting people to do the right things for the wrong reasons. When the discipline of evolutionary psychology is sufficiently developed, we can look forward to the age when people do the right things for the right reasons.

Friday, September 7, 2018

#43. A Discovery of Hackers [population, evolutionary psychology]

PO     EP     
Red, theory; black, fact.

9-07-2018: I was saving this for the Sunday before Halloween, but decided that it couldn't wait. The basic idea of this post is that the hacker phenomenon is psychologically and sociologically akin to what was once called witchcraft. Let me hasten to clarify that I am talking about witchcraft the social phenomenon, because I don't believe in anything supernatural. However, the height of the witchcraft hysteria in Europe occurred during the sixteenth century, when there were no computers. (I focus on Europe here because my ancestors came from there as did those of most people I know.) It was, however, a time of unprecedented scientific advance, and if science paced technology then as now, quite a few new technologies were coming into knowledge for the first time.

I suggest that the defining toxic ingredient in black-hat hacking is new technology per se. We should therefore expect that with time, computer hacking will spread to new-technology hacking in general and that the computer-centric version must be considered the embryonic form. This is bad news because there has never been so much new technology as now, but at what point in history has this statement not been true?

Belief in and persecution of witches is so widespread across human cultures that it must be considered a cultural universal. Scholars focus on the persecution part, blithely assuming that there is absolutely nothing real driving it, and that the subject people of the study are, by implication, a bunch of blithering idiots, and sadists to boot. I find this stance elitist. Never judge a man until you have walked a mile in his shoes. These people all have brains in their heads built to the exact same design as our own, and the role of education may be overrated when cultural universals are in play.

I suggest that the defining idea of the witch/technology-hacker (tacker) is viewing new technology as a possible means to increased personal power. To produce a tacker, this idea must be combined with a mad-dog rejection of all morality. 

A technology ideal for tacking/witchcraft must be usable without the identity of the agent coming into general knowledge, and is thus sociologically similar to the ring of Gyges mentioned in Plato's Republic. The anonymity conferred by the Internet makes it one of our worst rings of Gyges, but just wait. More will be discovered in other realms of technology as the hackers branch out, perhaps in unholy alliance with the currently popular Maker movement. Makers, wake up! It's not too early for a manifesto!

How common are Gygean technologies? Hard to say, but it may help to list some.
  • Ionizing radiation was known from the work of Roentgen in 1895 (x-rays) and Villard in 1900 (gamma rays) and for the first time, a means to destroy healthy, living tissue silently and through walls solid enough to conceal all signs of the agent, had become available. (See my blog "Journalist's Progress," at (Link under reconstruction)https://xrra.blogspot.com )
  • The lead pencil, introduced in the sixteenth century already alluded to, was originally made with actual lead metal (instead of graphite and clay mixtures), which we now know to be insidiously neurotoxic, especially to children--knowledge to warm the heart of any proper witch.
  • In the time of Christ in the Middle East, the Roman occupiers knew of ten or so plant-derived poisons, including opium. The very concept of a poison could have been new in those days, and poisons are the classical hard-to-detect weapons. If the weapon is hard to detect, so is the agent. A crypto-technological explanation for some of the events of the New Testament seems possible.
Gygean weapons are doubly "invisible" when based on new technology because these modi operandi are not yet on any body's radar, so the first x number of people who spot them are likely to be disbelieved and their sanity questioned.

Witches have always operated in the zone of perceptual blindness to abuses that transiently opens up after the introduction of any new technology. The psychological invisibility of weapons based on new technology is probably the factor that led witches to become associated with magic. 

Moreover, since the technology is unprecedented in human evolution, the levels of resentment that become inducible in the victims are potentially unprecedented and unphysiologically intense, leading to grotesquely disproportionate punishments being meted out to discovered witches, and this for strings of crimes that would have been extremely serious even considering strictly proportionate punishments. I suspect that the historical accounts of witch-burnings have all been cleaned up for a squeamish readership.

Why were a majority of European witches female? At the height of the anti-witch hysteria, the Black Death was raging and the local human population was probably having trouble keeping its numbers up. On general adaptationist assumptions, all kinds of social forces would have been working to reduce women to baby-making machines, whatever their endowments or aptitudes. This would have created an inevitable push-back in the most intelligent women to reclaim some of their personal power, and witchcraft would have seemed an attractive option for doing this.

Today, the hackers (soon-to-be tackers) are mostly male and the demographic challenge is too many people, not too few. Calhoun's overpopulation experiments on rodents imply that people will become more aggressive if forced to live at higher population densities, and such a relentless increase in aggressiveness may be driving the current reemergence of the witch/tacker. 

It doesn't help that organized religion, the traditional great enemy of witchcraft, is withering on the vine in this country, probably due to the intellectual fallout from Darwin's theory of evolution combined with the failure of the public to understand that a scientific world-view is never finished.

9-08-2018: Proposed definition of "witch": a person in moral free fall under the corrupting influence of technologies that lend themselves to secret abuse for the increase of personal influence.

Wednesday, July 25, 2018

#42. Corporate Sin [evolutionary psychology]

Red, theory; black, fact.

7-25-2018: A moment's reflection reveals that not all of humanly willed unhappiness is due to two persons interacting, either in a sadness cycle or an anger cycle. Wars of depopulation and wars of dispersal represent these interactions promoted to the level of entire societies. This promotion theory assumes that the same hard-wired wetware is being used for both levels, but with the addition of a few more bits of code to support the social level.

Theologians such as Bishop Baycroft, writing in "The Anglican Way," are well aware of this extra dimension of human misery, referring to it as "corporate sin," and admit that it is a more difficult problem than individual sin. The advice I give in "Signaletics for Salvation" (https://nightbull.blogspot.com) will not help you efficiently if your unhappiness has its roots in corporate sin (for example, if you are caught up in a military draft or are a slave), but it may be better than nothing. But let's see what we can surmise about those extra bits of code.

The basic design seems to be to transform a tiff between two individuals into a tiff between two leaders, then copy the emotions of the leaders into the heads of all the followers on both sides. Thus, a political leader is a kind of emotional conductor. This is why we have leaders.

By this theory, World War II was a tiff between Adolf Hitler and Winston Churchill, both famous for their speeches in which they inspired passions in their followers.

How do you get to be leader? The simplest answer seems to be that you just get famous and you are also someone who doesn't see a way to end his pain without involving the whole world. <07-21-22: As for how I ended my own pain, minding my own business and reaching out to family at times of need seems to have sufficed. I also had a talk with my federal MP at one point.>

An attractive theory about fame, in turn, is that all fame is 90% being-famous-for-being-famous, and 10% (or less) is being famous for something else, call it the predisposing factor. Human inter group interactions have the form we observe because these predisposing factors are not random but are due to natural selection. Furthermore, they are conditional upon prevailing conditions, such as the price of bread relative to wages. Finally, they already exist at the individual level. The process of garnering the absurd 90% of fame is the by-now familiar phenomenon of going viral, and its earlier historical equivalents. 

I imagine that this process is a positive feedback loop in the brain that involves the attentional system and Hebbian plasticity, the latter well known among students of neuroscience for having a built-in positive feedback. We also know that emotions are contagious (See: Hatfield E, Cacioppo JT, Rapson RL. Emotional Contagion. New York: Cambridge University Press, 1994).

The final bit of code we need to produce leaders and thus corporate sin is a tendency of this contagiousness to be potentiated by the famousness of the emoter one is observing. This mechanism of social control is distinctly different from the snowball effect that I likened to a black hole in an earlier post. It will take more thinking to decide which is more accurate.

Friday, July 20, 2018

#41. The Sadness Cycle [evolutionary psychology, neuroscience]

EP     NE     
Red, theory; black, fact.

7-20-2018: This post builds on "Signaletics for Salvation," a post in the companion blog, "Experimentalist's Progress, " at https://nightbull.blogspot.com. The theory part of that post is reprinted below with slight modification for the convenience of the reader.

The anger cycle and the sadness cycle reach their full flower in wars of dispersal and wars of depopulation, respectively. These were discussed in the post "Two Kinds of War" in this blog.

Wars of depopulation serve to prevent Malthusian disasters such as general famine. The sadness cycle is a form of altruism that facilitates this depopulation by making a portion of the population sad and suicidal and the remainder contemptuous and entitled. The contemptuous ones take everything the sad ones have, ultimately their lives, and the sad ones let them.

If the sacrificial lambs were fighting what is essentially a form of cannibalism tooth and nail, the transfer of property would leave the heritors with many injuries, which would defeat the purpose of the whole process, which is to leave the residual population stronger and healthier than before under conditions of restricted food supply. However, always bear in mind that the sad ones and the contemptuous ones are playing two roles within the same adaptation; if you can play one role, you can play the other. However, if you unfortunately carry some unfavorable mutation, you will be predisposed to the sad role. This is another way the adaptation leaves the population more robust than before.

Since no altruism can evolve in the presence of selfishness unless the altruists are only altruistic to other altruists, a signaling cycle is required to lock the altruists together to the exclusion of non-altruists. Thus, sadness induces contempt and contempt induces sadness, and so on in a vicious cycle leading to the complete destruction of the sad ones and the transfer of all their property specifically to the contemptuous ones. This dynamic could be the origin of elder abuse and clinical depression.

Macchiavelli wrote, "He is made contemptible who is held to be changeable, light, effeminate, pusillanimous, irresolute, and from these the Prince must guard himself as from a reef." The traits listed appear to be the symptoms of unacknowledged sadness, and were no doubt quite lethal in Macchiavelli's time. Due to the present skyrocketing of the world population with the concomitant "Calhoun effect" from crowding stress, we are no doubt due for a remacchiavellianization of daily life. For example, should I even be sharing these insights with you instead of keeping them to myself to my own advantage or at least posting them on a commercialized blog? Does my slowness to commercialize indicate suicidally self-giving tendencies that will one day prove fatal?

6-29-2018: The Anger Cycle (reprinted)
Much of human unhappiness comes from destructive, escalating signaling cycles, usually between two persons. Examples: arguments, feuds, schools of thought, gang wars, revolutions. The signals exchanged are initially personal expressions of anger. Importantly, these expressions are multi modal, and therefore highly redundant. (e.g., threatening utterances, tones of voice, facial expressions, gait, crashing and banging things, spying, following, etc.) Your anger comes out of you "through every pore."

These signals are too many and varied for conscious control, which is why most people remain enslaved by their signals and cycles. The anger cycle is presumed to escalate until one of the parties must leave the country. When people are threatened, they seek allies, so all of society eventually gets drawn in and polarized as the escalation proceeds apace, like a black hole. Therefore, it is a group that must eventually leave, not a single individual, which is the basis of the refugee phenomenon. 

In ecological terms, the refugee phenomenon is clearly sub serving the function of dispersal. However, dispersal-producing behavior is fundamentally altruistic in a backhanded way. The benefit to the supposed loser, the group that eventually gets driven out, is that occasionally they find a newly-emptied vacant habitat in which to settle and therefore can reproduce without competition. This is a tremendous benefit in evolutionary terms and may once have been great enough to redeem all the waste and suffering of human-style dispersal. 

However, altruistic behavior cannot evolve in the presence of non-altruists unless a signaling system is established to ensure that altruists are only altruistic to other altruists. That is why I lay so much emphasis on signaling here. The reason why the signals are so multi modal is that the altruism program probably breaks down occasionally because of the short-term advantages of being a non-altruist. This has probably happened many times in the past and the broken algorithm was repaired each time by natural selection with the addition of yet another signal component. 

Multi modality implies the existence of a neuronal OR-element somewhere on the sensory side, and the amygdalae could be these OR-elements. More precisely, the amygdalae could be specialized for providing OR-elements generally to the brain by virtue of a characteristic, unique amygdalar cytoarchitecture.

7-20-2018: The various signal cycles may reinforce each other. The four signal cycles that seem to form the framework of human life seem to have such an interdependence. These are: mother-child bonding, which could potentiate man-woman bonding, which could potentiate the anger cycle (via jealousy), which could potentiate the sadness cycle. These insights come from introspection and my own biographical data.

Friday, June 1, 2018

#40. The 1950 Ramp [population, genetics, evolutionary psychology, engineering, neuroscience]

PO     EN     EP     NE     GE     
Red, theory; black, fact.

6-01-2018; 
Since about 1950, the world population has been increasing along a remarkably steady ramp function with no slackening in the rate of increase yet apparent, although one cycle of oscillation in the slope occurred during the Sixties. Malthusian reasoning predicts an exponential increase, which this is not. From several lines of evidence, I keep coming back to the idea that humans must have a subconscious population controller in their heads, and yet such a controller would have leveled out the increase by now. Until now, no theory has sufficed to explain the facts.

I here propose that the natural population curve for humans in good times is a saw-tooth waveform, with population ramps alternating with political convulsions that result in a large group being expelled permanently, resulting in the precipitous but limited drop in local population density that ends the saw-tooth cycle. This cycle accomplishes the ecological dispersal function to which I allude many times in these pages. The population must ramp up for a time to sustainably create the numbers needed for the expulsions. The WHO population curve shows only a ramp because it is a worldwide figure and therefore population losses in expelling regions are balanced by population increases in welcoming regions. This also implies that human population has been increasing in a way unrestrained by food or resource availability or any other external constraint since 1950, to now.

Clearly, human population is being controlled by instinctive factors, but not to a constant absolute density, but rather to a constant rate of increase. Population density would go up along the much faster, steeper, and more disastrous exponential curve of Malthus if there were actually no controller.

My formal training in engineering and neuroscience justifies a bit of speculation as to mechanisms at this point. Look first for such a controller in the hypothalamus, already known to control other variables, such as temperature, by feedback principles.

In school, I was taught that nature does not reinvent the wheel, which I understand to mean that once a brain structure evolves to serve a particular computational function, it will be tapped for all future needs for such a calculation. This process may make it grow larger or develop sub-nuclei, but additional, independent nuclei for the same computation will never evolve.

I will continue to assume that the controller is a conventional PID controller, as in previous posts. To make it control rate of increase rather than absolute population density, you put a differentiator in the feedback pathway. Look first in the amygdala for such a differentiator. If you are of the opinion that human population control is urgent, then you must knock out this differentiator and replace it with a simple feed-through connection. Fortunately, one common way for evolution to implement differentiation in mammals is to begin with such a feed-through connection and supplement it with an inhibitory, slow, parallel feed-forward connection. If this is the case here, then you just inhibit the feed-forward pathway pharmacologically as specifically as may be, and the job is done. Subjectively, the effect of such a drug would be to take away people's ability to get used to higher population density in deciding how many children to have. An increased propensity to riot should not occur.

I assumed in the last post that the political convulsions that produce dispersal are triggered by the value on the integrator of the PID controller rising above a threshold. However, in the above design solution, the convulsion would be triggered by the raw, undifferentiated population-density signal rising above some threshold. Look in the amygdala for this signal as well. Consistent with this, bilateral removal of the amygdalae and hippocampi in monkeys is known to have a profound taming effect accompanied by hypersexuality, known as the Kluver-Bucy syndrome.

6-17-2018: To be consistent, I would have to say that the differentiator for the population signal is more likely to be in the hippocampal formation by the argument of nature not reinventing the wheel, because in an earlier post, I interpreted the hippocampus as the site of four successive differentiations that carry out a Fourier transform by mapping sinusiodal waves back onto themselves at a particular best frequency, in the presence of a map of such best frequencies.

However, this setup would require the creation of two neuron-to-neuron connections for its evolution; a first connection to send the amygdalar raw population signal to the hippocampus, and a second to send the differentiated result back for further processing. At best, this would require two simultaneous mutations. Either change by itself would be at best useless and could never be selected. This appears to be another example of irreducible complexity requiring the bi-mutation mechanism described in the previous post. 

The mechanisms usually offered to explain cases of apparent irreducible complexity, such as spandrelling, exaptation, and scaffolding, all appear to lack time efficiency and processiveness. I previously said that in evolution there are no (absolute)  deadlines, but relative deadlines can easily be created by an interaction of processes. In the presence of relative deadlines, such as adaptive footraces to be the first clade to exploit a newly-habitable area or a new niche, time is of the essence and selection for speed and evolvability can be expected. Such selection will create mechanisms such as crossing over that enhance evolvability.

Saturday, May 26, 2018

#39. Can Irreducible Complexity Evolve? [genetics, evolution]

EV     GE     
Red, theory; black, fact.

5-26-2018: Influential biologist Richard Dawkins wrote in "The God Delusion" that a genuine case of irreducible complexity will never be found in biology. A case of irreducible complexity would be some adaptation that would require an intelligent designer because it could never evolve one mutation at a time, and Dawkins believes there is no such intelligent designer in biology.

In classic natural selection, each mutation must be individually beneficial to its possessor in order for selection to increase its prevalence in the population to the point where the next incremental, one-mutation improvement becomes statistically possible. In this way, all manner of wondrous things are supposed to evolve bit by tiny bit.

However, I am seeing irreducible complexity all over the place these days. For example, your upper-jaw dentition must mesh pretty accurately with that of your lower jaw or you can't eat. Thus, the process of evolutionary foreshortening of the muzzle of the great apes to the flat human face could never have happened, assuming that a single mutation affects only the upper or lower jaw. But it did. (Let us gloss over the fact that that is an assumption, because the contrary seems to require non-local rules in development.)

Furthermore, how can any instinctive signaling system evolve one mutation at a time? At a minimum, you always need both the transmitter adaptation and the receiver adaptation, not to mention further mutations to connect the receiver circuit to something useful. The evolution of altruism presents a similar problem. The lonely first altruist in the population is always at a disadvantage in competition with the more selfish non-mutants unless it also has a signaling system that lets it recognize fellow altruists (initially, close relatives) and a further mutation that places the altruistic behavior under the control of the receiver part of this system. Thus, altruists would only be altruistic to their own kind, the requirement for altruism to be selected in the presence of selfishness. Finally, the various parts of this system must be indissolubly linked in a way that the non-altruists cannot fake.

My solution is to label the crossing-over events that occur during meiosis as "tetra-mutations." In crossing over, two homologous chromosomes pair up along their length and swap a long segment of DNA, a process requiring four double chain breaks and their corresponding repairs. Because of the presence of single-nucleotide polymorphisms, the homologous chromosomes are not exactly the same, so that each of the upstream sides of the four chain breaks ends up in a subtly different genetic environment. If the break point falls between a cis-acting regulatory element and the corresponding structural gene, for instance, the former may now control the expression of a slightly different protein. Thus, there could be as many as four distinct functional consequences of one crossing-over event. Why not call that a tetra-mutation?

In this way, a concerted change affecting four distinct sites becomes possible. The two ends of the recombinant segment can in principle be functionally unrelated initially. They become related if both are affected by the same tetra-mutation and the entire change increases fitness and is thus selected.

A single tetra-mutation could in principle produce viable altruism at one stroke because of the number of simultaneous changes involved. 

The probability of a combination of simultaneous local changes being beneficial to the organism is much smaller on mathematical grounds than is the probability of a given single-nucleotide change being beneficial. However, these unfavorable statistics are at least partly offset by the existence of a dedicated system for producing tetra-mutations in large numbers, namely meiosis, part of the process of maturation of egg cells and sperm cells.

In the big picture, tetra-mutations provide a way for a species to discontinuously jump into new niches as they open up, possibly explaining how a capacity for this kind of mutation could spread and become characteristic of surviving species over time. This idea also provides a ready explanation for the lack of transitional forms in the fossil record.

5-30-2018: Here is the search description again, in case you missed it or could not see all of it: Sexual reproduction may allow the evolution of irreducible complexity by increasing the intrinsic complexity of the basic building block of change, the mutation.

6-12-2018: Upon further reflection, it seems that the tetramutation construct described above lacks validity because during gamete maturation it falls apart into two bi-mutations, both of which cannot contribute to the same zygote. The bi-mutation is stable, however, because of the intervening translocated DNA segment. It is harder to see how a complex adaptation like altruism could evolve out of nothing but mono-mutations and bi-mutations, but that does not mean the theory put forward in this post is necessarily wrong. One must not argue from lack of imagination. It is an interesting question, actually, what is the minimum set of all mutation types necessary to account for all known adaptations.

8-27-2019: In my ignorance, I have undersold the bi-mutation idea. A very far-reaching change to the genetic information can occur during crossing-over that is not at all subtle and is termed unequal crossing-over. This form of the process arises because of inaccuracies, sometimes major, in the initial alignment of the homologous chromosomes prior to crossing-over. When the process is finished, one chromosome has been shortened and the other has been lengthened, with gene duplication. This is the major source of gene duplication, which, in turn, is a major source of junk DNA, the part that is classified as broken genes. Two questions come to mind. The first is, are anatomical features such as jaw length and axon targets somehow controlled by variations in gene dose? The second, which is a tangent, is, are broken genes really broken or just temporarily switched off by genetic drift at some mutational hot spot in the recognition site of some transcription factor? The analogy here is to a generator in a power plant that has been placed in stand-down mode because of a temporary decrease in the demand for electrical power.