[Paleopsych] is evolutionary change stockpiled?

HowlBloom at aol.com HowlBloom at aol.com
Mon Nov 22 23:41:34 UTC 2004

Greg Bear just sent me an amazing paper he delivered to the American 
Philosophical Society.  I've enclosed a copy below.

The paper points out that evolution appears to occur in short bursts followed 
by long periods of stability.  He points out that this is more meaningful 
than at first it seems.  Evolutionary changes, he says, are apparently stored up 
but are kept from expressing themselves.  Then, when the right signal comes, 
they come out of hiding and change the organism in which they've been hiding.  
They don't just change one organism.  They make that change in a massive crowd 
of organisms--and in crowds of crowds.  

In one of my papers, The Xerox Effect (see 
http://physicaplus.org.il/view_eng1.html), I've called the spontaneous and simultaneous precipitation of 
protons, galaxies, and stars supersimultaneity and supersynchrony.  In Greg's view, 
this supersimultaneity and supersychrony also occurs in the evolution of life.

But how does it work?  How do evolutionary changes stack up in storage?  Do 
they go through any sort of pretesting, any process of natural selection, any 
tryouts in the obstacle course of the real world?  How do they do this if 
they're not expressed in bodyplans or bodychanges that can be put through their 
paces to see if they work?

And, as Greg asks, when this host of changes comes out of hiding in a bunch 
of creatures simultaneously, what's the trigger that sets off the explosion of 
change?  Howard

ps the boldfaced sections and those in yellow are my ways of highlighting 
material for myself.  Ignore the bolding and yellowing.

By Greg Bear
I’m pleased and honored to be asked to appear before the American 
Philosophical Society, and especially in such august company. Honored... and more than a 
little nervous! I am not, after all, a scientist, but a writer of fiction--and 
not just of fiction, but of science fiction. That means humility is not my 
strong suit. Science fiction writers like to be provocative. That’s our role. 
What we write is far from authoritative, or final, but science fiction works 
best when it stimulates debate.
I am an interested amateur, an English major with no degrees in science. And 
I am living proof that you don’t have to be a scientist to enjoy deep 
exploration of science. So here we go--a personal view.
A revolution is under way in how we think about the biggest issues in 
biology--genetics and evolution. The two are closely tied, and viruses--long regarded 
solely as agents of disease--seem to play a major role.
For decades now, I’ve been skeptical about aspects of the standard theory of 
evolution, the neo-Darwinian Modern Synthesis. But without any useful 
alternative--and since I’m a writer, and not a scientist, and so my credentials are 
suspect--I have pretty much kept out of the debate. Nevertheless, I have lots of 
time to read--my writing gives me both the responsibility and the freedom to 
do that, to research thoroughly and get my facts straight. And over ten years 
ago, I began to realize that many scientists were discovering key missing 
pieces of the evolutionary puzzle. 
Darwin had left open the problem of what initiated variation in species. 
Later scientists had closed that door and locked it. It was time to open the door 
Collecting facts from many sources--including papers and texts by the 
excellent scientists speaking here today--I tried to assemble the outline of a modern 
appendix to Darwin, using ideas derived from disciplines not available in 
Darwin’s time: theories of networks, software design, information transfer and 
knowledge, and social communication--lots of communication. 
My primary inspiration and model was variation in bacteria. Bacteria initiate 
mutations in individuals and even in populations through gene transfer, the 
swapping of DNA by plasmids and viruses. 
Another inspiration was the hypothesis of punctuated equilibrium, popularized 
by Stephen Jay Gould and Niles Eldredge. In the fossil record--and for that 
matter, in everyday life--what is commonly observed are long periods of 
evolutionary stability, or equilibrium, punctuated by sudden change over a short span 
of time, at least geologically speaking--ten thousand years or less. And the 
changes seem to occur across populations.  
Gradualism--the slow and steady accumulation of defining mutations, a 
cornerstone of the modern synthesis--does not easily accommodate long periods of 
apparent stability, much less  rapid change in entire populations. If punctuated 
equilibrium is a real phenomenon, then it means that evolutionary change can be 
put on hold. How is that done? How is the alleged steady flow of mutation 
somehow delayed, only to be released all at once? 
I was fascinated by the possibility that potential evolutionary change could 
be stored up. Where would it be kept? Is there a kind of genetic library where 
hypothetical change is processed, waiting for the right moment to be 
expressed? Does this imply not only storage, but a kind of sorting, a critical editing 
function within our DNA, perhaps based on some unknown genetic syntax and 
If so, then what triggers the change? 
Most often, it appears that the trigger is either environmental challenge or 
opportunity. Niches go away, new niches open up. Food and energy becomes 
scarce. New sources of food and energy become available. Lacking challenge or 
change, evolution tends to go to sleep--perhaps to dream, and sometimes to rumple 
the covers, but not to get out of bed and go for coffee.
Because bacteria live through many generations in a very short period of 
time, their periods of apparent stability are not millennia, but years or months 
or even days.
The most familiar mutational phenomenon in bacteria--resistance to 
antibiotics--can happen pretty quickly. Bacteria frequently exchange plasmids that carry 
genes that counteract the effects of antibiotics. Bacteria can also absorb 
and incorporate raw fragments of DNA and RNA, not packaged in nice little 
chromosomes. The members of the population not only sample the environment, but 
exchange formulas, much as our grandmothers might swap recipes for soup and bread 
and cookies. How these recipes initially evolve can in many instances be 
attributed to random mutation--or to the fortuitous churning of gene 
fragments--acting through the filter of natural selection.  Bacteria do roll the dice, but 
recent research indicates that they roll the dice more often when they’re under 
stress--that is, when mutations will be advantageous. Interestingly, they 
also appear to roll the dice predominantly in those genetic regions where 
mutation will do them the most good! Bacteria, it seems, have learned how to change 
more efficiently.
Once these bacterial capabilities evolve, they spread rapidly. However, they 
spread only when a need arises--again, natural selection. No advantage, no 
proliferation. No challenge, no change.
But gene swapping is crucial. And it appears that bacteria accept these 
recipes not just through random action, but through a complicated process of 
decision-making. Bacterial populations are learning and sharing. In short, bacteria 
are capable of metaevolution--self-directed change in response to 
environmental challenges. 
Because of extensive gene transfer, establishing a strict evolutionary tree 
of bacterial types has become difficult, though likely not impossible. We’re 
just going to have to be clever, like detectives solving crimes in a town where 
everyone is a thief. 
Perhaps the most intriguing method of gene swapping in bacteria is the 
bacteriophage, or bacterial virus. Bacteriophages--phages for short--can either kill 
large numbers of host bacteria, reproducing rapidly, or lie dormant in the 
bacterial chromosome until the time is right for expression and release. Lytic 
phages almost invariably kill their hosts. But these latter types--known as 
lysogenic phages--can actually transport useful genes between hosts, and not just 
randomly, but in a targeted fashion. In fact, bacterial pathogens frequently 
rely on lysogenic phages to spread toxin genes throughout a population. 
Cholera populations become pathogenic in this fashion. In outbreaks of E. coli that 
cause illness in humans, lysogenic phages have transported genes from 
shigella--a related bacterial type--conferring the ability to produce shiga toxin, a 
potent poison. 
Thus, what at first glance looks like a disease--viral infection--is also an 
essential method of communication--FedEx for genes.
When genes go walkabout, bacteria can adapt quickly to new opportunities. In 
the case of bacterial pathogens, they can rapidly exploit a potential 
marketplace of naïve hosts. In a way, decisions are made, quorums are reached, genes 
are swapped, and behaviors change.
What lies behind the transfer of bacterial genes? Again, environmental 
challenges and opportunities. While some gene exchange may be random, bacterial 
populations overall appear to practice functions similar to education, 
regimentation, and even the execution of uncooperative members. When forming bacterial 
colonies, many bacteria--often of different types--group together and exchange 
genes and chemical signals to produce an organized response to environmental 
change. Often this response is the creation of a biofilm, a slimy polysaccharide 
construct complete with structured habitats, fluid pathways, and barriers 
that discourage predators. Biofilms can even provide added protection against 
antibiotics. Bacteria that do not go along with this regimen can be forced to 
die--either by being compelled to commit suicide or by being subjected to other 
destructive measures. If you don’t get with the picture, you break down and 
become nutrients for those bacterial brothers who do, thus focusing and 
strengthening the colony.
A number of bacteriologists have embraced the notion that bacteria can behave 
like multicellular organisms. Bacteria cooperate for mutual advantage. Today, 
in the dentist’s office, what used to be called plaque is now commonly 
referred to as a biofilm. They’re the same thing--bacterial cities built on your 
In 1996, I proposed to my publishers a novel about the coming changes in 
biology and evolutionary theory. The novel would describe an evolutionary event 
happening in real-time--the formation of a new sub-species of human being. What 
I needed, I thought, was some analog to what happens in bacteria. And so I 
would have to invent ancient viruses lying dormant in our genome, suddenly 
reactivated to ferry genes and genetic instructions between humans. 
To my surprise, I quickly discovered I did not have to invent anything. Human 
endogenous retroviruses are real, and many of them have been in our DNA for 
tens of millions of years. Even more interesting, some have a close 
relationship to the virus that causes AIDS, HIV. 
The acronym HERV--human endogenous retrovirus--became my mantra. In 1997 and 
1998, I searched the literature (and the internet) for more articles about 
these ancient curiosities--and located a few pieces here and there, occasional 
mention in monographs, longer discussions in a few very specialized texts. I was 
especially appreciative of the treatment afforded to HERV in the Cold Spring 
Harbor text Retroviruses, edited by Drs. Coffin, Varmus, and Hughes. But to my 
surprise, the sources were few, and there was no information about HERV 
targeted to the general layman.
As a fiction writer, however, I was in heaven--ancient viruses in our genes! 
And hardly anyone had heard of them. 
If I had had any sense, I would have used that for what it seemed at face 
value--a ticking time bomb waiting to go off and destroy us all. But I had 
different ideas. I asked, what do HERV do for us? Why do we allow them to stay in 
our genome?  
In fact, even in 1983, when I was preparing my novel Blood Music, I asked 
myself--what do viruses do ­for us? Why do we allow them to infect us? I 
suspected they were part of a scheme involving computational DNA, but could not fit 
them in...not just then. HIV was just coming into the public consciousness, and 
retroviruses were still controversial. 
I learned that HERV express in significant numbers in pregnant women, 
producing defective viral particles apparently incapable of passing to another human 
host. So what were they--useless hangers-on? Genetic garbage? Instinctively, I 
could not believe that. I’ve always been skeptical of the idea of junk DNA, 
and certainly skeptical of the idea that the non-coding portions of DNA are 
deserts of slovenly and selfish disuse. 
HERV seemed to be something weird, something wonderful and 
counter-intuitive--and they were somehow connected with HIV, a species-crossing retrovirus that 
had become one of the major health scourges on the planet. I couldn’t 
understand the lack of papers and other source material on HERV. Why weren’t they 
being investigated by every living biologist?
In my rapidly growing novel, I wrote of Kaye Lang, a scientist who charts the 
possible emergence of an HERV capable of producing virions--particles that 
can infect other humans. To her shock, the HERV she studies is connected by 
investigators at the CDC with a startling new phenomenon, the apparent mutation 
and death of infants.  The infectious HERV is named SHEVA. But SHEVA turns out 
to be far more than a disease. It’s a signal prompting the expression of a new 
phenotype, a fresh take on humanity--a signal on Darwin’s Radio.
In 1999, the novel was published. To my gratified surprise, it was reviewed 
in Nature and other science journals. Within a very few months, news items 
about HERV became far more common. New scientific papers reported that ERV-related 
genes could help human embryos implant in the womb--something that has 
recently been given substantial credence. And on the web, I encountered the 
fascinating papers of Dr. Luis P. Villarreal.
I felt as if I had spotted a big wave early, and jumped on board just in 
time. Still, we have not found any evidence of infectious HERV--and there is 
certainly no proof that retroviruses do everything I accuse them of in Darwin’s 
Radio. But after four years, the novel holds up fairly well. It’s not yet 
completely out of date. 
And the parallel of HERV with lysogenic phages is still startling.  
But back to the real world of evolution and genetics.
The picture we see now in genetics is complex. Variation can occur in a 
number of ways. DNA sequence is not fate; far from it. The same sequence can yield 
many different products. Complexes of genes lie behind most discernible 
traits. Genes can be turned on and off at need. Non-coding DNA is becoming extremely 
important to understanding how genes do their work. 
As well, mutations are not reliable indicators of irreversible change. In 
many instances, mutations are self-directed responses to the environment. Changes 
can be reversed and then reenacted at a later time--and even passed on as 
reversible traits to offspring.
Even such neo-Darwinian no-nos as the multiple reappearances of wings in 
stick insects points toward the existence of a genetic syntax, a phylogenetic 
toolbox, rather than random mutation. Wings are in the design scheme, the bauplan. 
When insects need them, they can be pulled from the toolbox and implemented 
once again.
We certainly don’t have to throw out Mr. Darwin. Natural selection stays 
intact. Random variation is not entirely excised. But the neo-Darwinian dogma of 
random mutation as a cause of all variation, without exception, has been proven 
Like genetics, evolution is not just one process, but a collaboration of many 
processes and techniques. And evolution is not entirely blind. Nor must 
evolution be directed by some outside and supernatural intelligence to generate the 
diversity and complexity we see. Astonishing creativity, we’re discovering, 
can be explained by wonderfully complicated internal processes.
These newer views of evolution involve learning and teamwork. Evolution is in 
large part about communication--comparing notes and swapping recipes, as it 
It appears that life has a creative memory, and knows when and how to use it. 
Let’s take a look at what the scientists have discovered thus far. 
Viruses can and do ferry useful genes between organisms. Viruses can also act 
as site-specific regulators of genetic expression. Within a cell, 
transposable elements--jumping genes similar in some respects to endogenous 
retroviruses--can also be targeted to specific sites and can regulate specific genes. Both 
viruses and transposable elements can be activated by stress-related 
chemistry, either in their capacity as selfish pathogens--a stressed organism may be a 
weakened organism--or as beneficial regulators of gene expression--a stressed 
organism may need to change its nature and behavior. 
Viral transmission occurs not just laterally, from host to host (often during 
sex), but vertically through inherited mobile elements and endogenous 
Chemical signals between organisms can also change genetic expression. As 
well, changes in the environment can lead to modification of genetic expression 
in both the individual and in later generations of offspring. These changes may 
be epigenetic--factors governing which genes are to be expressed in an 
organism can be passed on from parent to offspring--but also genetic, in the 
sequence and character of genes.
Our immune system functions as a kind of personal radar, sampling the 
environment and providing information that allows us to adjust our immune 
response--and possibly other functions, as well.
These pathways and methods of regulation and control point toward a massive 
natural network capable of exchanging information--not just genes themselves, 
but how genes should be expressed, and when. Each gene becomes a node in a 
genomic network that solves problems on the cellular level. Cells talk to each 
other through chemistry and gene transfer. And through sexual recombination, 
pheromonal interaction, and viruses, multicellular organisms communicate with each 
other and thus become nodes in a species-wide network.
On the next level, through predation and parasitism, as well as through 
cross-species exchange of genes, an ecosystem becomes a network in its own right, 
an interlinking of species both cooperating and competing, often at the same 
Neural networks from beehives to brains solve problems through the exchange 
and the selective cancellation and modification of signals. Species and 
organisms in ecosystems live and die like signals in a network. Death--the ax of 
natural selection--is itself a signal, a stop-code, if you will.
Networks of signals exist in all of nature, from top to bottom--from gene 
exchange to the kinds of written and verbal communication we see at this event. 
Changes in genes can affect behavior. Sometimes even speeches can affect 
Evolution is all about competition and cooperation--and communication. 
Traditional theories of evolution emphasize the competitive aspect and 
de-emphasize or ignore the cooperative aspect. But developments in genetics and 
molecular biology render this emphasis implausible. 
Genes go walkabout far too often. We are just beginning to understand the 
marvelous processes by which organisms vary and produce the diversity of living 
For now, evolution is a wonderful mystery, ripe for further scientific 
exploration. The gates have been blown open once again. 
And as a science fiction writer, I’d like to make two provocative and 
possibly ridiculous predictions.
The first is that the more viruses may be found in an organism and its 
genome, the more rapid will be that organism’s rate of mutation and evolution.
And the second: Bacteria are such wonderful, slimmed-down organisms, lacking 
introns and all the persiflage of eukaryotic biology. It seems to me that 
rather than bacteria being primitive, and that nucleated cells evolved from them, 
the reverse could be true. Bacteria may once have occupied large, primitive 
eukaryotic cells, perhaps similar to those seen in the fossil Vendobionts--or 
the xenophyophores seen on ocean bottoms today. There, they evolved and swam 
within the relative safety of the membranous sacs, providing various services, 
including respiration. They may have eventually left these sacs and become both 
wandering minstrels and predators, serving and/or attacking other sacs in the 
primitive seas. 
Eventually, as these early eukaryotic cells advanced, and perhaps as the 
result of a particularly vicious cycle of bacterial predation, they shed nearly 
all their bacterial hangers-on in a protracted phase of mutual separation, 
lasting hundreds of millions or even billions of years. 
And what the now trim and super-efficient bacteria--the sports cars of modern 
biology--left behind were the most slavish and servile members of that former 
internal community: the mitochondria.
Which group will prove to have made the best decision, to have taken the 
longest and most lasting road?

Howard Bloom
Author of The Lucifer Principle: A Scientific Expedition Into the Forces of 
History and Global Brain: The Evolution of Mass Mind From The Big Bang to the 
21st Century
Visiting Scholar-Graduate Psychology Department, New York University; Core 
Faculty Member, The Graduate Institute
Founder: International Paleopsychology Project; founding board member: Epic 
of Evolution Society; founding board member, The Darwin Project; founder: The 
Big Bang Tango Media Lab; member: New York Academy of Sciences, American 
Association for the Advancement of Science, American Psychological Society, Academy 
of Political Science, Human Behavior and Evolution Society, International 
Society for Human Ethology; advisory board member: Youthactivism.org; executive 
editor -- New Paradigm book series.
For information on The International Paleopsychology Project, see: 
for two chapters from 
The Lucifer Principle: A Scientific Expedition Into the Forces of History, 
see www.howardbloom.net/lucifer
For information on Global Brain: The Evolution of Mass Mind from the Big Bang 
to the 21st Century, see www.howardbloom.net
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