"Changes in food availability, food type, or the way you get food can trigger evolutionary mechanisms to deal with those changes. The result can be increased brain size and cognition, changes in locomotion and even social changes—how you interact with others in a group."

I read about that somewhere; no wait... I published an article that detailed the molecular mechanisms of how it (i.e., adaptive evolution)occurs.

Kohl, J.V. (2012) Human pheromones and food odors: epigenetic influences on the socioaffective nature of evolved behaviors. Socioaffective Neuroscience & Psychology, 2: 17338.

Open access: http://dx.doi.org...i0.17338

In AWT the complex evolved fluctuations of vacuum (Boltzmann brains) are just those, which managed to travel a long path across time dimension at place. Our intrinsic complexity is just a condensate of mutual changes of life environment, which we managed to survive in the past. In accordance with it, the organisms, which are living in stable life environments (like the sharks and horseshoe crabs living at the bottom of oceans) are rather primitive.

Len, a human has more hair by mass and number of hairs than a chimp.

Besides plenty of species have been artifically selected to be hairless. It's not a stretch to assume natural selection could achieve the same effect. There's any number of explanations, take your pick.

There's any number of explanations, take your pick.

I do favor the Aquatic Ape combined with Population bottleneck theory, as it provides simple & common explanations for multiple morphological peculiarities of human race, not just the lack of fur.

Yeah I like the Aquatic Ape theory, but I know it has little to no support and not being an expert I'll defer to them.

Seems pretty simple... Change begets even more change.

Yeah I like the Aquatic Ape theory, but I know it has little to no support and not being an expert I'll defer to them.

The problem with the Aquatic Ape theory is that they try to explain the wrong traits. Humans have evolved to live in proximity to deep water. To prove this look at what happens when a baby (or an adult) enters the water. There are a number of specific changes which are not learned behavior. The most spectacular are summed up in the rescuer's mantra: "No one is dead until they are warm and dead." This ability to survive hours or days of immersion in cold water, with no breathing, no pulse, and no brain electrical activity has to have evolved due to some evolutionary pressure. Floods that occur at rare intervals, but wipe out populations (absent the adaptation) are an obvious source of the forcing. Also if you need to go into cold water for some (I hope serious) reason, get your head wet first. The rest of the body doesn't adapt until the head is wet. ;-)

Furtioutous perhaps, if the ancestral ape culture was adaptable enough.

@lengould: I think you reverse the causality. Clothing is a compensation and, granted, in some cases an extension of traits.

What has been most selected for in humans are sexual and immunosystem traits. Since remaining hair is mostly a sexual signal (emphasizing the sex in the groin, emphasizing healt on the signal area of the head), I presume sexual selection predicts why we lost it and retained it both.

Also, the Aquatic Ape theory is considered crackpot. [ http://www.aquaticape.org/ ] "One of the questions people often ask is why the anthropologists who deal with human evolution don't deal with the AAT/H in their writings. First of all, we have to note that they do sometimes (more about that below), but also that there are a couple of very good reasons why they don't spend more time on it. One can be seen by looking at the quality of the evidence used to support the AAT/H. ..."

[cont] The most basic problem with the AAT/H is that it uses extreme environmental determinism. The proponents do this apparently thinking they are using the quite legitimate evolutionary principle of convergent evolution, but they do so in a very mistaken manner which suggests they really don't understand it. I have a short explanation of convergent evolution here. It seems as though they've picked up the term without understanding what it actually means; most specifically they shy away from the fact that convergent characters are similar in function as well as in structure. That is, convergent features are similar in structure because they are similar in function due to environment , not simply similar in structure due to environment. ...

They make the mistake of supposing that even very distantly-related animals in a common environment should evolve the same mechanisms for dealing with any given problem, ..."

@ ValeriaT: Take your crackpot "AWT" off science sites. Observations rejected "aether" a century (!) ago.

Physics as such has little to do with biology, which is differential reproduction regardless of the specific environment. (You *do* need an environment that allows a genetic machinery - but you aren't discussing this minor point at all.)

"Evolution" is nearly synonymous with 'cumulative adaptation.'
Adaptation is driven by changes in needs, which occurs because previous adaptations are no longer adequate to meet current needs. Needs change because circumstances (often environmental in origin) change.
This is practically a syllogism.
The only alternative to Adaptation is Extinction, and we are obviously not extinct.

Observations rejected "aether" a century (!) ago

The whole AWT just begins with description of imbecility of physicists, who cannot realize, that the motion of any environment is undetectable with its transverse waves. You're apparently unable to intercept this information, despite I explained it many times here. You're like the religious troll, who just repeats "But Bible describes it differently".

Physics as such has little to do with biology

The thermodynamics is routinely applied just to evolution. And the thermodynamics is best described with Boltzmann gas.

I have a question:

How do they rule out something other than rapid climate shifts as the cause of a change in locacl vegitation?

A forest can give way to grassland in response to other things, can't it? For example, repeated wildfires can reduce a forest to the point that it cannot recover, and grass takes over until the forest fights its way back. Repeated insect plagues and/or tree diseases can also do this.

Also, I wonder if samples from other locations in the region correlate with the time spans they see from samples taken at this single location.

In the time span they are talking about, North America experienced repeated waves of glaciation. When the glaciers receded, nothing was left but bare rock. Forests did not recover in these places for many centuries. They make it sound like massive climate shifts in a few thousand years are a new discovery. I think you see the same evolutionary jumps in other species all around the world in that time.

GSwift7: "For example, repeated wildfires can reduce a forest to the point that it cannot recover"
Wildfires and their frequency are a product of climate(lightning, aridity, precipitation), and so are insects. That's why it's hard to rule out climate. It affects a lot.

So much for environmental factors driving evolution.
With so much change going on today, why is it that we do NOT observe ANY organism change from whatever it is into something else?
What with all the hype of evolution being bandied about, no one has any documented evidence to support the idea that one organism can change from whatever it is into another one. Even amongst viruses or the incredibly long-running experiment with multiple generations of microbes, the organisms remain exactly what they were. No new creatures have ever emerged.
The closest we can get to so-called evolution is the changing of a butterfly/moth from egg to larva to pupa to final flying insert. The incredible change in the pupa stage is highly irritating to the evolutionist, since it defies ANY evolutionary explanation but rather loudly proclaims design.

Where is the required rapid evolutionary change we should be seeing in the present? There should be extremely high rates of change and failure visible

Wildfires and their frequency are a product of climate(lightning, aridity, precipitation), and so are insects. That's why it's hard to rule out climate. It affects a lot

Yes, that's true. However, as long as alternatives are possible, you MUST eliminate them with evidence before you can draw the above conclusion. As you say, climate can increase the likelyhood of fires, insects, disease, etc. On the other hand, seasonal weather, totally seperate from climate shifts can do the same. For example, lets say there's an early and wet Spring. Insects like this, and so do plant parasites like fungus and mold. Despite the warm and wet weather, forests can suffer and have trees die off. With trees dying, the undergrowth thrives. Throw in a dry hot summer and a thunder storm and you have the ingredients for a millenial scale forest fire. That isn't a climate shift, just weather. Those chance events CAN happen repeatedly in regions.

continued:

Anyway, that's just a pet peeve I have with articles that skip over things.

I looked up the source paper for the above article, and it turns out that the press release wasn't written very well. My doubts were valid, and the actual authors of the research covered them in the study.

It seems that they double-checked their assumptions by cross-checking the climate record with other sources. They compared to ocean sediment cores that show changes in monsoons. They also showed correllation with a major shift in the orbit and rotation of the Earth at the time in question. Here's a quote from the abstract:

where open C4 grasslands abruptly transitioned to closed C3 forests within several hundreds to thousands of years. Carbon-isotopic signatures correlate most strongly with Earth's orbital geometry (precession), and tropical sea-surface temperatures are significant secondary predictors in partial regression analyses

So, precession was the cause of evolution.

Those who posit wildfire theory et al seem not to understand that it is the availability of nutrients and their metabolism to pheromones that is responsible for divergence in species from microbes to man.
"Changes in food availability, food type, or the way you get food can trigger evolutionary mechanisms to deal with those changes. The result can be increased brain size and cognition, changes in locomotion and even social changes—how you interact with others in a group."

The molecular mechanisms of adaptive evolution have never changed, and that is what this article on the fluctuating environment restates for those who think random mutations or unknown natural mechanisms in different times and places alter adaptive evolution in different ways. Kohl, J.V. (2012) Human pheromones and food odors: epigenetic influences on the socioaffective nature of evolved behaviors. Socioaffective Neuroscience & Psychology, 2: 17338.

Open access: http://dx.doi.org...i0.17338

kevin:

So much for environmental factors driving evolution.
With so much change going on today

If you live in North America, then you should be familiar with the Africanization of the North American honey bee. That has happened in just a couple decades. Here's another example: The Influenza virus produces a new strain every year. How about pocket-sized dogs? They were once wolves. How about humans and the increase in height over the last two centuries? Even been on an old sailing ship? The ceilings are a bit low for my 6' tall head. I could go on and on and on, and those are only short term changes. Given thousands of years, species change to the point that they are so genetically different that they cannot breed with thier parent species. That's when they totally split into their own species. This is fairly simple stuff. If you don't understand, you should ask a fifth grader to explain it to you.

Those who posit wildfire theory et al seem not to understand that it is the availability of nutrients and their metabolism to pheromones that is responsible for divergence in species from microbes to man

I wasn't questioning the evolution part. I was questioning the assumption of rapid regional climate shift as suggested in the above article. As I said in my follow-up post, the authors of the actual study did double-check that assumption by cross-referencing against other sources. They must have agreed that there were other potential reasons for shifts in vegetation.

I would still argue that coincidence is not proof of causal relationship though. Personally, I think their assumption is a bit of a stretch. There are many other possible reasons for species adaptation, including pure random chance, or one tribe killing off all the other tribes, etc.

There are many other possible reasons for species adaptation, including pure random chance, or one tribe killing off all the other tribes, etc.

I'd love to learn more about adaptive evolution by random chance so the model (if any) could be compared to nutrient chemical metabolism to pheromones in a model where individual survival is nutrient chemical-dependent and reproduction is controlled by pheromones.

Human evolution is a real puzzle to me for several reasons.

Every other mammal dwelling on land above ground has a significant coat of hair or fur. Can the time from the development of clothing have been long enough for us to have evolved (essentially) hairless? (and I know, the folicles and tiny hairs still mostly exist). Hairlessness is normally an adaptation to living in water. Were our ancestors at some point sea creatures?

I guess you've never seen an elephant then? How about a rhino? A pig maybe? I get your point but there are examples of mammals without fur coats that do live a mostly terrestrial lifestyle. From what I've read our general hairlessness is an evolutionary adaptation to ridding our bodies of excessive heat generated in our big brains.

I'd love to learn more about adaptive evolution by random chance so the model (if any) could be compared

Errors in genes are random, and can be passes down genetically. If such an error becomes widespred it can become a common trait in a species.

in a model where individual survival is nutrient chemical-dependent and reproduction is controlled by pheromones

I find it difficult to explain white polar bears with only that mechanism.

Human evolution is a real puzzle to me for several reasons.

Every other mammal dwelling on land above ground has a significant coat of hair or fur. Can the time from the development of clothing have been long enough for us to have evolved (essentially) hairless? (and I know, the folicles and tiny hairs still mostly exist). Hairlessness is normally an adaptation to living in water. Were our ancestors at some point sea creatures?

Even old Uncle Neander wasn't particularly hirsute.

"Life always finds a way".

Errors in genes are random, and can be passes down genetically. If such an error becomes widespred it can become a common trait in a species.

But seriously, how does the error cause adaptive evolution. Errors are deleterious, not adaptive. Nutrient chemical intake and pheromone-controlled reproduction are adaptive (e.g., in species from microbes to man.)

Just quickly...the 'recessive' genes for "albinism' and for 'baldness' have been around for millennia. There must be sone evolutionary advantage to "someone, sometime" for them to survive human/natural selection that long. If the environment changes naturally to prefer albinism/baldness genes, then they will become the "dominant gene" for that new crop of humans so affected and 'selected' by new environment. Remember, in many so-called 'bald areas' of skin (whether on skull or other areas) are actually covered by 'hairy fuzz' of minuscule hairs whose follicles have been affected by hormonal/other physiological factors. So change in any factors may restore the follicle function/product to take advantage of any new environmental factor within and without the human body. Cheers!

...the 'recessive' genes for "albinism' and for 'baldness' have been around for millennia.

The same can be said for all nutrient chemical-dependent pheromone-controlled genes in all species from microbes to man. The mere fact that gene expression is controlled by nutrient chemicals and their metabolism to pheromones introduces a bottom-up approach to gene activation and top-down control of the processes from gene activation to behavior and back.
Are you trying to tell me that bottom-up and top-down processes involve simultaneous random mutations? If so, the mutations are not really random are they? In fact, they're not mutations at all. The changes are genetically predisposed, and driven by what organisms eat and how they communicate with each other. Simply put, the epigenetic landscape becomes the physical landscape via nutrient chemical-dependent pheromone-controlled chromatin remodeling, not via mutations. http://f1000.com/.../1092760

JVK:

Explain the evolution of citrate metabolism in Richard Lenski's E. coli experiment in the context of "nutrient chemical-dependent pheromone-controlled" evolution.

How does chromatin remodeling relate to the introduction of novel genes?

JVK:
Explain the evolution of citrate metabolism in Richard Lenski's E. coli experiment in the context of "nutrient chemical-dependent pheromone-controlled" evolution.

How does chromatin remodeling relate to the introduction of novel genes?

Ask the question in the context of my model, and I may answer it. If you want to debate nutrient chemical-dependent pheromone-controlled adaptive evolution,provide an alternative model for de novo gene expression and receptor-mediated behavior. I think what you're asking is for an explanation of someone else's work, so you can ignore mine.

Yeah I like the Aquatic Ape theory, but I know it has little to no support and not being an expert I'll defer to them.

-
FrankHerbert

This is the latest PM from FrankHerbert-

FrankHerbert 2 h 45 min ago:
Faglord

Brilliant.

Ask the question in the context of my model, and I may answer it. If you want to debate nutrient chemical-dependent pheromone-controlled adaptive evolution,provide an alternative model for de novo gene expression and receptor-mediated behavior. I think what you're asking is for an explanation of someone else's work, so you can ignore mine.

I did ask it in the context of your model. That's why I specifically said "in the context of "nutrient chemical-dependent pheromone-controlled" evolution."

Identification and origins of de novo genes: http://www.plosge....1002381

Obviously, not all evolution can be due to environmentally-induced gene modification because there's no top-down mechanism for the creation of novel enzymes. A bacteria can't just detect citrate and magically reverse engineer the gene for citrate lyase. Either the E. coli got it through hor. gene transfer from a contaminant or it evolved it de novo.

Obviously, not all evolution can be due to environmentally-induced gene modification because there's no top-down mechanism for the creation of novel enzymes.

Either you understand more about this than I do, or you are making ridiculous assumptions. Why must there OBVIOUSLY be top-down mechanisms for the creation of novel enzymes?

A bacteria can't just detect citrate and magically reverse engineer the gene for citrate lyase. Either the E. coli got it through hor. gene transfer from a contaminant or it evolved it de novo.

How many DNA switches are there in the microbe? I don't get the picture of magical reverse engineering that you're trying to paint. I see the picture more as an epigenetic tweaking of immense gene networks as detailed in my model.

If you look at one gene for anything what do you expect to see in the context of the 4.5 million DNA switches in the human genome, for example? What top-down mechanism gets you from microbes to man? Is it a mutation?

A bacteria can't just detect citrate and magically reverse engineer the gene for citrate lyase. Either the E. coli got it through hor. gene transfer from a contaminant or it evolved it de novo.

In Blount et al., a three-step process was proposed — "in which potentiation makes a trait possible, actualization makes the trait manifest, and refinement makes it effective." Where does your either/or statement about E. coli and hor. gene transfer from a contaminant or de novo gene expression come from?

Discussion doesn't work if you're just making stuff up. Ask yourself: "Is there a model for that?" If there is, let's compare it to mine. If there isn't, just say there's nothing for comparison.

It seems that maybe...just maybe...aroc91 was being facetious...possibly testing you.

Why must there OBVIOUSLY be top-down mechanisms for the creation of novel enzymes?

Read it again. That's not what I said.

I see the picture more as an epigenetic tweaking of immense gene networks as detailed in my model.

How does epigenetic tweaking result in a novel phenotype? In your model, how does the presence of citrate in a media influence the evolution of citrate lyase epigenetically?

Where does your either/or statement about E. coli and hor. gene transfer from a contaminant or de novo gene expression come from?

Logic. Where else would the genetic information come from? How does the presence of the substrate create the necessary gene?

I guess I just need clarification. Are you proposing a guided, top-down approach to new genetic information as opposed to the selection-driven, bottom-up mutation/natural selection approach?

It seems that maybe...just maybe...aroc91 was being facetious...possibly testing you.

Maybe... just maybe... I'm merely trying to gain clarification into something I haven't fully grasped.

I guess I just need clarification. Are you proposing a guided, top-down approach to new genetic information as opposed to the selection-driven, bottom-up mutation/natural selection approach?

My model is one for bottom-up / top-down reciprocity (i.e., from epigenetically altered gene expression to behavior and back).

"This model of systems biology ("biological embedding") represents....

Cut and paste the link if the poster doesn't automatically display: http://f1000.com/.../1092760

Did you even look at it?

JVK:

I see the picture more as an epigenetic tweaking of immense gene networks as detailed in my model.

aroc91 ignores the detailed model and asks:

How does epigenetic tweaking result in a novel phenotype? In your model, how does the presence of citrate in a media influence the evolution of citrate lyase epigenetically?

Here's where discussion proves to be pointless, which is why I asked for the question to be placed in the context of the model. Instead, anonymous discussants often expect to be educated about the entirety of the microRNA / messenger RNA balance required for responses to novel stimuli and for homeostasis despite no indication that they understand anything other than random mutations theory.

Nutrient chemical-dependent is "bottom-up." Pheromone-controlled is "top-down." Reciprocity is required as indicated in the Blount et al paper (with Lenski) that did not address the required molecular mechanisms. My model addresses the molecular mechanisms.

You keep saying the same thing over and over without any further explanation and expect people to completely understand you. I know what post-transcriptional modification is.

http://www.ncbi.n...19014274

Macrolide resistance and the corresponding change in the rRNA gene. Seems like mutation of the gene and selection to me. You should know this is not uncommon. How does your model account for drug resistance when we've known about chromosomal genome mutations leading to rRNA active site modification for quite some time?

You keep saying the same thing over and over without any further explanation and expect people to completely understand you.

No, I expect you to comment either on my published work or on its representation in the poster. You keep saying what's been said by evolutionary theorists for 150 years -- mutations are causal, when they obviously are not.

...we've known about chromosomal genome mutations leading to rRNA active site modification for quite some time?

You're saying the mutations cause adaptive evolution of the human brain and behavior, aren't you? And you will probably insist that I'm the one who continues to say the same thing over and over.

The context here is the fluctuating environment. What fluctuates is nutrient chemical availability that epigenetically effects intracellular signaling and stochastic gene expression as is required to link sensory input directly to gene expression, to behavior, and back.

What role are you proposing for mutations?

How does the presence of the substrate create the necessary gene?

The presence of citrate does not create anything -- except in ridiculous mutation theories. A three-step process requires the substrate to elicit a slight change in the genetic predisposition of a receptor. That potentiates change in intracellular signaling that makes actualization possible via exposure-driven de novo gene expression. If gene expression leads to a beneficial new trait (e.g., ability to use citrate), the metabolism of the new "nutrient" is incorporated into species-specific pheromones that enable top-down refinement of the bottom-up trait-based behavior (nutrient chemical acquisition). A primary epigenetic signature (e.g., presence of citrate) is reinforced by secondary and tertiary repressive intrachromosomal compaction and interchromosomal aggregation of genes. The cell exhibits secondary-process learning and memory which interface with tertiary-process adaptations to chemical input in my model.

So, essentially, you're describing quorum sensing? That's perfectly valid.

How does that result in new genomic information though? How does that mesh with the fact that we've tracked chromosomal mutations responsible for the emergence of drug resistance. The mutation that resulted in the evolution of the well-known peppered moth from its original wing pattern to the darker pattern has even been identified.

So, essentially, you're describing quorum sensing? That's perfectly valid.

Where does the validity of nutrient chemical-dependent pheromone-controlled reproduction (i.e., quorum sensing) end and mutation-driven adaptive evolution begin? Is there a model for that?

How does that result in new genomic information though?

That's what I've detailed, which makes your question merely annoying, again.

How does that mesh with the fact that we've tracked chromosomal mutations responsible for the emergence of drug resistance.

Obviously, my model does not mesh with any mutation theory. I am not scientifically illiterate! What caused the mutation?

The mutation that resulted in the evolution of the well-known peppered moth from its original wing pattern to the darker pattern has even been identified.

Was the mutation automagically driven, or was it nutrient chemical-dependent and pheromone-controlled as is species divergence from microbes to man?

Was the mutation automagically driven, or was it nutrient chemical-dependent and pheromone-controlled as is species divergence from microbes to man?

So DNA replication errors are only due to some ulterior, epigenetic, reverse engineering, pheromone-driven motives? How does a cell direct mutation with certainty in what that mutation will result in? That seems just as automagical to me as random mutation/selection does to you. Berkeley's on my side, by the way.

http://evolution....om.shtml

So DNA replication errors are only due to some ulterior, epigenetic, reverse engineering, pheromone-driven motives?

That is not what I detailed in my model; you have returned to making stuff up.

How does a cell direct mutation with certainty in what that mutation will result in?

You have not grasped the concept of epigenetic effects on stochastic gene expression or the vaguery of mutations.

That seems just as automagical to me as random mutation/selection does to you. Berkeley's on my side, by the way.
http://evolution....om.shtml

There are not two sides. There's my model compared to random mutations theory. There has never been scientific support for the theory. Common sense and everything neuroscientifically known support adaptive evolution via nutrient chemical-dependent pheromone-controlled reproduction in species from microbes to man.

Don't you like the way I incorporated Lenski's works at your suggestion?

"The presence of citrate does not create anything -- except in ridiculous mutation theories. A three-step process requires the substrate to elicit a slight change in the genetic predisposition of a receptor. That potentiates change in intracellular signaling that makes actualization possible via exposure-driven de novo gene expression. If gene expression leads to a beneficial new trait (e.g., ability to use citrate), the metabolism of the new "nutrient" is incorporated into species-specific pheromones that enable top-down refinement of the bottom-up trait-based behavior (nutrient chemical acquisition). A primary epigenetic signature (e.g., presence of citrate) is reinforced by secondary and tertiary repressive intrachromosomal compaction and interchromosomal aggregation of genes. The cell exhibits secondary-process learning and memory which interface with tertiary-process adaptations to chemical input in my model."

Wow... Say THAT 10 times real fast...

Wow... Say THAT 10 times real fast...

Just say "quorum sensing". That model of nutrient chemical-dependent pheromone-controlled reproduction extends across species from microbes to man. Anyone who can grasp that "take home message" should help to convey it to the folks at Berkeley or anywhere else where people are taught anything else. Here's the "take home message" again: There are not two sides. There's my model compared to random mutations theory. In my model, "Olfaction and odor receptors provide a clear evolutionary trail that can be followed from unicellular organisms to insects to humans." http://dx.doi.org...i0.17338

What evolutionary theorists think happens is based on their ignorance of biological facts and acceptance of other's ignorance in the context of levels of biological organization. What we've seen here in discussion on this topic exemplifies that ignorance, which is widespread and it has been irrepressible for more than 50 years.

Where is the required rapid evolutionary change we should be seeing in the present? There should be extremely high rates of change and failure visible

Only if the world were 6500 years old as you seem to think.

Kevin would probably fail to appreciate the language analogy of evolution. Languages evolve slowly or quickly depending on a number of factors. Dialects change until they can no longer be understood by the original speakers.

Its the same way with evolution. Animal populations diverge until they can no longer interbreed, and so become distinct species.

Languages evolve slowly or quickly depending on a number of factors. Dialects change until they can no longer be understood by the original speakers

Languages change in response to food supply-driven social-interaction which can be observed in all communications between living organisms from bacteria to man.

Sorry, just having fun with JVK's 'theory'. lol.

You may as well stop arguing with JVK. He's either a serious crackpot or he is trolling you. I laughed my @$$ off at this one:

Anyone who can grasp that "take home message" should help to convey it to the folks at Berkeley or anywhere else where people are taught anything else

I had already figured out that he was probably trolling us, but that one sealed it for me.

Kevin:

There should be extremely high rates of change and failure visible

Otto the fool:

Only if the world were 6500 years old as you seem to think.

Animal populations diverge until they can no longer interbreed, and so become distinct species.

What causes their divergence? If it's nutrient chemical-dependent and pheromone-controlled, the divergence is limited by the food chain. As intelligent omnivores, we're at the top of it. As fools, we ingest manufactured chemicals and are exposed to endocrine disruptors that cause changes in phenotypic expression.

Having potentially reached the limits of evolution, however, the exposure to all things natural, unnatural, and exposure to those who ingest such things, is probably what causes the majority of our physical and mental disorders -- especially those associated with aging. Perhaps we are doomed and can evolve no further than we already have during the past 5-10,000 years.

see http://dx.doi.org...ure11690

You may as well stop arguing with JVK. He's either a serious crackpot or he is trolling you. I laughed my @$$ off at this one:

Anyone who can grasp that "take home message" should help to convey it to the folks at Berkeley or anywhere else where people are taught anything else

I had already figured out that he was probably trolling us, but that one sealed it for me.

Do you know if the "Berkeley side" has learned anything about evolution of enzymes with multiple functions, which may include new functions that arise before gene duplication -- like the one required for citrate utilization in E. coli? Of course you don't!

That is what makes you the unwanted troll arriving late to the party. If not a troll tell us how a random mutation was responsible for nutrient uptake in a microbe that somehow adaptively evolved to the endpoint that some people might call intelligent human beings, if a few more could be found here. If not for Kevin, we'd have only the Berkeleys.

Languages change in response to food supply-driven social-interaction which can be observed in all communications between living organisms from bacteria to man.

Sorry, just having fun with JVK's 'theory'. lol.

That's the kind of LOL fun that only a troll can have. I don't have a theory; it's a detailed model of nutrient chemical-dependent pheromone-controlled adaptive evolution from microbes to man. It includes the evolution of language and the diversity of languages associated with differences in the supply of nutrient chemicals which determine the social niche construction that is the basis for everything known about our behavioral ecology.

You studied at Berkeley, didn't you?

Just say "quorum sensing". That model of nutrient chemical-dependent pheromone-controlled reproduction extends across species from microbes to man.

Okay, that's better. I am in complete agreement on the causal nature of evolution. It is how ALL things evolve...
From the environment affecting the epiginetic layer, then to the genetic layer of a biological entity. Seems simple enough.
Eric Andrulis calls the process a gyre or vortex, others call it evolution. And others call it whatever. No matter the name, the rose still smells as sweet...:-)

JVK:

Just say "quorum sensing". That model of nutrient chemical-dependent pheromone-controlled reproduction extends across species from microbes to man.

No matter the name, the rose still smells as sweet...:-)

Enter English literature with representations of biological facts not known to trolls coming late to the party or those on the "Berkeley side" who might advocate that our language is what makes the rose smell sweet; not its nutrient chemical-dependent secretions that help to ensure its reproduction. Does this not suggest to others that science at Berkeley is dead? I've always thought highly of Berkeley grads until aroc91 posted the link to the misinformation about mutations theory. Maybe they're trying to mislead others until they can patent something that beneficially alters the microRNA / messenger RNA balance as Moskal et al http://dx.doi.org...2012.246 have done.

http://evolution..../search:

"Pheromone" No Results
"Nutrient" 1 result
"Mutation" 358 Results
"Random mutation" 144 results

Rah! Rah! Rah! Everything I needed to know about random mutations, I learned before I ended my college education. The genetics course and cut and paste chromosome matching-labs were the last straw.

JVK, I'm not a biologist, and I didn't go to Berkley. I studied aerospace at Auburn. That being said, I don't need to be an expert to know BS when I see it.

The science of genetics is still a very young science. We just recently figured out that all that stuff we used to call "junk DNA" is far from being junk. We're still working on some of the most basic theory about how genes work.

So, when I see you going on and on about some theory that "explains it all", I know you are full of it. If you are actually correct, it would be entirely due to blind luck. Since the state of the art in the field is nowhere near conclusive at this time, trying to argue with their conclusions is kinda silly. They are still in the early theoretical stages of all this.

If your idea has any traction, then apply for a grant and get working on it. There's more money going into that kind of research right now than any other field in science. With that kind of money around, the good ideas float to the top

JVK, I'm not a biologist, and I didn't go to Berkley. I studied aerospace at Auburn. That being said, I don't need to be an expert to know BS when I see it.

That being said, if you intend to demonstrate any degree of intelligence akin to what might be expected of a rocket scientist in discussion here, you would first read what I, as a medical laboratory scientist, have published Kohl, J.V. (2012) Human pheromones and food odors: epigenetic influences on the socioaffective nature of evolved behaviors. Socioaffective Neuroscience & Psychology, 2: 17338. http://dx.doi.org...i0.17338

What kind of idiot ignores my publication history: books, journal articles, book chapters et al., and claims to know BS when he sees it, calls me a troll et al? (That was a rhetorical question.)

Did you intend to exemplify the type of person who believes in random mutations theory despite the complete lack of scientific evidence for it?