Exposing Cognitive Dissonance At The Core Of Human Origin Theory

An account of our origins based on accepted scientific data but intentionally using unfamiliar terminology.

This is simply to expose serious cognitive dissonance at the core of 70 years of mainstream scientific research into human origins.
Most particularly efforts to explain the rapid emergence of our colossal new brain and other anomalous traits while being restricted to the use of classic adaptive selection theory only.
All the while the same mainstream scientific research accepts our forest origins and a 50 million year plus seed disseminating symbiotic relationship ingesting the swollen ovaries of the angiosperms. 

Since the Killer Ape Theory was proposed in the 1950s' almost all efforts to understand our origins and our weirdly anomalous traits have centred around classic adaptive selection, usually in hostile environments.
Basically, some form of adaptive pressure that elicits a selective genetic response locking a beneficial new trait into our genome.


The results can be summarised here;

A selection of current contenders for an adaptive selection theory of human origins that attempt to explain the relevant data.
Unfortunately, as yet no coherent theory to explain what are some of the weirdest anomalous traits in all of biological evolution.

Why are there so many explanations for primate brain evolution?
A synthesis of the theories and concepts of early human evolution
12 Theories of How We Became Human, and Why They’re All Wrong
Modern human origins cannot be traced back to a single point in time



So how to cut through the confusion? It's not rocket science it is very basic developmental biology!


Our distant mammalian ancestor formed a 50 million year plus seed disseminating relationship with the flowering plants or angiosperms.

The angiosperm host provided us with swollen ovaries in return for spreading its seeds, a classic symbiotic relationship.

In co-evolving symbiotic relationships, the participating host (angiosperm) and symbiont (us) significantly influence each other's development and evolution.

Over time the boundaries between the symbiont and host can blur as they become more deeply integrated, the term 'symbiotic hybrid' can be used to describe these relationships.

Symbiotic hybrids can result in new or 'emergent' properties or structures that neither host nor symbiont could produce or maintain alone.

A well-known example is lichen thallus, the emergent structure of a fungal and plant symbiotic hybrid.
If the symbiotic organisms that make up the lichen are separated the emergent thallus cannot be sustained and disappears.

As is typical for co-evolving symbiotic relationships our basic physiological requirements were increasingly provided for by our angiosperm host.

This involved our daily suckling of 'juvenilising' angiosperm reproductive biochemistry via the intermittent ingestion of swollen angiosperm ovaries for tens of millions of years.

One more time, for tens of millions of years our symbiotic relationship revolved around drinking the juvenilising reproductive compounds of the angiosperms every day.

While the ingestion conduit may have been oral the result was effectively the same as being reinserted and implanted into a juvenilising reproductive system with an intermittent umbilical connection.

Spending millions of years essentially implanted in a reproductive system creates an extraordinarily rare hormonal and molecular ecology in which to evolve and develop or to put it quite literally, to gestate.

The ensuing perpetual state of gestation and being permanently immersed in juvenilising reproductive biochemistry incrementally fetalised our mammalian physiology with each generation.

The amplification and extension of the typical neural growth window induced the proliferation of a new layer of embryonic neural tissue.   

As each generation became more juvenilised than the previous generation the increasingly juvenile neuro-endocrine regime fed into the hybrid 'gestation' environment initiating an exponential feedback loop of increasing juvenility.

The typical mammalian developmental and maturational windows were inevitably slowed and extended.

Over time the accelerating expansion of a colossal mass of increasingly juvenile neural tissue emerged.

The very same mechanisms resulted in the uneven extension of windows of bone growth, our (hind) legs became disproportionately long, the result: Taller larger brained bipeds.

When these symbiotic relationships breakdown the emergent properties and hybrid structures begin to revert as the archaic mammalian hormone regime begins to reassert itself.


Gets weirder: Slowing of developmental windows to explain anomalies in human evolution is not a new idea.
 

Oddly enough there were several related theories and proposals centred around the slowing of normal developmental and maturational windows as a means of explaining a number of anomalous traits from our large brain to the retention of a number of juvenile features.
The thinking was that these unusual traits might be related and explained by a simple slowing of normal developmental windows that in turn allow for a longer widows of neural expansion and the retention of juvenile traits as the normal maturational and ageing processes were inhibited.

A selection of summaries and critiques of proposals that attempt to explain why humans exhibit juvenile traits including our extraordinarily large brain.

Neoteny and Heterochrony in Humans
Heterochrony in Human Evolution: The Case for Neoteny Reconsidered
Human neoteny revisited: The case of synaptic plasticity
The Role of Heterochrony in Primate Brain Evolution
Heterochrony: the Evolution of Development
Human Evolution through Developmental Change
Morphometric heterochrony and the evolution of growth

Interesting eh? If nothing else it tells us that all the pieces of the symbiotic jigsaw have been seriously considered in isolation as part of ongoing efforts to explain our strangeness. 
Unfortunately, no coherent mechanism or driver to explain how the maturational process could be slowed or the juvenile window extended was identified.


The missing juvenilising factor hiding in plain sight.

However, a recent analysis of factors relating to the holy grail of human evolution, the neural expansion enigma, revealed a solid correlation with the ingestion of swollen ovaries.
Is fruit eating responsible for big brains?
Primate brain size is predicted by diet but not sociality 

The connection between ingesting swollen ovaries and unusually large brains in primates is not new, this study was published in 1993 Diet and Primate Evolution.


Recent article with simple summary

Why Some Primates Have Bigger Brains


Fruit Bats

A similar correlation was found in fruit bats, slowed development and unusually large neocortex, this paper dates to 1977 Relative Brain Size and Feeding Strategies in the Chiroptera.
Also an interesting correlation between symbiotic diet and gut anatomy Functional Anatomy of the Alimentary Canal in the Fruit Bat, Eidolon helvum, and the Insect Bat, Tadarida nigeriae

Like everyone else, the authors try to explain their findings under the umbrella of adaptive selection rather than the direct juvenilising impact of the symbiotic relationship.

All you have to do is factor in the real-time impact of flooding a typical mammal with the juvenilising reproductive biochemistry of the angiosperms, then it all fits together.

This paper is at least asking relevant questions but as yet no connection between 'fruit' and hormonally juvenilising 'swollen ovary'. The Roles of Phytoestrogens in Primate Ecology and Evolution


​​​So some suggestions re joining the well tested jigsaw pieces.

Based on predictable and near axiomatic biological mechanisms (as close as you get to facts) you cannot permanently add or subtract a powerful juvenilising factor to or from a complex organism such as a mammal without a massive and predictable impact on every aspect of growth, development and function.

Add a powerful juvenilising factor to a typical mammal for millions of years such as a flood of juvenilising reproductive biochemistry and it will have a juvenilising effect by inhibiting and slowing normal maturation mechanisms.
By slowing and therefore extending normal developmental windows such as neural proliferation or limb extension you can end up with a large-brained and disproportionately stretched fetus like organism without the need for adaptive changes in DNA.

In fact based on elementary developmental biology, a large-brained and disproportionately stretched fetus like organism would be the predictable outcome if the symbiotic relationship with the angiosperm reproductive system was stable for evolutionary time scales.

Remove the juvenilising factor after millions of years and it will have an equally powerful maturational effect on mammalian physiology, the runaway juvenilising process stalls and initiates a slowly accelerating maturational process. The freakishly juvenilised large-brained and disproportionately stretched fetus like organism (us) will inevitably begin to mature. Emergent structures such as the highly anomalous proliferation of the neo-cortical tissue will inevitably exhibit increasingly serious developmental failure. The loss of the angiosperm reproductive host and its complex juvenilising transcription factors prevents what had become 'normal' symbiotic development. This results in structural failure and malformation of the embryonic neocortex due to differentiation and atrophication as the post symbiotic environment is by comparison extremely ageing.


Ironically 'normal' development in the symbiotic hybrid was the very opposite of typical mammalian development with every aspect of maturation and ageing eventually slowing to a glacial pace.


Summary

Is there any evidence for a 50 million year plus juvenilising symbiotic relationship that inhibited mammalian maturational and ageing hormones? Yes.
Is there now evidence for developmental failure in our new brain linked to the activity of maturational and ageing hormones? Yes.
Is there evidence for catastrophic atrophication and erosion of our new brain as 'normal' maturation and ageing progresses? Yes.
Relevant links here
Is there evidence for accelerating post symbiotic reversion and atrophication of our new brain in our recent evolutionary history? Yes. 
Selection for smaller brains in Holocene human evolution.



Also, though it may seem circular, if there was a major neurological and perceptual trauma in our distant past then it would be reasonable to expect surviving accounts alluding to what would have been a massive event in ancient mythology.


If our neo-cortex was an emergent or hybrid symbiotic structure it would inevitably exhibit increasingly serious developmental problems, atrophication and erosion once disconnected from its host and the unique transcription and biochemical environment required for its initial emergence and continued structural and functional integrity.


OK that was all a bit heavy duty so some light relief to put it all in perspective.

I remembered a scene from the 1970's TV series 'Planet of the Apes' that may well sum up our efforts to make sense of our ancestors and the mess we are in, it is a bit of a twisted analogy but you will hopefully get the point.

In this scene, the Ape Prefect 'Barlow' considers himself a scientist of sorts and attempts to make sense of the ancient 'primitive' artefacts he discovers.
It never occurs to him that his whole approach may be deeply flawed and it is he who is, by comparison, primitive and lacking the cognitive capacity to understand what he has found and what it means.