Epigenetic inheritance a new theory

[Bgoatgruff]

This looks like the ideal forum to request comments/criticism on a neural function/evolution hypothesis I have been developing. I have pieced together data observations etc and conducted a few experiments over the last 11 years, my conclusions are a little unexpected. To make the pieces fit I needed a non mendelian inheritance mechanism (a minor headache!) what I came up with based on some of the unusual aspects of human physiology was a variation on the accepted inheritance model that ran along side it.

 

It might shed some light on nakedness and other traits particularly neotony and the rapid expansion and stall of our brain etc

 

Below is an excerpt from recent correspondence. If you find it of interest visit http://www.kaleidos.org.uk and download chapt 4 its a rough draft in laypersons language.

 

Thanks

 

 

 

 

The hypothetical epigenetic mechanism I'm interested in is extremely simple in principle (my explanation may not be so simple!). Whether it ever played a part in primate/human evolution is another mater. If it did there are a small number of requirements that would need to be in place for it to work. (more later)

 

Anyway the basic mechanism is already part of the accepted inheritance /transcription mechanism though it is usually relatively stable. Rather than variation and inherited traits being transmitted via DNA and DNA mutation my proposal is that part of the DNA reading mechanism could provide variation and inheritance of that variation. In addition as the mechanism is based on variation in hormone levels/activity there is potential for blanket effects on all aspects of growth/development. Finally as there is the potential for an accelerating positive/negative feedback loop there is potential for fast track evolution of whole growth/development traits ie juvenile phase. This in turn can radically alter many specific traits.

 

Sex steroids ie estrogens, testosterone are central to DNA transcription and also play a role in development windows ie juvenility. The pineal produces melatonin and pinoline both modulate steroid activity. Melatonin also appears to play a direct role in DNA transcription.

Pineal activity is significantly regulated by neural activity, the accepted model of daylight regulation is incomplete.

 

So briefly, the neuroendocrine system of the adult female plays a significant role in the permanent structural/functional development of the early foetal neuroendocrine system.

 

 

A hypothetical scenario--- a change in steroid activity during early neural devolvement in the uterus permanently changes neuro-endocine function in such a way that it elevates life long melatonin production. When that foetal neuro-endocrine system reaches maturity and becomes pregnant (female line of course) it creates the same modified inutero hormone environment. A slight increment with each generation is all that is required, very rapid change will likely be detrimental, no change no evolutionary effect.

 

So a change in the hormone environment of the foetus slightly increases lifelong pineal activity. Melatonin and pinoline are both steroid modulating hormones and both play a role in the length of the juvenile window. So a direct effect on the structural development of the brain and an effect on the windows of neural development are initiated by the hormone environment in the uterus. If such changes are incremental ie more equals more then a potentially powerful inheritance mechanism exists. However as it is not locked into the genes it is potentially unstable with the capacity to rapidly accelerate into a runaway feedback loop or stall and reverse.

[Airmid]

Wow, that was quite a read! Now for some sensible comments.....

 

Unfortunately my knowledge about human genetics and endocrinology is only up to Discovery Channel level. I remember seeing a documentary that centered on these issues. I remember that one of the cases presented there was about a study of inherited responses to stress: children of a number of women who were subjected to severe stress during pregnancy had abnormal responses to stress themselves in later life. So at least some research has been done in that direction, but I have no idea of the scope or level of support for it.

If this research is valid, it would support your case. However, at evolution time scale, like you said, the mechanism is unstable. I think you will need support from research for this particular step most of all.

 

I have been reading a few chapters of your work. You haven't convinced me at all, and I particularly dislike the combination of doctrine ("stop poisoning your body!") and science ("on human evolution"). I'm quite surprised myself that I'm willing to take your work serious; probably because there's some interesting ideas in there, and because you are making an effort to find scientific support for your ideas. I think, however, that you should make a clear choice: either go for the doctrine, or the science. If you go for the doctrine, have fun; if you go for the science, be prepared to put in a lot more effort to read anything you can find on the subject, and not only weigh the pro's but also the con's you might find in there. Obviously I think the science way would be the better way *smiles*.

 

Good luck,

Airmid.

[Bgoatgruff]

Thanks for your comments, few responses that might clarify what I’m looking for and why.

 

Firstly if it was not already obvious I’m not a professional scientist, I have no formal qualifications in most of the areas I’m interested in other than plant sciences, have no organization and no funding. Like it or not this seems to make going down the science only route re peer reviewed journals etc a bit tricky. I did make a presentation of my embryonic theory at a small conference in the US in 1998 and a summary was reviewed and published. A couple invites emerged but due to lack of funds I could not attend. During that period there seemed to be an assumption that I had a doctorate in brain related science, when it would emerge that I did not attitudes seemed to change.

 

Anyway I have quite intentionally decided to go down the science mixed with ‘doctrine’ route in the format of a laypersons book. This approach is simply to create some interest/ controversy from which I hope to engage in more serious dialogue. That said my writing skills are abysmal so the draft manuscript was written by someone else who brought greater doctrinal element than I am comfortable with. The current/ongoing rewrite will address that to some degree. The web site is obviously in the same mould though I would hope that it is not too difficult to separate out accepted scientific data/observation from doctrine or speculation.

 

So much for my defense, What I’m really interested in at this stage is comment on the inheritance mechanism only, in principle and as a possible factor in primate evolution. If you like, separating out a more scientific element of the ‘story’.

 

I have been requesting comment from biologists for some time and thus far no specific problems have been brought to my attention. As already stated the mechanism is very simple in principle and is based on mechanisms that are accepted and are known to play a role in neural development and regulating the windows of neural development. I am aware of the examples you mention (and others) though the mechanism I’m proposing is distinct. I accept its is potentially unstable (something I required) however the unstable factors in this case are specific biochemical/hormonal elements found in a typical forest dwelling primates diet. These external elements (steroid modulating plant sterols) were present day in day out for tens of millions of years (pretty stable re evolutionary time scales) and may as well have been part of the endocrine system. I have proposed that these hormone modulating elements initiated and supported a change in endocrine activity. The loss of these factors even for a generation would be enough to destabilize the proposed modified endocrine function. Specifically leaving the forest ecology behind. Once the mechanism stalls it will not restart, any extension in juvenile phase or neural expansion will stall and show some reversal. I apologize if chapter 4 is not academic enough in its presentation though I think the basic elements are clear enough.

 

Thanks

 

Tony

[Airmid]

Thanks! Your reply cleared up things quite a bit. I apologize if I was a bit harsh in my first reply.

I'm glad to hear you're editing your work, and I'm sure you will do a good job with it. Don't think too little of yourself ("no formal qualifications" "abysmal writing skills"). Your subject is good, and I think it doesn't need whistles and bells to make it interesting to the layperson. "The Naked Ape" was a bestseller, wasn't it?

I'll leave the field now and hope that someone with better human biology skills than mine will make the next reply!

 

Airmid.

[Bgoatgruff]

Thanks again, the proposed inheritance mechanism could stand alone however its really just one part of an investigation into cerebral dominance/asymmetry. The overall proposal is that the left hemisphere is a hormonally damaged version of the right and we are looking at the problem with our perceptually limited left.

[Bgoatgruff]

In view of the lack of comment re epigenetic theories (too speculative I presume, though the individual elements are accepted) I thought I would mention an experiment I conducted in 1998.

 

I had predicted that if my basic neural evolution/function theory was anywhere near the mark there would be a significant differential in sleep requirement between the cerebral hemispheres, the non-dominant hemisphere requiring considerably less. This would be disguised by the perceptual effects of cerebral dominance i.e. the dominant hemispheres ‘batteries’ get low, the experience is tiredness and less function. We tend not to question this, go to sleep and wake up with our dominant sense of self recharged. This cycle tends to continue from birth till death and is reinforced perceptually/subjectively and objectively (sleep deprivation experiments) when significant periods without sleep occur.

 

This basic scenario is further complicated by a deficiency of essential biochemistry, poor build quality and the inertia of long term inhibition. These additional factors are only relevant to the potential functioning of the non-dominant hemisphere.

As previously posted the dominant hemispheres function is limited by design/transcription errors primarily in the uterus. The limits in function re structural flaws make redundant the potential limiting factors re biochemistry etc.

 

A trawl through the literature on sleep and cerebral dominance threw up enough anomalies and oddities that seemed to support such a scenario

 

It seemed reasonable to try running the neural system in a different way and observe any changes in function. Looking at it from an engineering perspective I did not (like pretty much everyone else) presume the brain was currently fully functional and decided to change a couple of variables simultaneously as my theory suggested this would be required to access any significant change in function.

 

So by looking at the basic research and development of the most complex delicate thing we know (following the engineering analogy)

I combined the accepted biochemistry present for tens of millions of years (thousands of complex delicate biochemical’s, the products of the highly advanced forest pharmaceutical labs (trees), in pristine condition i.e. without denaturing via heating and oxidizing) with repeated periods without sleep (up to 7 days). The subjective experience was most surprising, reducing windows of tiredness/dysfunction then an apparent reduction in tiredness an increasing sense of function (mental, physical) plus a feel good factor.

 

After two years of repeated informal experiments primarily involving myself and to a lesser degree a small number of volunteers I approached a university to objectivity test the most testable elements of the perceived changes. The sense of increased stamina, strength, balance and dexterity was something reported by several volunteers (as well as many perceptual changes). If these changes were real they would be measurable.

 

I discussed this with Professor Dave Collins then head of sports science at Manchester Metropolitan University UK (Now performance director with the UK athletics team).

 

He was intrigued but skeptical, having a military background with some experience of sleep deprivation he suggested the perceived improvements during prolonged sleep elimination were classic delusion.

He agreed to supervise an experiment to demonstrate the delusionary effects of sleep deprivation re physical function and publish the results.

 

So to cut a long ramble a bit shorter, a 5 day experiment was arranged, myself and another volunteer (previously retro fitted with the biochemistry accepted as integral to primate evolution for tens of millions of years) stayed awake under constant 24 hour supervision by a team of scientists (including some filming). We were tested every 3 hours for a number of functions.

 

Briefly, no decline as would be expected (a result in its self) and significant improvements across the board. Due to the inexplicable results (at least re current thinking) publishing was cancelled until further studies were conducted though no funding was available. The results are available and Professor Collins remains willing to go on the record to verify them.

 

This may seem somewhat removed from the evolution forum but it suggests latent and very advantageous function that is rarely accessed along the lines of savant function experiments at The Centre for the Mind (Australia). Whatever the merits or otherwise of my theory (which did predict such an outcome) an explanation is required??

[Bgoatgruff]

Still looking for some comments re epigenetic inheritance theory that proposes the human neuroendocrine system was significantly influenced by the chemistry of our archaic tropical forest diet. Thought I would add a link to a recent study that showed a correlation between plant sterols and endocrine function.

 

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12093826&dopt=Abstract

 

In this case feeding marmosets Soya baby formula as concerns have been expressed re the hormonal effects on human development. While I do not think Soya formula is an appropriate source of nutrition for human babies the study illustrated an interesting effect. Basically plant sterols can significantly alter 'normal' endocrine function. This in turn can alter the 'normal' growth and development of the infant including the hormone sensitive brain. Permanent neural functioning is significantly influenced by factors affecting early neural development. The Soya fed marmosets showed a very significant reduction in the neonatal testosterone surge, something considered normal in many primates including humans. While the sterols in Soya may not have been part of our evolution, the related sterols in a typical forest dwelling primate diet certainly were. These kinds of chemicals were present 24/7 for millions of years during all stages of growth and development including the hormonally sensitive foetal phase. If Soya fed during the early post natal phase can significantly alter the level of one of the most developmentally important hormones (testosterone) what effect would the permanent presence of related chemicals have had on our development. More importantly what effect does the relatively recent near absence of these chemicals create. Perhaps the 'normal' brain sculpting testosterone surge is not as normal as supposed. Unless of course one assumes the brain evolved in isolation from the thousands of hormonally active chemicals found in fruit and leaves?