View Full Version : Environmental factors in the etiology of ADHD(split from safety of stimulants thread)


SB_UK
07-17-15, 03:03 AM
That's interesting.

What we call ADHD is just a stress reaction.

The underlying cause of the stress reaction can either be through 'feature' (different logical structure to mind - see Stabile (paraphrase, on-site) 'a richer encoding of reality through necessity takes longer to form' cf developmental delay) or 'flaw' (FXS).

-*-

Haven't been able to (in a satisfying way) connect in cerebellum.

Have the connection between smooth movement - cerebellum and basal ganglia (substantia nigra, Parkinson's disease)
And perhaps the idea of 'learning' in the cerebellum.

Have noticed our kids have 'slurred' speech .. ... thinking 'education' of the cerebellum.
A bit like (Dore ??) which uses physical education (balance) to educate the cerebellum ??

Am noting a connection between physical co-ordination, speech co-ordination, complexity of language.
Between 'external' clumsiness and 'internal' clumsiness.

No real belief that people are 'genetically' clumsy - only that people fail to be taught or fail to learn.

Raises the interesting question of the importance - once again - of other aspects of life which we require for proper development - fine locomotor exercises eg badminton, table-tennis and arts eg drawing, painting and music ... ... perhaps elocution lessons (Speaking clearly).

Wondering whether crispness of movement in sports, playing an instrument, talking are all part of 'cerebellar' education which feed back into mind ?

This kinda' idea.Amazingly, the part of the brain that processes movement is the same part of the brain that's processing learning. http://www.pesoftware.com/resources/movelearn.html

Suddenly linking movement and thinking became inescapable.Particularly like the idea of fine motor activity in the external and internal world being 'shared'.

SB_UK
07-17-15, 04:40 AM
So - all of the above - places a different developmental schedule on ADDers - who when subject to inappropriate educaion / inappropriately (too) advanced education to the ADDer developmental delay (take longer to learn better) - react with stress - impedes learning, prevents learning - arrests development ?

So - the well documented ADDer developmental delay can result in arrested development in the absence of appropriate education ?

daveddd
07-17-15, 05:28 AM
That's interesting.

What we call ADHD is just a stress reaction.

The underlying cause of the stress reaction can either be through 'feature' (different logical structure to mind - see Stabile (paraphrase, on-site) 'a richer encoding of reality through necessity takes longer to form' cf developmental delay) or 'flaw' (FXS).

-*-

Haven't been able to (in a satisfying way) connect in cerebellum.

Have the connection between smooth movement - cerebellum and basal ganglia (substantia nigra, Parkinson's disease)
And perhaps the idea of 'learning' in the cerebellum.

Have noticed our kids have 'slurred' speech .. ... thinking 'education' of the cerebellum.
A bit like (Dore ??) which uses physical education (balance) to educate the cerebellum ??

Am noting a connection between physical co-ordination, speech co-ordination, complexity of language.
Between 'external' clumsiness and 'internal' clumsiness.

No real belief that people are 'genetically' clumsy - only that people fail to be taught or fail to learn.

Raises the interesting question of the importance - once again - of other aspects of life which we require for proper development - fine locomotor exercises eg badminton, table-tennis and arts eg drawing, painting and music ... ... perhaps elocution lessons (Speaking clearly).

Wondering whether crispness of movement in sports, playing an instrument, talking are all part of 'cerebellar' education which feed back into mind ?

This kinda' idea.http://www.pesoftware.com/resources/movelearn.html
Particularly like the idea of fine motor activity in the external and internal world being 'shared'.

im not even sure if FXS is even just a flaw as cause

I've read that its likely a strong diathesis that still needs a environmental stress component to activate

can the flaws in the gene they find be a product of that as a whole, misleading some to a strict genetic disease cause?

SB_UK
07-17-15, 05:30 AM
The net consequence of ^^^ in line with KD's OP is that meds would help to suppress the stress reaction which itself results in adverse downstram consequences for proper neural development.
But the key stressors are age inappropriate education, and in the absence of age appropriate education - development can't occur.

So - adverse educational (particularly cerebellar) environment leads to neural regression via stress -> ameliorated by stimulants.
But - adverse educational (particularly cerebellar) environment leads to lack of neural development - since 'learning' (development of appropriate neural structures) cannot occur.

The meds are only necessary in an adverse educational environment - may suppress damage but won't promote development unless education exposure appropriate.

Problem - how do we develop an appropriate educational environment ?

Simply factor in the developmental delay - we know that ADDers have a 3 - 4 year delay beginning at age x - normalizing at age y ... ... so to have the potential for a 2 stream system. Perhaps a system where classes aren't age restricted - although older students in the same class as younger students are often made fun of ... ... although this behaviour can be dispelled under the 'taking longer to learn better' model of ADHD ... ... if more widely accepted by society.

daveddd
07-17-15, 05:56 AM
That's interesting.

What we call ADHD is just a stress reaction.

The underlying cause of the stress reaction can either be through 'feature' (different logical structure to mind - see Stabile (paraphrase, on-site) 'a richer encoding of reality through necessity takes longer to form' cf developmental delay) or 'flaw' (FXS).

-*-

Haven't been able to (in a satisfying way) connect in cerebellum.

Have the connection between smooth movement - cerebellum and basal ganglia (substantia nigra, Parkinson's disease)
And perhaps the idea of 'learning' in the cerebellum.

Have noticed our kids have 'slurred' speech .. ... thinking 'education' of the cerebellum.
A bit like (Dore ??) which uses physical education (balance) to educate the cerebellum ??

Am noting a connection between physical co-ordination, speech co-ordination, complexity of language.
Between 'external' clumsiness and 'internal' clumsiness.

No real belief that people are 'genetically' clumsy - only that people fail to be taught or fail to learn.

Raises the interesting question of the importance - once again - of other aspects of life which we require for proper development - fine locomotor exercises eg badminton, table-tennis and arts eg drawing, painting and music ... ... perhaps elocution lessons (Speaking clearly).

Wondering whether crispness of movement in sports, playing an instrument, talking are all part of 'cerebellar' education which feed back into mind ?

This kinda' idea.http://www.pesoftware.com/resources/movelearn.html
Particularly like the idea of fine motor activity in the external and internal world being 'shared'.

I've been interested in coordination and development of mental illness

i can't shake one example , gurevitch, a russian psychologist came of with four motor types

categories had different labels then, but its easy enough to make the connection

https://books.google.com/books?id=IdP7AQAAQBAJ&pg=PA97&dq=gurevitch+motor+types&hl=en&sa=X&ved=0CCYQ6AEwAGoVChMIx92I-vHhxgIVS40NCh1eQACe#v=onepage&q=gurevitch%20motor%20types&f=false

SB_UK
07-17-15, 06:13 AM
im not even sure if FXS is even just a flaw as cause

I've read that its likely a strong diathesis that still needs a environmental stress component to activate

can the flaws in the gene they find be a product of that as a whole, misleading some to a strict genetic disease cause?


That's ^^^ interesting.

eg http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3697269/

Stress-Induced Modulators of Repeat Instability


Here, we review the regulation of mutation rate, with special emphasis on the roles of tandem repeats and environmental stress in genome evolution.When does trinucleotide expansion occur in development ?

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3175376/
Expansions in simple DNA repeats underlie ~20 severe neuromuscular and neurodegenerative disordersFunny

neuro and muscular
inescapable connection between thinking and movement

If our ultimate aim is to understand the mutational mechanism in humans


These findings imply that Base Excision Repair is involved in expansionDNA damage and autophagy. (http://www.ncbi.nlm.nih.gov/pubmed/21419786)

Unrepaired DNA damage has been linked to a variety of human disorders including cancer and neurodegenerative disease. Autophagy
- fasting ie food intake related.

eg Calorie restriction increases telomerase activity, enhances autophagy (http://www.ncbi.nlm.nih.gov/pubmed/25662949)

-*-

What's the backdrop ?

The Thrifty gene hypothesis is operating to switch us off carb dependence - however we haven't realised - are operating over a highly insulin-promoting diet - are deactivating autophagic / DNA repair mechanisms - are promoting Trinucleotide expansions - which - although valid methods used in genomic evolution - are no longer required.

So - mechanisms which promoted survival of the fittest ie food availability supported further genomic change - to favour continued survival of organisms at the level of genomic change (Think movie Highlander where each victory was accompanied by the quickening - and the individual getting stronger) ... ... these mechanisms are retained - and are inadvertently re-activated when we expose a system geared towards 'change' in the presence of carbs (animal-based protein + high GI carbs) - to these nutritional factors.

In The Highlander though - there could be only 1 - which would be the emergence of modern man with mind.
Genomic evolution ends here as we shift to a model or evolution employing only the nerve.
No further room for genomic change in the system - we switched to a neural model of evolution.

'Cept retained the evolutionary (primitive reward system) affection for pro-insulin expressing foods ... ... the journey to wisdom is about eliminating 'craving' or switching from a pro-anabolic to a maintenance (ketone) metabolic spectrum.

Carbs - hyperglycaemic / hypoglycaemic (drops below baseline) - duality of pleasure / pain
Ketones - unipolar state - as we know ketosis overcomes appetite (hunger) cf all of the many ketogenic weight-loss regimes.

-*-

Once again - a sliding scale of metabolic fuel from carbs to ketone bodies (minimally processed low GI vegetables) is suggested ?

SB_UK
07-17-15, 06:29 AM
I've been interested in coordination and development of mental illness

i can't shake one example , gurevitch, a russian psychologist came of with four motor types

categories had different labels then, but its easy enough to make the connection

https://books.google.com/books?id=IdP7AQAAQBAJ&pg=PA97&dq=gurevitch+motor+types&hl=en&sa=X&ved=0CCYQ6AEwAGoVChMIx92I-vHhxgIVS40NCh1eQACe#v=onepage&q=gurevitch%20motor%20types&f=false

Not in order ?

+ + - - fine locomotor
+ - + - gross locomotor

So - cerebellar education using first repetitive gross and then repetitive fine locomotor activities ?

SB_UK
07-17-15, 06:38 AM
So all of the above implies

Carb-driven (primitive energy source)
Genomic development of physical body (insulin mediated anabolic (growth) processes)

Fat (ketone)-driven (higher energy source)
Neural development of brain (the nerve doesn't divide - just re-arranges its connections)

See - wikipedia/HDAC inhibitor (eg ketone bodies, beta-hydroxybutyrate) acting as a growth suppressant (pharma targets for treating inflammatory conditions/cancer).

So - a fundamental switch in our blue-print from physical structure (genome governed) to informational structure (neurally governed).

Mitochondrial selection during evolution (fungus)
+
Melanin

--> radiotrophic fungus

Well-known idea that a major transition in our evolution from prokaryote to eukaryote involved colonization by mitochondria
- however we need to connect melanin into the picture.