View Full Version : How nutrition affects epigenetics (split from epigenetics thread)


Amtram
05-01-14, 05:57 PM
Epigenetics as a cause for ADHD is a much more complex and significantly less likely scenario than genetic inheritance, and requires an assumption, a HUGE assumption, that is not yet supported by any data whatsoever.

Evidence that glucose changes epigenetics is. . .unsupported. Every cell in the body requires glucose for energy and reproduction.

It is not magic. It happens no matter whether you change methylation or not. It is almost entirely heritable. We have extremely limited information about what methylates what CpG Islands, when that methylation has an impact, and whether that impact is positive, negative, or neutral. All we have is evidence of how it works and a few specific experiments with specific chemicals introduced at specific developmental stages that produce specific changes in gene expression.

Everything else is Baseless Speculation.

SB_UK
05-02-14, 07:24 AM
That page is interesting.

http://en.wikipedia.org/wiki/X-inactivation
Compared to the Xa, the Xi has high levels of DNA methylation, low levels of histone acetylationSo - we've the 2 effects of epigenetics - DNA and histone modification which're operating in tandem to result in:
growth -> maintenance transition.


--------------------
Human development
--------------------

Growth paradigm
Some genes will need to be switched off -
high levels of DNA methylation, low levels of histone acetylation [growth promoting requiring]
[glucose]

->- cortisol (eustress) - >- favours this transition

Maintenance paradigm
Some genes will need to be switched on -
low levels of DNA methylation, high levels of histone acetylation [aerobic respiration requiring]
[fat/ketone]

So human development is supposed to progress with development from attraction to glucose (pre-frontal cortex reward system) to 'loss of material world attachment' ie no further growth in the system.
A shift from carb-driven (hyperglycaemia/hypoglycaemia) to ketosis/fat (stable blood glucose).

The nerve - for its development doesn't require 'growth' as it doesn't as such grow - simply alters its pattern of connections; so we can see development of the nervous system towards 'quality' as being a post-physical body growth paradigm.

-*-

So stable epigenetically inherited marks on DNA AND histone - resulting in selection for 'maintenance' and not 'growth' phenotype.

-*-

But what happens to this system if we apply distress instead of eustress ?
Well - it'll certainly break the transition from growth to maintenance.

What should we do about it ?
Realise the human transition and change society accordingly.

But what about all of those people who've been broken through distress ?
Well - I guess it's never too late to practice eustress.
IE neuroendocrine resistance syndromes can be rendered 'sensitive' by application of eustress.

SB_UK
05-02-14, 08:03 AM
--------------------
Human development
--------------------

Growth paradigm
Some genes will need to be switched off -
high levels of DNA methylation, low levels of histone acetylation [growth promoting requiring]
[glucose]

->- cortisol (eustress) - >- favours this transition

Maintenance paradigm
Some genes will need to be switched on -
low levels of DNA methylation, high levels of histone acetylation [aerobic respiration requiring]
[fat/ketone]


- which is how cortisol can control 2 conflicting processes:
glucocorticoids function through interaction with the glucocorticoid receptor:

up-regulate the expression of anti-inflammatory proteins.
down-regulate the expression of proinflammatory proteins.



Pro-inflammatory - 'growth'
Anti-inflammatory - 'maintenance'

-*-

So - the idea is that blood glucose requirement will shift from high to low - with development.
Attraction for glucose elevation (the PFC selfish reward system) should wane as human physical development progresses.
Reduced attraction to glucose / reduced levels of blood sugar - increasing recruitment of cortisol to maintain blood glucose levels.
With time - cortisol epigenetically shapes the genome/histome into the maintenance/metabolism state.
At some point- upon development - we've a loss in the blood glucose elevating reward system.
We're in a healthy ageing paradigm - as we're going to arrest the rate of cell division (prolong healthy life).
The PFC reward system shifts to another reward system.
The neurone doesn't much care for growth/proliferation and is able to do its thing without actual cell division.
We shift from a physical paradigm, full on - to a neural paradigm.
That neural paradigm can be taken as living for quality.

Quality of sensory experience.

-*-

So the 'thinking mind' is simply a conduit from animal (living for food) into living for sensory quality.
We've arrested at the thinking stage - where 'I know that I know nothing' - is the key phrase.
Goal to develop a mind which is wholly consistent with species wellbeing.
Why ?
Generation of quality is something that other people can do for themselves and contribute (limitless paradigm) to you.

We need a social species in order to be able to work together.

The role of the human mind is simply to get our heads around the need for a collaborative structure in which we can all work on realising the highest possible quality of human experience - for one - and for all.

LynneC
05-02-14, 08:42 AM
Evidence that glucose changes epigenetics is. . .unsupported. Every cell in the body requires glucose for energy and reproduction.
Actually, there is some evidence that high blood glucose can cause epigenetic changes. This is not in the context of epigentic changes in expression of ADHD, but it is not accurate to say that glucose elevation has no effect on epigenetics. Full article...
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2556800/

SB_UK
05-02-14, 08:48 AM
So - the emergence of ADDer via epigenetic selection - suggests.

[1] ADDers born into fully optimised (low energy) epigenetically modified genome/histome.
[2] ADDers born into ACC and not PFC (blood glucose) reward system.
[3] ADDers - lower growth rates - but greater longevity given very specific - ketosis conditions ie conditions in which blood glucose usage is kept to a minimum.
[4] Exuberant growth in ADDers given either high blood glucose /distress.
Exuberant = deranged growth.

ADDers fall victim to diseases prematurely, when actually optimised to go on for longer in the correct environmental setting.

Eliminating Psych and Physical distress, and embracing eustress is key.

LynneC
05-02-14, 08:54 AM
The environment doesn't change the epigenetics, puberty is still the result.
But the change can happen sooner or later. Does this make sense to anyone but me?
I think it may be more accurate to say that the environment may cause epigenetic changes that can result in early puberty. By environment, I'm including chemical exposure, dietary considerations, etc.
I think another important thing to remember is that factors (such as environment) that cause epigenetic changes (and therefore altered expression of certain traits) in one individual may not cause the same epigenetic changes and altered expression in another individual because of differences in individual genomes.

SB_UK
05-02-14, 08:55 AM
Actually, there is some evidence that high blood glucose can cause epigenetic changes. This is not in the context of epigentic changes in expression of ADHD, but it is not accurate to say that glucose elevation has no effect on epigenetics. Full article...
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2556800/

"We show that transient hyperglycemia induces long-lasting activating epigenetic changes in the promoter of the nuclear factor κB"

... ... where NF-kB is strongly pro-inflammatory.

IE direct promotion of the pro-inflammatory state ('growth') via blood glucose fluctuation/usage/attraction.
Promotion of the anti-inflammatory state by ketone bodies.
HDAC inhibitors eg beta-hydroxybutyrate - strongly anti-growth/proliferation.

Since Ketone bodies are epigenetic modifiers, and blood glucose levels prevent ketone body production - then 'guilt by association' - blood glucose variability is tied into epigenetic change.

SB_UK
05-02-14, 09:05 AM
I think it may be more accurate to say that the environment may cause epigenetic changes that can result in early puberty.

Relationship between precocious puberty/hypersexual behaviour/teenage pregnancies and diet (hyperglycaemic) ?

IE exuberant growth given chronically high blood glucose levels.
eg
CONCLUSIONS/INTERPRETATION:

Age at menarche seems to be inversely associated with prediabetes and diabetes independent of confounding factors including current BMI. Women at risk for diabetes might be identified by a history of young age at menarche.
http://www.ncbi.nlm.nih.gov/pubmed/22170465

Lunacie
05-02-14, 09:27 AM
So - the emergence of ADDer via epigenetic selection - suggests.

[1] ADDers born into fully optimised (low energy) epigenetically modified genome/histome.
[2] ADDers born into ACC and not PFC (blood glucose) reward system.
[3] ADDers - lower growth rates - but greater longevity given very specific - ketosis conditions ie conditions in which blood glucose usage is kept to a minimum.
[4] Exuberant growth in ADDers given either high blood glucose /distress.
Exuberant = deranged growth.

ADDers fall victim to diseases prematurely, when actually optimised to go on for longer in the correct environmental setting.

Eliminating Psych and Physical distress, and embracing eustress is key.

:scratch: What's this about falling victim to diseases - prematurely?

Not everyone gets the same diseases as the same age, eh?

SB_UK
05-02-14, 09:43 AM
What would happen if we force fed 5 identical identical twin brothers 3000, 4000, 5000, 6000 and 7000 calories per day - and didn't allow them to burn it off ?
We'd find that the one eating the most 'd become afflicted by disease before the others (in order).
So - feeding 2 individuals - one of whom needs less calories or calories of a different type to another person - 'd similarly result in that other more efficient metabolism breaking prematurely relative to the 'less' efficient metabolism whose needs are being met.

In metabolic syndrome - low birth weight babies explode into grossly overweight Syndrome X'ers.
I don't think that this could occur on a [raw vegan] ketogenic diet
http://en.wikipedia.org/wiki/Metabolic_syndrome

Some have pointed to a variety of causes, including increased uric acid (http://en.wikipedia.org/wiki/Uric_acid) levels caused by dietary fructose (http://en.wikipedia.org/wiki/Fructose).The 'gourmet' raw vegan (MUFA/PUFA-centric) diet (in wikipedia) is relatively low protein and low fructose.

Amtram
05-02-14, 10:12 AM
Actually, there is some evidence that high blood glucose can cause epigenetic changes. This is not in the context of epigentic changes in expression of ADHD, but it is not accurate to say that glucose elevation has no effect on epigenetics. Full article...
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2556800/

I never said it has no effect on epigenetics. I never said that cortisol has no effect on epigenetics. What I'm saying is that the claims about the epigenetic effects of these chemicals is way, way overstated, and a long way away from being set in stone.

Unmanagable
05-02-14, 12:52 PM
Maybe it's just the strange way my brain works and no one else feels this way, but weren't many of the now proven facts once viewed as simply being "Baseless Speculation" by extremely skeptical peeps back in the day?

Amtram
05-02-14, 01:07 PM
Also, all the conclusive research I've seen on epigenetic changes related to dietary changes were from prenatal exposure. This in no way implies that postnatal dietary changes will in any significant way change gene expression.

SB_UK
05-03-14, 08:03 AM
If the ketone body is a HDAC inhibitor - and a HDAC inhibitor affects gene expression, then there can be no doubt that a dietary switch from hyperglycaemic to ketosis will have an effect on gene expression.
To carry out gene expression, a cell must control the coiling and uncoiling of DNA around histones (http://en.wikipedia.org/wiki/Histones).

It's absolutely inconceivable that a standard Western diet being switched to a ketosis lifestyle wouldn't have predictable consequences on gene expression, operating through epigenetic mechanism.

-*-

Even more so - physical activity 'cements' ketosis ('hitting the wall') and so we can extend nutrition/physical activity via epigenetic modification directly into the modification of gene expression - from wikiP/HDi ... ... towards selection of a non-growth/non-proliferative phenotype.

Dizfriz
05-03-14, 10:22 AM
Maybe it's just the strange way my brain works and no one else feels this way, but weren't many of the now proven facts once viewed as simply being "Baseless Speculation" by extremely skeptical peeps back in the day?
Yes but so many speculations are presented without evidence. There is an old rule in science that ideas presented without evidence can be rejected without evidence.

So yes some of the speculations did, in time, gain evidence and were accepted but the ones that never were able to develop evidence remain as just that, speculation. Evidence is the key.

There is nothing wrong with speculation but it is good to keep in mind that it is indeed speculation and not, as some do, take speculation as fact.

Dizfriz

Amtram
05-03-14, 01:24 PM
Maybe it's just the strange way my brain works and no one else feels this way, but weren't many of the now proven facts once viewed as simply being "Baseless Speculation" by extremely skeptical peeps back in the day?

No, they started off with knowledge that led to the idea that there might be a basis for speculation. There had to be enough information to form a hypothesis, not just some random ejaculation of ideas.

And proof is for math and alcohol. Not science.

Amtram
05-03-14, 01:29 PM
If the ketone body is a HDAC inhibitor - and a HDAC inhibitor affects gene expression, then there can be no doubt that a dietary switch from hyperglycaemic to ketosis will have an effect on gene expression.

In fetuses?


It's absolutely inconceivable that a standard Western diet being switched to a ketosis lifestyle wouldn't have predictable consequences on gene expression, operating through epigenetic mechanism.

It's absolutely inconceivable that this would be the case, given the dearth of robust evidence pointing to dietary changes in adult human beings causing noticeable changes in gene expression.


Even more so - physical activity 'cements' ketosis ('hitting the wall') and so we can extend nutrition/physical activity via epigenetic modification directly into the modification of gene expression - from wikiP/HDi ... ... towards selection of a non-growth/non-proliferative phenotype.

How about from peer-reviewed, published data in reputable academic journals? If you don't have full-text access, I can look it up for you. Wikipedia has its benefits, but it's not the go-to source for up to date research results or analysis of data.

Shenpen G
06-10-14, 05:47 PM
... given the dearth of robust evidence pointing to dietary changes in adult human beings causing noticeable changes in gene expression...


This might help:



Mitochondrial biogenesis in the anticonvulsant mechanism of the ketogenic diet.

RESULTS: Most striking was a coordinated upregulation of all (n = 34) differentially regulated transcripts encoding energy metabolism enzymes and 39 of 42 transcripts encoding mitochondrial proteins, which was accompanied by an increased number of mitochondrial profiles, a higher phosphocreatine/creatine ratio, elevated glutamate levels, and decreased glycogen levels. Consistent with increased energy reserves, synaptic transmission in hippocampal slices from KD-fed animals was resistant to low glucose.

INTERPRETATION:
These data show that a calorie-restricted KD enhances brain metabolism. We propose an anticonvulsant mechanism of the KD involving mitochondrial biogenesis leading to enhanced alternative energy stores.

http://www.ncbi.nlm.nih.gov/pubmed/16807920