View Full Version : Epigenetics and ADHD, a simplified view


Dizfriz
03-31-14, 03:44 PM
I think a general understand of epigenetics may turn out to be important in the understanding of ADHD so I am going to discuss it a little.

Be aware that I am not an expert so this is a layman's approach to the subject and I am very open to corrections from those more knowledgeable. Also keep in mind that epigenetics is not settled science but subject to a lot of hypothesis testing. Science does not know a lot about the subject yet so anything said is somewhat tentative.

I am trying to write this in short paragraphs to help ADHDers read in short segments and I will try to make it as short as possible. This will result in some very important stuff left out. Hopefully I can address some of this down the road.

Also be aware that this is a complicated subject and I am presenting a very simplified version. Really, that is all I am capable of presenting. This stuff is complex.

A good bit of this cribbed from the book The Epigenetics Revolution by Nessa Carey. I take full responsibility for anything in this essay, anything I get wrong is not her fault.

So let us begin.

Just for the record, epigenetics generally is defined as the set of modifications to our genetic material that change the ways genes are switched on or off, but which don't alter the genes themselves. This is what the agreed on consensus opinion currently is.

It is easier to understand epigenetics using metaphors. There are several metaphors for epigenetics. Carey uses one of a script of a play

She presents the DNA genetic make up of an individual as a script of a play, Macbeth for example.

Let us look at epigenetics as the director and actors that put on the play.

You may have two groups putting on the same play in different towns. The script is the same but the interpretations of the director and actors may make both plays quite different in presentation. The actors and director do not change the script but their interpretation of how to present the play. Think of genetic markers as director and actor notes on the script.

In the play, the words from the script don't change but there is an opportunity for different interpretations of that script. That variation is part of epigenetics.

With a set of identical twins the scripts are identical but, due to a number of factors, each plays out a little different.

Another good working definition of epigenetics is the dynamic that explains the differences between two genetically identical organisms.

Also note that most of the research is done with strains of mice that are genetically identical. The working assumption is that any differences between individuals is the result of epigenetics.

Epigenetics is part of genetics. Epigenetics is what translates the script into action. Epigenetics is what tells the cells and proteins what, when and how to do.

Epigenetics is busily at work after the egg and sperm are joined. The fertilized egg develops undifferentiated cells. Epigenetics tells cells to become arm cells, neuron cells, liver cells, skin cells and so forth.

Epigenetics turns on genes, turns them off and turns them back on when the time is right.

During all this, DNA (the script) is not replaced, it remains the same. Here, life experiences (of the actors etc) can change the expression of the words.

But this is not an infinitely malleable process. Take the twin studies involving ADHD. Somewhere around 80-90% is directly traceable to the script (genes) but there is also 10-20% variation involved that is probably in some way epigenetic in nature.

This is why identical twins are so identical but not totally so. Same script, different director and actors. This is likely why two people may have the genetic markers for ADHD but only one will exhibit the symptoms enough for a diagnosis.

Epigenetic markers chart the development of the individual but when the sperm and egg are formed, most but not quite all of the markers are wiped clean and the zygote started anew with a clean slate so to speak.

Some epigenetic modifications are passed between parent and offspring by the sperm and the egg. This type of inheritance is pretty rare, but Carrey does report a belief that there must be some epigenetic modifications that are special. She relates that they don't get replaced when the egg and sperm fuse to form the zygote. So, although the vast majority of the mammalian genome does get reset when the egg and the sperm fuse, a small percentage of it is immune from this reprogramming.



There is a lot more to this but I think that this is a reasonable start as I did not want to get to long or complicated trying to touch all bases. Look at this as a quick introduction to the subject and nothing more. I hope it helps understanding of the subject at least a little.


Dizfriz

mildadhd
03-31-14, 07:37 PM
"Epigenesis: This biological principal suggests that individual development arise from gradual, individualized differentiation of each organism,

a process that is now being understood at a genetic level.


While the mammalian genome (successive DNA base pairs) establishes the primal template for body and brain construction (genotype),

a more complex and variable process of gene-expression controls the production of the final organismic forms (phenotype).


It is recognized that these developmentally variable "epigenetic" processes enable differential expressions of the genotype,

allowing environmental control over the final phenotypes.


The biochemistry of epigenetics involves modifications in the degree to which gene expression can be controlled by histone methylation

and related changes of nuclear chromatin, which provide for fine-tuning of patterns and intensities of gene expressions during development,

along with the mechanisms by which gene expressions can be amplified or silenced."





-Panksepp/Biven, "From the Couch to the Lab: Trends in Psychodynamic Neuroscience", (Box 9.1 Definitions) p 146.



i!i

Dizfriz
03-31-14, 08:27 PM
-Panksepp/Biven, "From the Couch to the Lab: Trends in Psychodynamic Neuroscience", (Box 9.1 Definitions) p 146.

What's the point of this?


Dizfriz

mildadhd
03-31-14, 10:01 PM
What's the point of this?


Dizfriz


A definition of epigenesis/epigenetics.

You don't agree?



Peripherals

Dizfriz
03-31-14, 10:30 PM
A definition of epigenesis/epigenetics.

You don't agree?



Peripherals
I gave two definitions of epigenesis, why do we need another? Are you proposing a different way of describing epigenetics than the ones I gave?

Dizfriz

Dizfriz
03-31-14, 10:59 PM
-Panksepp/Biven, "From the Couch to the Lab: Trends in Psychodynamic Neuroscience", (Box 9.1 Definitions) p 146.


I just looked this up. Neither Panksepp nor Biven are listed as authors of the book. The authors listed are Aikaterini Fotopoulou, Donald Pfaff and Martin A. Conway.
http://www.amazon.com/From-Couch-Lab-Psychodynamic-Neuroscience/dp/019960052X

Dizfriz

namazu
03-31-14, 11:15 PM
I just looked this up. Neither Panksepp nor Biven are listed as authors of the book. The authors listed are Aikaterini Fotopoulou, Donald Pfaff and Martin A. Conway.
http://www.amazon.com/From-Couch-Lab-Psychodynamic-Neuroscience/dp/019960052X

You're both partly right -- Fotopoulou, Pfaff, and Conway are the editors of the book, but Panksepp and Biven are the authors of Chapter 9, "A meditation on the affective neuroscience view of human and animalian MindBrains". (If you "search inside the book" on Amazon you can see a snippet of the chapter.)

Dizfriz has presented an explanation of epigenetics in the opening post of the thread, with the intent to help those less familiar with the science understand what it's all about. Peripheral has quoted another explanation of epigenetics from the book chapter referenced above. Let us please keep this discussion narrowly focused on the science of epigenetics, in general and as it relates specifically to ADHD. Please avoid getting personal or straying too far afield from the mechanisms of epigenetics. If you wish to discuss the possible contributions of social/emotional environment on the development of ADHD in this thread, please keep your posts focused on the specific biological mechanisms by which these environmental conditions influence epigenetic processes.

mildadhd
03-31-14, 11:53 PM
You're both partly right-


How ironic! :D

environment (Peripheral) and genetics (Dizfriz) = both right.

1 genetic + 0 = 1 (no change) no relationship

1 environment + 0 = 1 (no change) no relationship

1 environment + 1 genetic = epigenetic

1 + 1 = 2 (change) Relationship

Life is equal to 2.

1 Relationship between 2 (or more).


- Fotopoulou, Pfaff, and Conway are the editors of the book, but Panksepp and Biven are the authors of Chapter 9


I take full responsibility for wrongly labeling Panksepp/Biven as the editors.

My apologies to Fotopoulou, Pfaff, Conway, Biven, Panksepp, and Dizfriz

My mistake was not intentional, and I appreciate the correction.

A extra thanks to Namazu for her quick detective work, and easy to understand explanation.





Peripherals

dvdnvwls
04-01-14, 12:12 AM
How ironic! :D

environment (Peripheral) and genetics (Dizfriz) = both right.

1 genetic + 0 = 1 (no change) no relationship

1 environment + 0 = 1 (no change) no relationship

1 environment + 1 genetic = epigenetic

1 + 1 = 2 (change) Relationship

Life is equal to 2.

1 Relationship between 2 (or more).

I don't believe that any of this is fair to conclude from any evidence. It looks pretty on the screen, but it isn't right.

mildadhd
04-01-14, 01:00 AM
I don't believe that any of this is fair to conclude from any evidence. It looks pretty on the screen, but it isn't right.

That was my simplified view of epigenetics and ADHD.

Epi + genetic

We know what "genetic" is.

What is "epi"?

Originally Posted by Peripheral View Post
How ironic!

environment (Peripheral) and genetics (Dizfriz) = both right.

1 genetic + 0 = 1 (no change) no relationship

1 environment + 0 = 1 (no change) no relationship

1 environment + 1 genetic = epigenetic

1 + 1 = 2 (change) Relationship

Life is equal to 2.

1 Relationship between 2 (or more).


Peripheral

mildadhd
04-01-14, 01:20 AM
I gave two definitions of epigenesis, why do we need another? Are you proposing a different way of describing epigenetics than the ones I gave?

Dizfriz

Dizfriz,

I think you forgot about the "primal template", (lower subcortical genetic instinct, all humans are born with, before experiences occur), that during epigenetic processes, the higher cortical areas implicated in ADHD, are built upon, in your OP.


Example:


"While the mammalian genome (successive DNA base pairs) establishes the primal template for body and brain construction (genotype),

a more complex and variable process of gene-expression controls the production of the final organismic forms (phenotype) (see post # 2 (http://www.addforums.com/forums/showpost.php?p=1632638&postcount=2))




-Panksepp/Biven




Take Care.

Peripherals

Dizfriz
04-01-14, 09:58 AM
How ironic!

environment (Peripheral) and genetics (Dizfriz) = both right.

1 genetic + 0 = 1 (no change) no relationship

1 environment + 0 = 1 (no change) no relationship

1 environment + 1 genetic = epigenetic

1 + 1 = 2 (change) Relationship

Life is equal to 2.

P, some of what I am trying to explain is that the epigenetics is not that simple. The evidence currently is that genetics plays a much larger part in causation of ADHD (80-90%) than environment (10-20%). Where environment plays a larger role is in how the disorder is expressed. Parenting styles, for example, play an important role in how ADHD plays out.

So you are right that the environment plays an important role with ADHD just not as powerful a one as genetics.

When I speak of environment, I am talking about unique individual experiences such as with identical twins. While genetically identical, each twin experiences life is a different way. For twins raised in the same environment these experiences may be very similar, with twins raised in different environments, those experiences are often very different.

The physical and behavioral similarities in the twins especially in the second case can be best explained by genetics while differences probably are best explained by epigenetics.

Keep in mind that epigenetics is a new field and all this is subject to change but this is what the evidence seems to strongly indicate.

So personal experience (environment, epigenetic change) can cause variation in how genetics (DNA) expresses in the phenotype but as I said it is not an infinitely malleable process. It normally can vary the play so to speak but not the script. The effects of epigenetics in this case, while important, can only be a variation of the script. Its effects are real but limited.

I want to think namazu for the update on Panksepp. I was puzzled on this and should have gone deeper. P, I apologize for not doing that.

Also, I want to keep the discussion more or less focused on what I wrote. I am trying to give readers a little background on the subject and to have the thread diverge into a struggle over things that really do not relate is not productive. I am probably as much fault as P and will try to do better.

Dizfriz

Dizfriz
04-01-14, 10:51 AM
OK in all fairness I will address Panksepp's definition of epigensis.

"Epigenesis: This biological principal suggests that individual development arise from gradual, individualized differentiation of each organism, a process that is now being understood at a genetic level.

While the mammalian genome (successive DNA base pairs) establishes the primal template for body and brain construction (genotype), a more complex and variable process of gene-expression controls the production of the final organismic forms (phenotype).

It is recognized that these developmentally variable "epigenetic" processes enable differential expressions of the genotype, allowing environmental control over the final phenotypes.

The biochemistry of epigenetics involves modifications in the degree to which gene expression can be controlled by histone methylation and related changes of nuclear chromatin, which provide for fine-tuning of patterns and intensities of gene expressions during development, along with the mechanisms by which gene expressions can be amplified or silenced." While this is a good description, I do not see very much difference in what I said and this and I felt mine said the same thing and was a lot shorter, simpler and more relevant to ADHD.

Note that he is talking about "fine-tuning" of gene expression and not major changes.

I did not see the need for another description of epigenesis unless there is a point to be made or that it showed a differing opinion or viewpoint. If this is the case, please explain it and we can discuss it. If I was too short then I apologize.


As a quick add on, it was asked "What is "epi"? In the context of the thread, it means the study of mitotically (http://en.wikipedia.org/wiki/Mitosis) and/or meiotically (http://en.wikipedia.org/wiki/Meiosis) heritable changes in gene function that cannot be explained by changes in DNA sequence."[19] (http://en.wikipedia.org/wiki/Epigenetics#cite_note-isbn0-87969-490-4-19) The Greek prefix epi- in epigenetics implies features that are "on top of" or "in addition to" genetics; thus epigenetic traits exist on top of or in addition to the traditional molecular basis for inheritance.http://en.wikipedia.org/wiki/Epigenetics

In simpler words, it simply means the processes that operate "on top" of DNA genetics. Epigenetic markers or methylation(no need to go into that in this context) that change or alter the expression of genes without changing DNA itself.

Hope this helps a little on that.


Dizfriz

namazu
04-01-14, 11:36 AM
Dizfriz,

I think you forgot about the "primal template", (lower subcortical genetic instinct, all humans are born with, before experiences occur), that during epigenetic processes, the higher cortical areas implicated in ADHD, are built upon, in your OP.

Actually, I think that "primal template" is exactly what Dizfriz is describing as the genetic "script" upon which epigenetic processes can operate.

It is not limited to the lower subcortex, but encompasses all DNA-based instructions for "body and brain construction (genotype)", as Panksepp and Biven stated.

mildadhd
04-01-14, 01:17 PM
Actually, I think that "primal template" is exactly what Dizfriz is describing as the genetic "script" upon which epigenetic processes can operate.

It is not limited to the lower subcortex, but encompasses all DNA-based instructions for "body and brain construction (genotype)", as Panksepp and Biven stated.



At birth, the lower subcortical emotional "primal template" brain areas are more mature, than the higher cortex "primal template".

The lower affective subcortical genetic instincts, fine tune the higher cognitive cortex genetic instincts, with experience.

Primal crying mechanisms precedes attention and inhibition. Attention and inhition are fine tuned on top of the primal genetic emotional instinct.

At birth, we move(primary motor), breath (primary homeostasis), touch(primary sensory), cry (emotion primary)...Focusing on the brain development.

On top of that, the mechanisms for attention and self regulation are developed fine tuned.

The instinctual primal emotions (genetic) experienced at birth, are not regulated yet.


At birth,

Higher self regulation systems, implicated in ADHD, are fine-tuned, on top of, "crying" systems (7 primal emotion).

Ground up development, before the age of 1-4, is dominated by primal emotion (affective consciousness.)

After the age of 4-6, til adulthood the higher self regulation, (cognitive consciousness.)

Super duper simplified. (to keep things simplified, I left out important prenatal topics for later discussion).

I disagree with Dizfriz's statistics, but will leave that disagreement, for a different thread.



Peripherals

Dizfriz
04-01-14, 01:43 PM
At birth, the lower subcortical emotional brain areas are more mature, than the higher cortex.

The lower affective subcortical genetic instincts, fine tune the higher cognitive cortex genetic instincts, with experience.

Crying precedes attention and inhibition.

At birth, we move(primary motor), breath (primary homeostasis), touch(primary sensory), cry (emotion)...Focusing on the brain development.

On top of that, the mechanisms for attention and self regulation are developed fine tuned.

The instinctual primal emotions (genetic) experienced at birth, are not regulated yet.


At birth,

Higher self regulation systems, implicated in ADHD, are fine-tuned, on top of, "crying" systems (7 primal emotion).

Ground up development, before the age of 1-4, is dominated by primal emotion (affective consciousness.)

After the age of 4-6, til adulthood the higher self regulation, (cognitive consciousness.)

Super duper simplified. (to keep things simplified, I left out important prenatal topics for later discussion).

I disagree with Dizfriz's statistics, but will leave that disagreement, for a different thread.



Peripherals

Could you tie this into the OP and the subject under discussion which is the mechanics of epigenetics and how they specifically relate to ADHD?

If you want to get into more general developmental issues, perhaps another thread might be better. The purpose of this thread was to help general readers understand a little more about epigenetics and that is all so can we keep it there?

Dizfriz

mildadhd
04-01-14, 02:13 PM
ADHD also has a window of opportunity and vulnerability.

When brain development is most affected by the environment.

Before the age of 4-10.

Peaking at Age 1 with a slight decline to the age 4-10, is when impaired areas of brain implicated in ADHD, are the most influenced by environment.

During the early period of affective consciousness dominance. (before four)

Specifying what age of epigenetic processes occur, is very relevant to the definition and ADHD.


4. Windows of opportunity/windows of vulnerability: The sequential development of the brain and the activity-dependence of many key aspects of

neurodevelopment suggest that there must be times during development when a given developing neural system is more sensitive to experience than others.

In healthy development, that sensitivity allows the brain to rapidly and efficiently organize in response to the unique demands of a given environment to express

from its broad genetic potential those characteristics which best fit that child’s world.

If the child speaks Japanese as opposed to English, for example, or if this child will live in the plains of Africa or the tundra of the Yukon, different genes can be

expressed, different neural networks can be organized from that child’s potential to best fit that family culture and environment.

We all are aware of how rapidly young children can learn language, develop new behaviors and master new tasks.

The very same neurodevelopmental sensitivity that allows amazing developmental advances in response to predictable, nurturing, repetitive and enriching

experiences make the developing child vulnerable to adverse experiences

Sensitive periods are different for each brain area and neural system and therefore, for different functions.

The sequential development of the brain and the sequential unfolding of the genetic map for development mean that the sensitive periods for neural system

(and the functions they mediate) will be when that system is in the developmental ‘hot zone’ – when that area is most actively organizing.

The brainstem must organize key systems by birth; therefore, the sensitive period for those brainstem-mediated functions is during the prenatal period.

The neocortex, in contrast, has systems and functions organizing throughout childhood and into adult life.

The sensitive periods for these cortically mediated functions are likely to be very long.


The simple and unavoidable conclusion of these neurodevelopmental principles is that the organizing, sensitive brain of an infant or young child is more

malleable to experience than a mature brain.

While experience may alter the behavior of an adult, experience literally provides the organizing framework for an infant and child.

Because the brain is most plastic (receptive to environmental input) in early childhood, the child is most vulnerable to variance of experience during this time.


http://centerforchildwelfare2.fmhi.usf.edu/kb/chronicneglect/childexperience.pdf


i!i

Lunacie
04-01-14, 02:35 PM
Thank you Dizfriz. The comparison to the written script and the interpretation by the director and actors is very helpful to me.

The script does not change at any age, but the way it is acted out may change.

Either we are born with the script (genes) that describe ADHD or a different script that is not ADHD.

If the script is about ADHD, the director and actors may change the way the ADHD is presented.

If the script is not about ADHD, it doesn't matter what the director and actors do, it still won't be about ADHD.

sarek
04-01-14, 03:17 PM
Peaking at Age 1 with a slight decline to the age 4-10, is when impaired areas of brain implicated in ADHD, are the most influenced by environment.

During the early period of affective consciousness dominance. (before four)

Specifying what age of epigenetic processes occur, is very relevant to the definition and ADHD.



Are you asserting epigenetic processes are at work in the brain at ages 4 and over?

Lunacie
04-01-14, 03:44 PM
Are you asserting epigenetic processes are at work in the brain at ages 4 and over?

If I may answer the question ...?

Yes, the epigenetic process is at work past the age of 4, however it does not change the basic DNA/genes, it only signals them to be active or inactive.

This seems to fit in with Dizfriz's explanation:

Tightly associated with the genome, the epigenome represents an ensemble of biochemical marks present on the DNA itself. These marks modulate the DNA’s activity and functions, but occur without any change in the DNA sequence. Instead, various enzymes add epigenetic marks to the DNA. The marks stamp genes with a unique signature that signals the gene to be active or silent.

Unlike the DNA sequence, epigenetic processes are dynamic and not fixed, although some can persist for long periods of time, up to several years or a lifetime -

See more at: http://dana.org/Cerebrum/Default.aspx?id=39461#sthash.2XMq2S3d.dpuf

mildadhd
04-01-14, 04:04 PM
Are you asserting epigenetic processes are at work in the brain at ages 4 and over?

Yes, but mostly before the age of 4, in regards to dramatic rate and areas of brain development specifically impaired in ADHD.

Example

The critical period of neural brain development, related to ADHD mechanisms, when "automatic set points" are established and fine tuned by epigenetic process,

is around age 1-4.

(attention mechanisms are one example , but not the only mechanisms involved in ADHD, I'm leaving out other mechansims and prenatal topics out of the discussion,

for simplification, but the concept is the similar.)

Specifics would depend on the brain area being discussed. ( age,environment and predispositon, etc, give or take)

When a sensitive infant is distressed, perceived or real, fine tuning of attention mechanisms, may be interrupted over a period of time, development becomes stuck,

as the rate of development declines. (after the specific critical period of development)

Not because plastisticity is impossible, but because the rate of development and sensitivity to environmental influences that affect development are less.

ADHD Symptoms may not be obvious til about 7-10.

Partly because all people have underdeveloped attention mechanisms/function during early infancy/childhood.

Also some hyperactive children are not ADHD, but can take a little longer to develop, than there peers.






Peripherals

mildadhd
04-01-14, 04:31 PM
"..it only signals them to be active or inactive".. (Lunacie)



active = ADHD

inactive = no ADHD


Peripherals

Lunacie
04-01-14, 04:45 PM
active = ADHD

inactive = no ADHD


Peripherals

I disagree.

In the link I posted, it is said that "Unlike the DNA sequence, epigenetic processes are dynamic and not fixed."

That means that the genes (the script) are not dynamic, they are fixed and do not change.

Epigenetics can make the ADHD active or inactive, but they do not have anything to do with "writing the script."

mildadhd
04-01-14, 05:06 PM
I disagree.

In the link I posted, it is said that "Unlike the DNA sequence, epigenetic processes are dynamic and not fixed."

That means that the genes (the script) are not dynamic, they are fixed and do not change.

Epigenetics can make the ADHD active or inactive, but they do not have anything to do with "writing the script."


The script is genetic.

This thread is about epigenetics.

Environment and genes, not just only genes.

Example

DRD4 is a gene variant.

DRD4 variants tend to be more susceptible to environmental influences, whereas other variants are less susceptible

http://www.ncbi.nlm.nih.gov/gene/1815


The variants can be passed from generation to the next, but the environment, at least partly has an influence on which variants become active or inactive.

I am interested in any protective factor(s) in the environment (internal or/and external) involved on top of genetics.) Epigenetics

Peripherals

mildadhd
04-01-14, 05:28 PM
Some people do have more gene variant combinations, associated with ADHD, that mathematically make the person more likely to have ADHD.

But that doesn't negate any protective factors that may be present in the environment.

If I remember correctly, less than a third of ADHDers actually have any known genetic variants, associated with ADHD?

I am not disputing any know genetic factors, I just don't think there is enough biological evidence, to back up more than a 50:50 environment and genetic = epigenetic causation, at this point in history.







Peripherals

ginniebean
04-01-14, 05:47 PM
Thank you dizfriz, that was very helpful.

Dizfriz
04-01-14, 06:02 PM
Are you asserting epigenetic processes are at work in the brain at ages 4 and over?
Just to touch base on this. As I understand it some areas of the genome are susceptible to epigenetic changes throughout life and some are fixed at conception or shortly after.

If you are interested, I could do a little digging. Let me know.

Dizfriz

Dizfriz
04-01-14, 06:07 PM
active = ADHD

inactive = no ADHD

We do not know nearly enough about epigenetics and ADHD to make anywhere near this kind of statement. What you are presenting is simply unsupported conjecture. Right now we do not know the genes involved except for a few much less the epigenetic effects of those.

The Carey book is quite good if you want to do some relevant reading on the subject. I might suggest that. You can probably pick it up at your library.

Dizfriz

Dizfriz
04-01-14, 06:12 PM
ADHD also has a window of opportunity and vulnerability.

When brain development is most affected by the environment.

Before the age of 4-10.

Peaking at Age 1 with a slight decline to the age 4-10, is when impaired areas of brain implicated in ADHD, are the most influenced by environment.

During the early period of affective consciousness dominance. (before four)

Specifying what age of epigenetic processes occur, is very relevant to the definition and ADHD.


http://centerforchildwelfare2.fmhi.usf.edu/kb/chronicneglect/childexperience.pdf


I looked at the article and it had nothing to say about ADHD. Can we keep this on topic.

Dizfriz

Dizfriz
04-01-14, 06:16 PM
I am interested in any protective factor(s) in the environment (internal or/and external) involved on top of genetics.) Epigenetics

Wouldn't that be better on another thread? Protective factors are not a topic under discussion here. We need to stay on task.


Dizfriz

Dizfriz
04-01-14, 06:21 PM
I am not disputing any know genetic factors, I just don't think there is enough biological evidence, to back up more than a 50:50 environment and genetic = epigenetic causation, at this point in history.

I do not think you have the evidence to back this up but if you feel you do, I would be very interested in seeing it. Again, this would probably be better on another thread since this one is about how epigenetics works although it is on topic enough it could fit in at least to some degree.

Dizfriz

daveddd
04-01-14, 06:30 PM
if someone where to develop, say ptsd

at age 12-13

would that be epigenics

i think its pretty conclusive a predisposition is required for it?

Dizfriz
04-01-14, 06:55 PM
if someone where to develop, say ptsd

at age 12-13

would that be epigenics

i think its pretty conclusive a predisposition is required for it?

You are getting past my knowledge but on a quick bit of research it would seem to be likely. I have not kept up with this and at first blush I would have said that genetic predisposition would not be found to any real degree but apparently this is a real possibility.

In this case, it would very likely to be a case of epigenetic involvement but I don't have the knowledge to say. My knowledge and understanding of epigenetics is on a pretty basic but hopefully reasonably accurate level.


Dizfriz

daveddd
04-01-14, 07:10 PM
yea adhd might even be the predisposition
http://www.ncbi.nlm.nih.gov/pubmed/23561240

i know nothing about epigenetics

that was just an example

Dizfriz
04-01-14, 07:22 PM
yea adhd might even be the predisposition
http://www.ncbi.nlm.nih.gov/pubmed/23561240

i know nothing about epigenetics

that was just an example
Thanks for the cite.

I have long suspected that ADHD was part of a genetically connected cluster of disorders. These might include bipolar, Tourette's, autism, now PTSD and possibly several others with epigenetics very probably involved in some way. There have been some intriguing hints at this but, as far as I know, nothing beyond that.

Good point, thanks.

Dizfriz

daveddd
04-01-14, 07:38 PM
Thanks for the cite.

I have long suspected that ADHD was part of a genetically connected cluster of disorders. These might include bipolar, Tourette's, autism, now PTSD and possibly several others with epigenetics very probably involved in some way. There have been some intriguing hints at this but, as far as I know, nothing beyond that.

Good point, thanks.

Dizfriz

yea it was more of a question

i didn't know if there was a cut off age for epigenics or something

Dizfriz
04-01-14, 08:25 PM
yea it was more of a question

i didn't know if there was a cut off age for epigenics or something
Sarek asked a simular question. I felt I knew the answer but wanted to check it out to be sure. Epigenetic processes are ongoing throughout the life span.

The thing to consider is that pretty much all that involve changes in our body is a result of epigenetics. Every time a new neuronal circuit is developed due to experience and learning, for example, epigenetics is involved.

The top layer of skin cells, (the epidermis) is replaced about every five weeks from constantly dividing stem cells in the deeper layers of that tissue. These stem cells always produce new skin cells, and not, for example, muscle cells. It is epigenetics that controls this. Epigenetics instructs the undifferentiated cell to become a skin cell. From this, I think you can see that the epigenetic process goes on throughout the life span.

A person's genetics sets the script and epigenetics sets it into motion so to speak and that process never stops in one form or another as long as the play is running.

Hope this helps.

Dizfriz

Amtram
04-01-14, 08:26 PM
If you want to get an example of epigenetics that we all see, and most of us (fortunately) get to experience, let's look at puberty.

Each change in our bodies that takes place during our journey to sexual maturity is an example of epigenetics at work. The instructions for our adult bodies' characteristics are encoded in our DNA, and the process that changes all our cells from childhood to adolescence to adulthood is epigenetics. This is not a process that's driven by environment - it's a process that's in our genetic destiny, but our epigenome kick starts it.

The fact that various environmental factors *may* change gene expression in no way implies that epigenetics *is* the interaction between genes and environment. Amy Lossie, who is a postdoc studying epigenetics, provided this explanation on Quora:

You have billions of cells in your body. Each of those cells has, for the most part, the identical DNA sequence. If you were to read the DNA in your cells like a very long book, the words would be in the exact same order in every cell. Why then, does your liver tell a different story from your heart, from your skin? How can that be?

The answer is that just like in books, your cell has punctuation that it uses to interpret your DNA. For example:

"Let's eat Grandma!" has a very different meaning than, "Let's eat, Grandma."

There are about 40 different types of epigenetic punctuation marks. The combinations of these marks is different in the books of DNA that make up your liver compared to the books that make up your skin, your heart.

These different combinations of punctuation marks allow your cells to tell the story that is specific to each cell, and ensures that your brain is not telling the liver's story.

And Cath Ennis, who did postdoctoral research on human genome evolution, in a different section of Quora, tried to put it in layman's terms like this:


If you consider your DNA as the text of an instruction manual that explains how to make a human body, epigenetics is as if someone's taken a pack of highlighters and used different colours to mark up different parts of the text in different ways. For example, someone might use a pink highlighter to mark parts of the text that need to be read the most carefully, and a blue highlighter to mark parts that aren't as important.

There are different types of epigenetic "marks", the same way there are different coloured highlighters, and each mark tells the proteins in the cell to process those parts of the DNA in certain ways. For example, DNA can be "tagged" with tiny molecules called methyl groups that stick to some of its letters. There are proteins in the cell that specifically seek out and bind to methylated DNA, and shut it down so that the genes in that region don't get expressed. So DNA methylation is a like a blue highlighter telling the cell "you don't need to know about this section right now".

In contrast, there are some epigenetic marks that actually affect the proteins (called histones) that DNA wraps itself around, rather than the DNA itself. Different molecular "tags" can stick onto different locations on the histone proteins, each one having a different effect. Some tags in some locations loosen the attachment between the DNA and the histone, making it more accessible to the proteins that are responsible for activating the genes in that region; this is like a pink highlighter telling the cell "hey, this part's important". Other tags in other locations do the opposite, or attract other proteins with other specific functions.

So, even though every cell in the body has the same basic DNA, the text has different patterns of highlighting in different types of cell - a liver cell doesn't need to follow the same parts of the instruction manual as a brain cell. And when the DNA is copied, some of the highlighting also gets copied - just like in a photocopier.

Dizfriz
04-01-14, 08:34 PM
Amtram, nice explanation.

Dizfriz

tazoz
04-29-14, 07:25 PM
Moderator note:

Please keep all scientific discussion of newly published or old material concerning Epigenetics to this thread. All other threads that deal with Epigenetics will be closed and new threads will be merged with this thread.

This is only relevant with relation to threads posted in this subsection (The Scientific iscussion section)

Thank you

mildadhd
04-29-14, 10:28 PM
The effect of changing air pressure on growing vegetation, is the simplest example an epigenetic relationship, that I can think of.

Epigenetics (epigenesis) is a multi-layered spectrum of internal and external biological relationships, occurring between environments and genes.

I am interested in learning about social emotional environments, that may promote the genetic expression of PLAY instincts.



P

mildadhd
04-29-14, 11:37 PM
That example doesn't fit the explanation Amtram posted above.

I was referring to a previous thread.

See thread, High pressure influences on gene and protein expression
(http://www.addforums.com/forums/showthread.php?p=1639693#post1639693)

SUMMARY

Elevated hydrostatic pressure can influence gene and protein expression in both 1 atmosphere-adapted and high pressure-adapted microorganisms.

Here we review experiments documenting these effects and describe their significance towards under-standing the molecular bases of life in deep-sea high pressure environment~

http://bartlettlab.ucsd.edu/Publications_files/Bartlett1995.pdf





The choices of atmospheric pressure within spaceflight and extraterrestrial habitats are not merely engineering considerations but are biological

considerations of the highest order, and modern molecular tools can be employed to increase understanding of the biological consequences of pressure

engineering decisions.

http://gravitationalandspacebiology.org/index.php/journal/article/viewFile/1/1




P

SB_UK
04-30-14, 03:44 AM
Saw this yesterday !
http://www.nhs.uk/news/2013/02February/Pages/altitude-elevation-obesity-weight-BMI-link.aspx

Generally we think of people who can exercise at altitude as being fitter - more aerobically fit.

Surely the point is to aspire towards as high a level of aerobic fitness as possible.

Is life at high altitude related to epigenetic changes ?
http://www.scienceofrunning.com/2011/12/altitude-babies-rats-and-epigenetics.html
A study in the Journal of Applied Physiology was recently published that took a bunch of rats that were at high altitude in Bolivia and made a group of them live in a simulated sea level environment. So you basically had an altitude group and a sea level group, but it was only from 1 day before birth to 15 days after birth when they were in these two different environments. Then they were brought together and lived their normal rat lives together. Well, they checked them periodically through their life and ultimately at 600 days post birth.
What is interesting is that those 16 days during development affected parameters for the rest of their lives. For example, the “normoxia/oxygen” group had lower hemoglobin and hematocrit for the rest of their lives. They also had “reduced right ventricular hypertrophy (both sexes); lower air space-to-tissue ratio in the lungs (males only); reduced CO2 production rate, but higher oxygen uptake (males only);”

But yet again - the overwhelming message is that epigenetics senses stress (including low oxygen availability) and changes 'us' the only way it knows how - to make us into more efficient aerobic organisms.

So - this works through low food availability, low oxygen availability ... ... ...

Looks like the global goal of epigenetic modification is in line with the Thrifty gene ie to make an organism which can survive on less.

Which isn't ideal in a world of boredom, plentiful comfort 'food' and Xbox.

Amtram
04-30-14, 08:49 AM
I was referring to a previous thread.

See thread, [URL="http://www.addforums.com/forums/showthread.php?p=1639693#post1639693"]High pressure influences on gene and protein expression


What you are referring to is not epigenetics that is in any way relevant to the normal processes that affect humans in daily life. That's the problem. It is unlikely that any of us will experience epigenetic changes from space travel.

The locations on our DNA that can be epigenetically changed are limited. The effects of those changes may be completely inconsequential, affecting only a few cells at a time and producing no noticeable change beyond the molecular level. The majority of epigenetics is predetermined by our DNA and is highly stable.

Where can we see epigenetic changes? On unmethylated cytosine-guanine pairs that are outside of promoter regions of the DNA. What are the most common epigenetic changes in humans? Puberty. Ageing. Cancer.

Why? Because epigenetics is how cells clone themselves prior to apoptosis (cellular "suicide.") Changing the epigenetic instructions that have been built into the DNA, and transcribed into the RNA for the purposes of creating the proteins necessary for cells to grow a new nucleus and split results in *defective* cells. Rather than being a "magic bullet" to turn you into superman, it's more likely to mess you up if it does anything.

SB_UK
05-01-14, 05:25 AM
Here's a simple epigenetic mechanism which could explain the emergence of ADHD, apparent high heritability of human diseases ... ...

To be explained in more detail if required.

During the process of development/growth, stress produces histone modifications which just happen to be on whichever viral-derived cellular growth factor (ie c-src from v-src) that happens to be functional when 'stress' (cortisol) is applied.
We know that cortisol operates through histone modification.
We know that cortisol is anti-growth/anti-proliferation.
We know that HDAC inhibitors are anti-growth/proliferation.
We know that cortisol is anti-viral.

If these histone modifications are retained (ie anti-growth processes) - which they will be ie strongly selected because of the increased survival fitness of an organism with physiology that requires less energy - then we'll observe a form of heritability of conditions which either reflects the usage of that particular gene in development or subsequently - when it's re-used later in life.

So - we've a method of stress-based selection of low energy requiring genomes, with a form of 'memory' built in - because it's the stress suffered at defined points in life which will be inherited via the histome.

So - the presumed pattern 'd be something like - upon completing silencing of these 'exuberant' viral derived genes - that a new more energy efficient organism (aerobic) 'd pop into existence.

ADDers - the thrifty histome.

-*-

So the saying is that 'what doesn't kill you makes you stronger' - thinking that what has happened is survival through stress (most notably lack of food availability) simply inhibits all viral derived growth processes encoded within the human genome - whereby the trend is towards generating a perfectly aerobic organism - a more efficient organism
- but everything goes wrong when efficient organisms are fed glucose fluctuating foods.

Psychological stress is an added difficulty for us to factor in - because how would the psychological stress alter this system.
This entire system is more optimised for physical stress - when psychological stress enters the fray, are we simply going to see an acceleration in the level of these processes occurring ie mother, child, kid, adult under constant chronic stress resulting in rapid histome modification/emergence of ADDer type ... ... or make things generally worse for us.

The conclusion though that's returned appears to be to live life in a very low psych DIstress, very low physical DIstress, very high psych EUstress, very high physical EUstress environment.

Where that appears to be to permit the individual


perfectly moral operation (eliminating psych DISTRESS),
an organic vegan low GI diet (eliminating physical DISTRESS from reactive hypoglycaemic episodes to glucose spikes),
to allow the individual to invest themselves in mental pursuits which the individual finds personally rewarding (hobbies - very high psych EUstress as the individual strives to better him/her self),
hitting the wall training to stabilze blood glucose levels (very high physical EUstress environment).

We need to operate at a level which increases aerobic fitness whilst keeping blood glucose levels stable within a moral framework.



So - cheating with high GI sugar water supplements isn't to be encouraged.

-*-


The point is that ADD reflects a 'good thing' which goes badly wrong in a psychologically and physically DIstressful environment, which do not permit psych. and physically EUstressful behaviours.
Underneath it all - we've simply selection for an organism with lowest growth rates - which is good - because our cells only have a certain number of replications in them before they fail through telomere shortening.
However - feed a 'low energy' requiring organism high energy - and I think what we observe is over-exuberant growth (compared to nonADDers) resulting in massively increased susceptibility to diseases of ageing (cancer etc).

SB_UK
05-01-14, 06:07 AM
The basic point is that epigenetics will appear to produce all manner of really unpleasant effects ie cancer, ageing
- but none of that's the complete truth.

It's a more efficient metabolism which goes horribly horribly (premature cancer/ageing) awry if rock steady blood glucose levels aren't maintained.

Lunacie
05-01-14, 12:51 PM
What you are referring to is not epigenetics that is in any way relevant to the normal processes that affect humans in daily life. That's the problem. It is unlikely that any of us will experience epigenetic changes from space travel.

The locations on our DNA that can be epigenetically changed are limited. The effects of those changes may be completely inconsequential, affecting only a few cells at a time and producing no noticeable change beyond the molecular level. The majority of epigenetics is predetermined by our DNA and is highly stable.

Where can we see epigenetic changes? On unmethylated cytosine-guanine pairs that are outside of promoter regions of the DNA. What are the most common epigenetic changes in humans? Puberty. Ageing. Cancer.

Why? Because epigenetics is how cells clone themselves prior to apoptosis (cellular "suicide.") Changing the epigenetic instructions that have been built into the DNA, and transcribed into the RNA for the purposes of creating the proteins necessary for cells to grow a new nucleus and split results in *defective* cells. Rather than being a "magic bullet" to turn you into superman, it's more likely to mess you up if it does anything.

And environment can work in tandem with epigenetics?
For example, girls are beginning puberty at an earlier age because of changes in diet.

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?

Dizfriz
05-01-14, 02:35 PM
And environment can work in tandem with epigenetics?
For example, girls are beginning puberty at an earlier age because of changes in diet.

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 you may be correct but I do not know for sure. There is so much we don't know about epigenetics yet. This is all so new, we did not get a good working definition of the term until 2008 so it can be seen just how new it is.

Anyway, interesting question and I suspect you may be correct but don't ask me to back it up.

Dizfriz

Dizfriz
05-01-14, 02:42 PM
The thing about epigenetics that I don't think some realize, it is not infinitely plastic. It is not some magic wand one can wave to make all things possible. It is restricted as to what it can do. It cannot change the DNA script of the organism, it can only modify its expression to some limited degree.

I keep emphasizing that we don't know a lot bout epigenetics yet, it is far too new to be able to say much definitively.

Consider that most of the research has been done with mice. The reason is that strains of mice can be developed in which each individual has the same genetics as any other individual in the strain. Because of this, much of what we know about epigenetics is limited to mice.

From that specific mechanisms can be explored discounting different DNA. It is one variable that doesn't have to be taken into account which makes research into epigenetics easier. With these mice, you can hypothesize that any differences between individuals is due to epigenetics and not DNA

New findings on the subject are coming in all the time but there is a danger of trying to take it far past what can be supported or applying it where the research is not available. Epigenetics of plants under pressure, for example, does not apply to humans nor especially to ADHD humans.

Just a word of caution, unsupported conjecture is not very useful nor helpful in a support setting.

Dizfriz

SB_UK
05-01-14, 03:35 PM
Thing about cortisol - is why does a small non-descript hormone from the centre of the body which just tries to ensure that we've a stable blood glucose - also appear to stop growth/proliferation.
The grand change in biology was from glycolysis to mitochondrial respiration.
It's very clear that mitochondrial respiration is favoured over glycolysis for generating energy.
It's shown that cancer cells acquire their energy (Warburg effect) via glycolysis and so relegating it into the background would appear to be a great idea.
So - we've:
glucose - glycolysis - viral growth - cellular growth (virus grows best in fast dividing cells)
= proliferative
vs
cortisol - ketone - mitochondrial aerobic respiration
= anti-proliferative

Return to the previous comment of we've only a certain number of cell divisions in us before our telomeres shorten beyond repair.

A low energy state would definitely select.

However - a stable blood glucose is absolutely required - ensured in ketogenic metabolism since blood glucose is spared for all but the rbc/liver ?

Let's hear it for interval training on the gourmet raw vegan diet in a fair global society (no money), where people can choose their speciality based on personal interest/personal reward acquired.

mildadhd
05-01-14, 03:41 PM
Here is a link interesting link about ADHD and some possibly related types of epigenetic processes.

I got to run, I have other links related to the OP topic that I want to discuss and present in the future.

Thought I would post this now to give other members interested a chance to read the material and to help guide the discussion about ADHD and epigenetic processes.

P



Interestingly, like the other examples discussed above, these epigenetic changes only occur during a specific critical period --in this case immediately after birth.


Pre- and peri-natal environmental risks for attention-deficit hyperactivity disorder (ADHD): the potential role of epigenetic processes in mediating susceptibility (http://epigenomicslab.com/Publications/2008%20-%20Pre-%20and%20peri-natal%20environmental%20risks%20for%20attention-deficit%20hyperactivity%20disorder%20(ADHD)%20the% 20potential%20role%20of%20epigenetic%20processes%2 0in%20mediating%20susceptibility.pdf)




P

SB_UK
05-01-14, 03:59 PM
- then we'll observe a form of heritability of conditions which either reflects the usage of that particular gene in development or subsequently - when it's re-used later in life.

- from above is meant to mean this

Peripheral's paper
These observations concur with the DOHaD
hypothesis, increasingly supported in relation to
chronic metabolic disorders such as diabetes and
coronary heart disease, which postulates that the
environment during various critical developmental
periods is crucial in determining the onset of dis-
eases later in life.

Dizfriz
05-01-14, 04:32 PM
Here is a link interesting link about ADHD and some possibly related types of epigenetic processes.

I got to run, I have other links related to the OP topic that I want to discuss and present in the future.

Thought I would post this now to give other members interested a chance to read the material and to help guide the discussion about ADHD and epigenetic processes.

P

In your own words, what do you think the article is saying? What is its importance? Can you summarize that the authors are trying to accomplish in the article?

Just posting a study without comment is not all that useful in this context. What about the study makes it worth taking the time to look at?

Dizfriz

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.

daveddd
05-01-14, 09:06 PM
i see where they are going towards epigenetics and adhd


can you expand on it?

i think I'm misunderstanding, it seems they say environment can effect epigenetic

http://books.google.com/books?id=SfswPYqNJOIC&pg=PA2071&dq=adhd+epigenetic+nigg&hl=en&sa=X&ei=j-5iU_2YK8bqoATptYKYAw&ved=0CE8Q6AEwBA#v=onepage&q=adhd%20epigenetic%20nigg&f=false

Amtram
05-01-14, 09:34 PM
Yes, environment can affect epigenetics, but only under some very limited circumstances. There's a lot of potential for influencing epigenetics way, way, way in the future, but right now the research is more along the lines of learning how it works and seeing what ways it can be altered, mostly with insects, but sometimes with rodents.

As I had mentioned, I have three posts on my blog on simplified epigenetics that have been praised by people who actually do epigenetic research. I'm also working on several papers they suggested trying to "translate them into English," with their support and guidance. It's a slow go because I've been away from home caring for my parents, but what it's teaching me is that what epigenetics does primarily is exactly what the DNA tells it to do, and that even changing methylation does not produce miracles, because it usually happens on genetic sites that don't code for much.

Where gene expression is strongly determined by the DNA, you can't really change the methylation without destroying the organism. So far. Again, in the distant future when we know everything and can work miracles, that may change.

daveddd
05-01-14, 09:41 PM
is mental illness one of the limited circumstances which environment can effect epigenetics?

daveddd
05-01-14, 09:54 PM
Here's a simple epigenetic mechanism which could explain the emergence of ADHD, apparent high heritability of human diseases ... ...

To be explained in more detail if required.

During the process of development/growth, stress produces histone modifications which just happen to be on whichever viral-derived cellular growth factor (ie c-src from v-src) that happens to be functional when 'stress' (cortisol) is applied.
We know that cortisol operates through histone modification.
We know that cortisol is anti-growth/anti-proliferation.
We know that HDAC inhibitors are anti-growth/proliferation.
We know that cortisol is anti-viral.

If these histone modifications are retained (ie anti-growth processes) - which they will be ie strongly selected because of the increased survival fitness of an organism with physiology that requires less energy - then we'll observe a form of heritability of conditions which either reflects the usage of that particular gene in development or subsequently - when it's re-used later in life.

So - we've a method of stress-based selection of low energy requiring genomes, with a form of 'memory' built in - because it's the stress suffered at defined points in life which will be inherited via the histome.

So - the presumed pattern 'd be something like - upon completing silencing of these 'exuberant' viral derived genes - that a new more energy efficient organism (aerobic) 'd pop into existence.

ADDers - the thrifty histome.

-*-

So the saying is that 'what doesn't kill you makes you stronger' - thinking that what has happened is survival through stress (most notably lack of food availability) simply inhibits all viral derived growth processes encoded within the human genome - whereby the trend is towards generating a perfectly aerobic organism - a more efficient organism
- but everything goes wrong when efficient organisms are fed glucose fluctuating foods.

Psychological stress is an added difficulty for us to factor in - because how would the psychological stress alter this system.
This entire system is more optimised for physical stress - when psychological stress enters the fray, are we simply going to see an acceleration in the level of these processes occurring ie mother, child, kid, adult under constant chronic stress resulting in rapid histome modification/emergence of ADDer type ... ... or make things generally worse for us.

The conclusion though that's returned appears to be to live life in a very low psych DIstress, very low physical DIstress, very high psych EUstress, very high physical EUstress environment.

Where that appears to be to permit the individual


perfectly moral operation (eliminating psych DISTRESS),
an organic vegan low GI diet (eliminating physical DISTRESS from reactive hypoglycaemic episodes to glucose spikes),
to allow the individual to invest themselves in mental pursuits which the individual finds personally rewarding (hobbies - very high psych EUstress as the individual strives to better him/her self),
hitting the wall training to stabilze blood glucose levels (very high physical EUstress environment).

We need to operate at a level which increases aerobic fitness whilst keeping blood glucose levels stable within a moral framework.



So - cheating with high GI sugar water supplements isn't to be encouraged.

-*-


The point is that ADD reflects a 'good thing' which goes badly wrong in a psychologically and physically DIstressful environment, which do not permit psych. and physically EUstressful behaviours.
Underneath it all - we've simply selection for an organism with lowest growth rates - which is good - because our cells only have a certain number of replications in them before they fail through telomere shortening.
However - feed a 'low energy' requiring organism high energy - and I think what we observe is over-exuberant growth (compared to nonADDers) resulting in massively increased susceptibility to diseases of ageing (cancer etc).

you're actually a scientist right SB?

because this seems really accurate

http://books.google.com/books?id=MxOH7VPpGzwC&pg=PA529&dq=a+study+by+uddin+and+colleagues&hl=en&sa=X&ei=svxiU7LwO43voAS8q4CYDg&ved=0CDUQ6AEwAQ#v=onepage&q=a%20study%20by%20uddin%20and%20colleagues&f=false

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.

Amtram
05-02-14, 08:15 AM
*sigh* daveddd, many people cherry-pick science looking only for pieces of information which, taken out of context, support their own agendas. There are many chemicals that can cause methylation or acetylization, but they don't have a universal effect, and they don't work on all nucleotides in DNA, and they most certainly don't automatically cause an improvement in health or prevent a negative outcome or produce any of these inevitable results that are being stated as definitive.

You can't take results from in-vitro, single-cell studies and assume they operate the same way in a living creature. In a petri dish, water kills all cancer, for example. For the same reason, the things glucose or cortisol or whatever the chemical of the day is said to do in laboratory conditions does not automatically apply to a living creature, in which not only do those chemicals perform other vital functions, but in which there are a huge variety of other chemicals also interacting with and confounding the same process.

Even experiments in insects and animals don't automatically translate into human results. First, because the lab animals have been bred or genetically engineered to knock out as many confounding factors as possible, and strongly express the characteristic that's being studied. Second, because we are not the same as animals. We see this all the time in, for example, drug studies that show that a medication does just what it's supposed to in animals, but doesn't work or has a negative effect in humans.

While someone who has some scientific knowledge may know more about something than someone who doesn't, they know the most about their own specialized field - and less than another scientist who specializes in the field in question. Argument from authority is a logical fallacy in the first place, and in science, it is trumped by scientific consensus (which means the evidence universally supports a conclusion, not that scientists took a vote on what conclusion they'd support.)

sarek
05-02-14, 10:29 AM
Since this thread has been veering off into a discussion of nutritional effects on epigenetics I have taken the liberty of moving those posts to this thread (http://www.addforums.com/forums/showthread.php?t=161446) so as to keep the aspect of nutrition separate from the original subject of the present thread. If you desire to continue discussing the nutritional aspect, I kindly refer everyone to the split off thread.

Dizfriz
05-02-14, 11:25 AM
is mental illness one of the limited circumstances which environment can effect epigenetics?Likely so but right now we don't understand enough about it to say much with any degree of confidence.

Dizfriz

Amtram
05-02-14, 01:06 PM
It's more like the other direction. Epigenetics affects mental illness. Usually by carrying out the orders of the DNA, and building a different brain model.

SB_UK
05-02-14, 01:16 PM
How about ?

http://www.sciencedirect.com/science/article/pii/S0306452212011414
Moreover, major treatments for schizophrenia over the past 40 years have included the drugs lithium and valproate, both of which we now know are histone deacetylases.I thought they were bipolar treatments ... ... anyway ???

How about ?
[1]
Physical development complete (essentially) at birth - end of developmental biological program (stand alone entity able to survive in isolation) - so everything's in place bar the brain's neural connections.
[2]
Birth into ketone usage (lithium,valproate) as the ideal epigenetic platform ie stable genome/histome
[3]
For experience to lead to re-wiring of the brain/learning.

So - the point in thsi post being that epigenetics represents a program of instructions which're followed in utero - but upon birth, and the 'brain' taking over - that program has completed - and we're expected to 'freeze' the completed epigenetics program in 'metabolism' mode - whereby under ketogenic metabolism - a gentle re-wiring of connections occurs in response to experience.

There has to be a reason why so many human conditions are fixed by ketones/HDAC inhibitors - including physical, neurological and psychiatric - cancer and immunologic.

SB_UK
05-02-14, 02:27 PM
Significance of epigenetics for understanding brain development, brain evolution and behaviourhttp://www.sciencedirect.com/science/article/pii/S0306452212011414
-1-
Two major environmental developments have occurred in mammalian evolution which have impacted on the genetic and epigenetic regulation of brain development. The first of these was viviparity-2-The extensive neocortical development which takes place post-natally[1] In utero
So physical growth (all basic cellular differentiation events have occurred).

[2] In the big wide world
Nerves re-associate over an epigenetically complete (growth/proliferation/differentiation process complete) ie 'finished' histome/genome whereby what now counts is experience/sensory exposure in association/reassociation of nerves into networks -

or as one big neuro guy once said - don't talk to me about molecular biology/genetics to help understand the brain/mind.
It's of no use.

Maybe of no use ?
We need to maintain the ideal physiological milieu for neurones to do their thing.

The ideal physiological milieu for pregnant mother to permit foetal development.

Human beings don't do well when distressed.

Amtram
05-02-14, 07:41 PM
How about ?
[1]
Physical development complete (essentially) at birth - end of developmental biological program (stand alone entity able to survive in isolation) - so everything's in place bar the brain's neural connections.
[2]
Birth into ketone usage (lithium,valproate) as the ideal epigenetic platform ie stable genome/histome
[3]
For experience to lead to re-wiring of the brain/learning.

So - the point in thsi post being that epigenetics represents a program of instructions which're followed in utero - but upon birth, and the 'brain' taking over - that program has completed - and we're expected to 'freeze' the completed epigenetics program in 'metabolism' mode - whereby under ketogenic metabolism - a gentle re-wiring of connections occurs in response to experience.

There has to be a reason why so many human conditions are fixed by ketones/HDAC inhibitors - including physical, neurological and psychiatric - cancer and immunologic.

That is the opposite of what this paper says, and further, the "points" that you make are not even mentioned in the research and are therefore unrelated and speculative. I've put in a request for the full text, but none of this is even implied in the abstract.

Amtram
05-02-14, 07:53 PM
-1-
-2-[1] In utero
So physical growth (all basic cellular differentiation events have occurred).

[2] In the big wide world
Nerves re-associate over an epigenetically complete (growth/proliferation/differentiation process complete) ie 'finished' histome/genome whereby what now counts is experience/sensory exposure in association/reassociation of nerves into networks -
The ideal physiological milieu for pregnant mother to permit foetal development.

Human beings don't do well when distressed.

Again, this is an example of what I said to daveddd about "cherry picking," with the added feature of Baseless Speculation.

The idea of epigenetic changes in the brain postnatally caused by environment has pretty much zero biological plausibility. Epigenetic changes in the brain that were established at conception, yes. Those are plausible and are being researched. Brain injuries that occur postnatally do not cause epigenetic changes, they cause brain damage.

In order for there to be an epigenetic change, cells need to be reproducing themselves and then apoptosing. This does not happen with neurons. If it did, we would all be babbling idiots, because what affects our function is the connections between neurons. Make a new neuron and destroy the old one, all those connections are gone and need to be re-established from scratch. We would have perpetual bouts of amnesia, loss of learning, cognitive, perceptual, and emotional difficulties in an endless cascade throughout the course of our lives.

When neurons grow new axonal branches, synapses rearrange, and dendrites spread, this is not epigenetics. This is plasticity. It does not involve cell production, but cell growth. No cell production, no epigenetics.

daveddd
05-02-14, 08:04 PM
It's more like the other direction. Epigenetics affects mental illness. Usually by carrying out the orders of the DNA, and building a different brain model.

no, this doesn't sound right

people aren't pre programmed to get ptsd

thats about as extreme bioreductionism as I've ever seen

daveddd
05-02-14, 08:12 PM
Likely so but right now we don't understand enough about it to say much with any degree of confidence.

Dizfriz

so yes we know environment can effect epigenetic and produce different phenotypes

it seems a lot of things in psychology haven't been proven

it doesn't mean they can't be talked about

i feel like science impedes psychology in this way

Dizfriz
05-02-14, 08:17 PM
so yes we know environment can effect epigenetic and produce different phenotypes


Yes but it appears that this is rather limited and I don't think any generalizations can be made right now.

Dizfriz

Dizfriz
05-02-14, 08:24 PM
Amtram It's more like the other direction. Epigenetics affects mental illness. Usually by carrying out the orders of the DNA, and building a different brain model. Daveddd: no, this doesn't sound right

people aren't pre programmed to get ptsd

thats about as extreme bioreductionism as I've ever seen I have to go along with Amtram here. If the genetics are not there, epigenetics has nothing to do. If the genetics are present then epigenetics can be a factor. With mental illness, we don't know a lot about it yet but the idea of the individual's genetics controlling the possibilities is pretty well supported.

Dizfriz


Dizfriz

daveddd
05-02-14, 08:28 PM
I have to go along with Amtram here. If the genetics are not there, epigenetics has nothing to do. If the genetics are present then epigenetics can be a factor. With mental illness, we don't know a lot about it yet but the idea of the individual's genetics controlling the possibilities is pretty well supported.

Dizfriz


Dizfriz

yea, its very common knowledge genetics predisposes to mental illness, it just doesn't predetermine

like you always say, genetics is not destiny

Dizfriz
05-02-14, 09:10 PM
yea, its very common knowledge genetics predisposes to mental illness, it just doesn't predetermine

like you always say, genetics is not destiny

This is quite true but genetics can have a huge effect on the odds.

Dizfriz

daveddd
05-02-14, 09:31 PM
i agree totally

and most gene by environment theories, i imagine are incredibly hard to test, i don't think that should lead to them being dismissed though

the only promise i can think of (which may be and seems to have been possible for some ) is breaking down the phenotype through therapeutic strategies

stripping it down to the genotype which is much less life destroying, and solving what was once thought strictly biological

i feel simply switching off the genome (sorry if I'm using the wrong word) through genetic medicine would leave unhealthy traces of the phenotype,

simple genetic based emotional reactions to the environment(not caused by anyone or parent) may cause epigenetic changes that can be much more impairing than the emotions themselves

Amtram
05-02-14, 09:36 PM
no, this doesn't sound right

people aren't pre programmed to get ptsd

thats about as extreme bioreductionism as I've ever seen

This paper isn't about PTSD, therefore using PTSD as an example is not relevant. PTSD is potentially a G x E condition, and there may or may not be an epigenetic involvement. All we know is that there is a genetic predisposition that may make it more likely when a person is exposed to the trigger of traumatic stress. In this case, the environmental trigger is clear, so it's far less necessary to try to attribute it to some more complex process.

Bioreductionism is more along the lines of assuming that environment causes everything because epigenetics.

daveddd
05-02-14, 09:37 PM
ptsd is a good mental illness to start with because everyone can agree its genes by environment

the others will follow

its a good place to start

Amtram
05-02-14, 09:53 PM
i agree totally

and most gene by environment theories, i imagine are incredibly hard to test, i don't think that should lead to them being dismissed though



The problem lies in assuming that all G x E conditions are epigenetic in nature. And looking now at the full text of the paper cited by SB above, there is no evidence in it supporting any of the claims that were made. It's more about how maternal imprinting during fetal development is influenced by heritable epigenetics that are then reinforced by social structure - and how they are mutually self-reinforcing. In mice and chimpanzees.

It also mentions how post-mortem findings in human brains from people who suffered late-onset psychiatric disorders like schizophrenia and bipolar and some types of psychosis showed hypomethylation of GABA-ergic neurons in the prefrontal cortex, which means that where methylation was supposed to take place (as a protective against these problems, to put it a little more simply) it didn't - and that is assumed to take place prenatally, based on animal studies. It is also assumed to be maternally inherited, at least in the models used in this study.

No mention anywhere of ketones or stress - just heredity.

daveddd
05-02-14, 09:56 PM
i tend to assume SB would know something i didn't

he is a top notch scientist in molecular medicine

Amtram
05-02-14, 09:57 PM
ptsd is a good mental illness to start with because everyone can agree its genes by environment

the others will follow

its a good place to start

It's a good place to start if you're studying PTSD. Regardless, you need to find the genes first in order to establish genetic predisposition. And the genes or pieces of genes we might find are conclusively associated with vulnerability to PTSD are not necessarily going to have anything to do with other mental illnesses.

As I've said elsewhere, you can't find one thing in one situation with one set of variables and then assume it applies exactly to everything else that is similar in some way or another. Maybe in Math or Physics, perhaps in Chemistry, but no way is Biology that cut-and-dried.

daveddd
05-02-14, 10:01 PM
thats where we will have to agree to disagree

you have a much more specific biological stance on mental illness then me

if you read two paragraphs , this is the view i agree with


http://books.google.com/books?id=Tna-9d_ykPIC&pg=PA63&dq=theodore+millon+biosocial&hl=en&sa=X&ei=Ek5kU-3IHoqlyATU-4LICg&ved=0CDwQ6AEwAw#v=onepage&q=theodore%20millon%20biosocial&f=false

Amtram
05-02-14, 10:09 PM
i tend to assume SB would know something i didn't

he is a top notch scientist in molecular medicine

Everyone knows something someone else doesn't. However, I'm looking at full text articles in peer-reviewed academic journals and checking with scientists who are actively researching in these fields and getting complete disagreement with his statements. Scientific consensus is based on data and evidence, and the consensus in this case disagrees completely with the statements SB is making.

I would also like to think that a top notch scientist wouldn't direct people to an published paper and then misrepresent the data in that paper to make it say something that it does not, even in the slightest. Nowhere in this paper does it talk about diet or stress. No epigeneticists talk about regulatory transcription errors taking place in the brain post-natally, because it doesn't happen. And in this paper in particular, it's talking about investigating transcription errors by testing placental tissue - that definitely says that it's not about postnatal diet or stress. i.e., using this particular paper to say what SB said it says is, well, inaccurate.

daveddd
05-02-14, 10:13 PM
while its great your constantly checking with scientists to prove people wrong

I've seen very little progress by scientists in the field of psychology, that seems to make you dismissive of everything

although in psychology these theories are being made into treatment strategies that are greatly helping people, scientific proof or not

SB_UK
05-03-14, 06:24 AM
i tend to assume SB would know something i didn't

he is a top notch scientist in molecular medicine

Not any good really
- just finding it really hard to find a way that molecular genetics will lead to a curative (as opposed to a preventative) approach, particularly to any psychiatric disorder.

As far as I can see physiology defines operational bounds which can be handled.
So ... ... wikP/stress
stress, based on years of empirical research, "should be restricted to conditions where an environmental demand exceeds the natural regulatory capacity of an organism"Now - presumably stress during development is going to have an effect.
How will stress outside of the natural regulatory capacity of the developing foetus work ?
Epigenetically.

So - there's a connection between physiology, homeostasis and epigenetics.

So - just as Peripheral has described the pO2 having an epigenetic effect on the growth of plants - so environmental factors which compromise the survival of the developing foetus - at any point in time, operates to restore homeostasis at any developmental time-point via epigenetic modification - operating through cortisol - which (exactly as mentioned by Peripheral above) selects for a 'maintenance' and not a 'growth' phenotype.
Growth arrest occurs reactively to withdrawing oxygen - continued growth would result in the organism dying.

Stress will select for an energetically more efficient organism - using that basic idea.
But here's the problem - presumably too much stress will 'overselect' ... ... (don't know) ... ...

So - we've the idea of manageable versus unmanageable stress which we're going to have to turn into distress vs eustress, glycolysis versus mitochondrial respiration, glucose versus fat.

"prenatal cortisol exposure, as a predictor of infant cognitive development"http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2872196/

So - the question might be - how do we ensure that the developing foetus is subject to ONLY manageable stress ?

Presumably - we need to look at the level of distress under which mother (and her parents) were placed; to take away the distress to permit a perfect physiological medium in which the developing foetus may develop ?

From the perspective of the developing foetus - the perfect physiological medium can only represent the presentation of factors required for growth (oxygen,glucose).
As these factors are varied - so are reactive epigenetic marks put down - to correct disruption in homeostasis.

So epigenetics operating perfectly reactively to physiological environment.

But what is the ideal physiological medium for the foetus to develop pre-natally and for the brain/mind to develop post-natally ?

Well - we need to identify the physical distressors of man (eg alcohol, cigarette smoke discovered through epidemiological verification), and the psychological distressors (eg educational and workplace insecurity discovered through epidemiological verification) of man
- and correct them - noting that for the most part - human beings are driven into physical distressors (particularly a high fat / high sugar diet) because of its activation of the opiate system (stress relief) because of an adverse psychological (immoral) environment.

So - once again - what's reported back is to suspend people within a moral environment (in which education teaches global logical consistency with the wellbeing of man (the species)) ... ... and that no longer psychologically distressful life will no longer express itself through physical distress through reaching for stress relief (the wrong foods, the wrong psychoactive compounds), will no longer result in reactive epigenetic change which impedes development, will no longer express itself in disease later on in life for the epigenetically over-sculpted child.

-*-

So - the net conclusion of all of that - is that there's nothing really wrong with any human being (from the perspective of the common disease); all that's wrong is that we're living life in a world which doesn't make sense - the lack of sense translates into distress which expresses itself epigenetically by deviating the developmental trajectory of the developing foetus from ideal into deranged -
- with the net effect being disease.

Correct social structure (psychosocial stress) and the rest (physical distress,physiological disruption,undesirable epigenetic modification) will
correct.

-*-

The slight problem I'm having is that I'm trying to suggest that selection for an optimally efficient energetic organism occurs through epigenetic route, and also that (above) distress can epigenetically sculpt the organism into disease.

So - which one is it to be ?

I think the answer is that:
eustress at all levels -> results in optimal selection for energetic efficiency
distress at all levles -> results in potentially adverse epigenetic modifications, which can express themselves in disease.

-*-

But! what's the overarching pattern.

A shift away from blood glucose (as terribly inefficient) usage - into fat usage.

So ... ... perhaps we can take away the idea that eustress (and the positive epigenetic modifications which it implies) is manifest in the individual through exercise and diet - developing into as efficient an aerobic organism as possible.

As mentioned previously we've compiled a list of factors which drive mitochondrial biogenesis - and so if we see those as representing the entire set of eustressful factors - and apply those through life - then we'll end up with positive selection for a health-promoting epigenetic profile, which'll reward us with a healthy life span which does not include significant levels of sickness prior to a premature death.

-*-

Live like a Jedi (alliance with morality, aerobically fit) and live a long life; otherwise epigenetics gonna' getcha'.

SB_UK
05-03-14, 06:44 AM
thats where we will have to agree to disagree

you have a much more specific biological stance on mental illness then me

if you read two paragraphs , this is the view i agree with


http://books.google.com/books?id=Tna-9d_ykPIC&pg=PA63&dq=theodore+millon+biosocial&hl=en&sa=X&ei=Ek5kU-3IHoqlyATU-4LICg&ved=0CDwQ6AEwAw#v=onepage&q=theodore%20millon%20biosocial&f=false


Excellent stuff.

That's it.

"biological maturation is dependent upon a favourable environmental experience"

or optimal physical (in utero) and neural/mental (post-natally) development occurs through a maximally eustressful, minimally distressful environment

ie a moral social landscape (equality) [psych] in which optimal aerobic efficiency [phys.] is sought.

-*-

Epigenetic modification reactively to deviations from physiological homeostasis - so the tools of physiology represent epigenetic modification.
All's well and good as long as we chase the eustressful idea, falls apart when the other path (the Dark side) is chosen.

SB_UK
05-03-14, 06:50 AM
Just to be clear - this is a complete summary of what I think underlies optimal human development and (when it fails) - all of the diseases that the planetary people are collapsing from:

"biological maturation is dependent upon a favourable environmental experience"

ie genetics/epigenetics at the level of physical, neural and mental development is WHOLLY subservient to the environment.

Placing emphasis on genetics/epigenetics rather than the environment is a bit like looking at some tools and wondering why they're not fixing a car.
Yes they can - but they require the environmental influence of somebody who knows what they're doing to use them.

But sure enough - with the right environmental influence, no repair can be fixed without tools.

-*-

All of this translates environmental modification as the basis to the alleviation of human disease/suffering.
And genetics/epigenetics as an 'academic' discipline - which can be researched, if a mechanism of operation (of environmental exposure) is desired.

But - that mechanism isn't going to prove very easy to unravel - developmental epigenetics (the state of all genome and histone modifications and recording ALL environmental influences simultaneously) is so much harder than genetics (find a broken gene) in terms of reproducibility.

So - epigenetics/genetics instead of environment - places the cart before the horse - places environmental consequence before exposure.

Amtram
05-03-14, 01:39 PM
while its great your constantly checking with scientists to prove people wrong

I've seen very little progress by scientists in the field of psychology, that seems to make you dismissive of everything

although in psychology these theories are being made into treatment strategies that are greatly helping people, scientific proof or not

There are amazing things happening with psychology, but not acknowledging them in the context of molecular biology doesn't mean I don't appreciate them. You will also find that I am not praising the advances in bionic prostheses, computer engineering, or alternative energy sources. This does not mean at all that I disdain them, just that they are irrelevant in this particular context.

Dizfriz
05-03-14, 02:32 PM
while its great your constantly checking with scientists to prove people wrong What she appears to be doing is what anyone with a strong interest in science should do, trying to show herself wrong.

This is how science is done. You keep on trying to falsify your ideas and the they more they hold up to this, the more confidence you can have in then. Science never proves only supports or falsifies.

If you try to prove yourself right then you are in a very big danger of confirmation bias, only looking at ideas that agree with you.

I've seen very little progress by scientists in the field of psychology,Actually I have seen quite a lot over the years. Go back about 20 years and see where we were then and compare to where we are now; big difference.

That seems to make you dismissive of everything I don't see that with her. She seems to be dismissive of ideas that are presented without evidence and while I tend to be a bit more patient, I also run in that direction.

although in psychology these theories are being made into treatment strategies that are greatly helping people, scientific proof or not This is where you are having problems. Science doesn't do proof and no one is trying to make it do proof as we understand the nature of the critter.

It is not my job to defend Amtram as she is more than capable of taking care of herself but while I sometimes take a somewhat different approach, I usually agree with what she has to say when taken from her viewpoint and her research is first class so I felt the need to make a statement on that.

Dizfriz

Amtram
05-03-14, 02:51 PM
ie genetics/epigenetics at the level of physical, neural and mental development is WHOLLY subservient to the environment.

And this is WHOLLY incorrect. Epigenetics is almost completely subservient to RNA transcription of DNA. This is where the credibility of your statements about epigenetics completely falls apart. We have a handful of examples of artificial methylation of histones resulting in changes in gene expression - and this means that it is an interrruption in a process that already has direction and mechanism that operates on its own, without the need for environmental pressure of any kind.


All of this translates environmental modification as the basis to the alleviation of human disease/suffering.
And genetics/epigenetics as an 'academic' discipline - which can be researched, if a mechanism of operation (of environmental exposure) is desired.

No, it does not. Because altering genetic expression is just as likely to lead to horrible outcomes with the limited knowledge we have now. This is purely magical thinking with no basis in any of the evidence that has been collected in research. We are so far from being able to manipulate histone methylation in order to guarantee universally beneficial results that this claim is outrageous.

One of the first epigenetic manipulations that was tested in animals and found to be relevant to humans was folic acid. We have long advised pregnant women to increase their intake of folic acid to prevent spina bifida. Animal tests showed that too much folic acid, though, actually caused spina bifida. Folic acid is a methylator, and in children who were born with spina bifida despite their mothers taking the supplement to prevent it, sure enough - those gene loci were hypermethylated.

So, no, "environmental modification" has already been demonstrated to not alleviate disease and suffering.


So - epigenetics/genetics instead of environment - places the cart before the horse - places environmental consequence before exposure.

If you want the right answers, you don't start with the conclusion you want to reach and then manipulate or cherry pick data to support that conclusion. This is what you are doing, and there are already more examples that your conclusion is flawed than correct.

LynneC
05-07-14, 01:50 PM
One of the first epigenetic manipulations that was tested in animals and found to be relevant to humans was folic acid. We have long advised pregnant women to increase their intake of folic acid to prevent spina bifida. Animal tests showed that too much folic acid, though, actually caused spina bifida. Folic acid is a methylator, and in children who were born with spina bifida despite their mothers taking the supplement to prevent it, sure enough - those gene loci were hypermethylated.
Are you saying that folic acid supplementation may have caused spina bifida, or that in those cases folic acid didn't prevent spina bifida?

Amtram
05-07-14, 04:58 PM
Actually, it was causing the spina bifida. When you're methylating an unmethylated gene, (I know I said this before, but don't remember where) you can turn on something beneficial or detrimental, or turn off something beneficial or detrimental. In this case, there's more to discover regarding the predisposition that increased susceptibility to spina bifida. i.e., in some individuals, the folic acid activated the expression of spina bifida OR turned off the protection against spina bifida.

dvdnvwls
05-07-14, 05:44 PM
while its great your constantly checking with scientists to prove people wrong

I've seen very little progress by scientists in the field of psychology, that seems to make you dismissive of everything

although in psychology these theories are being made into treatment strategies that are greatly helping people, scientific proof or not
Science is not about proving people wrong; it's about proving ideas wrong. If we start operating by personal attacks and accusations, we'll get so bogged down in that that nothing will ever get done.

If some idea can be proved wrong, then it should be proved wrong, as quickly as possible so we can get back to business.

No idea can really ever be perfectly proved right, because someone could (theoretically) always come along tomorrow and show that there's a case where it doesn't happen that way. But proving things wrong is how science works, and if an idea is proved wrong then seriously what could anyone want a wrong idea for? If there's good reason to believe that some wrong theory was partly on the right track, then - well, "back to the drawing board", that's science in action.

Presenting not-fully-tested hunches as if they're proven is not really very helpful. Trying out such a hunch on yourself and finding that it works for you is great - but it doesn't suddenly mean the hunch is true for everyone; in fact it doesn't mean much of anything yet, just that it seemed to work, once, for one person. A good start. Worth exploring.

mctavish23
05-07-14, 08:54 PM
TUT spelled backwards is still TUT.

u r welcome :cool:

Amtram
05-08-14, 01:54 PM
Argh. I'm looking for the study about the excess folic acid, and can't find it. There's too much new research on it. A lot of it is good, but densely packed with scientific vocabulary, so it won't make a lot of sense to too many people for me to share it. I'll keep digging.