View Full Version : Branche from I've been saying this for years thread


mildadhd
02-28-13, 12:30 PM
This is the first clue that specific genes and pathways may cause a broader susceptibility to a number of disorders. Now the important work will be to figure out how this actually happens," said Smoller


Smoller noted these genetic risk factors may only account for a very small part of the risk driving these disorders, and just how big a share they account for isn't yet known.

So, looking for these genes in an individual now would not be considered a diagnostic tool. "They are not enough to predict any individual's risk. And you might carry all of these variants and never develop a psychiatric disorder," Smoller said.

http://healthyliving.msn.com/diseases/adhd/shared-genes-may-link-adhd-autism-and-depression






Not all people who carry these genes develop psychiatric disorders. (Same with other genes shown to be related to ADD)

What environmental factors are involved in gene expression,

that might result in a actual psychiatric disorder?

Does the research mention anything about similar environmental factors that might be involved in the actual expression of these genes ?

Why don't all people with these genes develop a disorder?


.

SB_UK
02-28-13, 01:36 PM
Large number of those conditions mentioned here:
http://en.wikipedia.org/wiki/Delta_wave

Slow waves / calcium waves / delta waves covered here years and years ago.

SB_UK
02-28-13, 01:46 PM
In the cortex, the suprachiasmatic nuclei have been shown to regulate delta waves, as lesions to this area have been shown to cause disruptions in delta wave activity.
The suprachiasmatic nucleus (SCN), i.e., the biological clock of the brain, shows lower vasopressin production and a smaller circadian amplitude in depression, which may explain the sleeping problems in this disorder and may contribute to the strong CRH activation. The hypothalamo-pituitary thyroid (HPT)-axis is inhibited in depression. These hypothalamic peptidergic systems, i.e., the HPA-axis, the SCN, the SON and the HPT-axis, have many interactions with aminergic systems that are also implicated in depression. CRH neurons are strongly activated in depressed patients, and so is their HPA-axis, at all levels, but the individual variability is large.

The matched stressors of stress (CRH) and depression -> depress -> the SCN leading to defects in calcium channel regulated deep sleep which manifests itself as a whole host (eg those in the article and wikiP) of very serious disorders.

-*-

As simple as that - stress/depression (particularly chronic) messes with 'urrr 'eds ?

SB_UK
02-28-13, 01:51 PM
There is something very, very, very, very special about the 0 Hz EEG.

SB_UK
02-28-13, 02:46 PM
http://www.psychologytoday.com/blog/sleepless-in-america/201010/the-mystery-deep-sleep
Unfortunately deep sleep is very vulnerable to the effects of stressThe reason why ADDers have no memory (see line 1 of signature) and
http://www.bbc.co.uk/news/health-21199949 (http://www.addforums.com/forums/)
"the quality of deep sleep [impaired by stress] hampers the ability to store memories."

Amtram
02-28-13, 02:53 PM
Not all people who carry these genes develop psychiatric disorders. (Same with other genes shown to be related to ADD)

What environmental factors are involved in gene expression,

that might result in a actual psychiatric disorder?

Does the research mention anything about similar environmental factors that might be involved in the actual expression of these genes ?

Why don't all people with these genes develop a disorder?


.

That's why it's important to see the genes in context. They found that the people who had these disorders all had a set of genes in their DNA that didn't exist in any of the control (non-disordered) subjects. What they think they've found is not a single gene, which I don't think they've been looking for for years) but a group of genes together that are appearing in the DNA only of people who have one of these five conditions.

Amtram
02-28-13, 02:58 PM
What ever Abi? Environment is part.

Not until after the fact. This is about the phase of development when the brain itself is being built, before any chemicals influence methylation or nurturing influences psychology. This is about the part that may one day allow us to make a definitive diagnosis using a serum test and address the post-birth environment factors before they become detrimental issues.

TygerSan
02-28-13, 03:07 PM
Slow waves / calcium waves / delta waves covered here years and years ago.

There are 2 types of calcium channels: L-type and T-type. The gene in question codes for a subunit (building block) of an L-type channel.

Interestingly, while delta waves seem to involve calcium signalling, my understanding is that it involves T-type channels more than L-type channels.

Another interesting point is that both of these channels are really important in cardiac function and other non-brain functions as well.

Also very interesting is that a known mutation in the same gene as mentioned in the article (CACNA1C) causes Timothy syndrome. Aside from having heart issues and other physical abnormalities, a large number of children with Timothy syndrome are on the autism spectrum.

http://ghr.nlm.nih.gov/condition/timothy-syndrome

SB_UK
02-28-13, 03:18 PM
There are 2 types of calcium channels: L-type and T-type. The gene in question codes for a subunit (building block) of an L-type channel.

Interestingly, while delta waves seem to involve calcium signalling, my understanding is that it involves T-type channels more than L-type channels.

Another interesting point is that both of these channels are really important in cardiac function and other non-brain functions as well.

Also very interesting is that a known mutation in the same gene as mentioned in the article (CACNA1C) causes Timothy syndrome. Aside from having heart issues and other physical abnormalities, a large number of children with Timothy syndrome are on the autism spectrum.

http://ghr.nlm.nih.gov/condition/timothy-syndrome

Aye ... ... just about to post that ... ... pity - the story was shaping up nicely.

:(

Not getting any obvious mechanistic connections with L type !

SB_UK
02-28-13, 04:07 PM
Trying to keep the dream alive with this paper:
http://www.jneurosci.org/content/27/14/3823.full.pdf

- suggesting that L- and T- calcium channels may act on nerve cells to produce 2 markedly different patterns of firing.

[extending a little bit too far out of my comfort zone - don't know whether this L- & T- Ca2+ channel co-localization reflects a more ubiquitously seen 'duality' in activation of nerve cells. more generally throughout the brain]

SB_UK
02-28-13, 04:17 PM
Continuing the logic from the hypothalamic SCN setting of delta slow wave rhythm (one mode of firing) in deep sleep (T calcium channel implicated) ... ... is it possible that the other side of the coin - when we're wide awake is a faster rhythm of firing (the other mode of firing) ... ... representing an L calcium channel mediated function ?

It'd be nice to see whether L and T calcium channels are to be found in the same place (on the same cells) throughout the brain.

SB_UK
02-28-13, 04:28 PM
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1299527/

Exact same bimodal pattern seen in T- and L-type Ca2+ channels in heart muscle as cerebellar nerve cell.

We showed that Ca2+ admitted through either T- or L-type Ca2+ channels is capable of initiating contraction and that the contractions depended on Ca2+-induced Ca2+ release from the sarcoplasmic reticulum (SR). The contractions, however, had different properties. T-Type and L-Type Ca2+ Conductances Define and Encode the Bimodal Firing PatternThose initiated by Ca2+ entry through T-type Ca2+ channels had a longer delay to the onset of shortening, slower rates of shortening and relaxation, lower peak shortening, and longer time to peak shortening. These differences were present even when L-type Ca2+ current amplitude, or charge entry, was less than that of T-type Ca2+ current, suggesting that Ca2+ entry through the T-type Ca2+ channel is a less effective signal transduction mechanism to the SR than is Ca2+ entry through the L-type Ca2+ channel.

mildadhd
02-28-13, 07:51 PM
That's why it's important to see the genes in context. They found that the people who had these disorders all had a set of genes in their DNA that didn't exist in any of the control (non-disordered) subjects. What they think they've found is not a single gene, which I don't think they've been looking for for years) but a group of genes together that are appearing in the DNA only of people who have one of these five conditions.

According to one of the link you provided the underlined is not accurate.

People can have these genes and not develop a psychiatric disorder.

"They are not enough to predict any individual's risk. And you might carry all of these variants and never develop a psychiatric disorder," Smoller said.

http://healthyliving.msn.com/diseases/adhd/shared-genes-may-link-adhd-autism-and-depression

silivrentoliel
02-28-13, 08:03 PM
I know I'm not the most scientific person in the world... in fact, most of it goes right over my head.... but I'm missing the correlation between calcium and newly found genes within a DNA strand. (Granted, I didn't understand much about what was said about calcium.... but I don't see the correlation)

mildadhd
02-28-13, 08:24 PM
Originally Posted by Peripheral
What ever Abi? Environment is part.

Reply by Amtram ;Not until after the fact. This is about the phase of development when the brain itself is being built, before any chemicals influence methylation or nurturing influences psychology. This is about the part that may one day allow us to make a definitive diagnosis using a serum test and address the post-birth environment factors before they become detrimental issues.



Amtram,

The fact is all people who have these genes, don't develop a psychiatric condition. There must be more factors, than just having these genes to develop a psychiatric condition?

Surely your not going to label everyone with these genes with a psychiatric condition?

I do agree that some people might be more inherently sensitive (genetic predisposition) in the more genetically ancient "hard wired", (sub-cortex) primary emotional systems,

but the higher brain (cortex) is shaped in a relationship with the environment and the middle and lower areas of the emotional brain (sub cortex) at the same time.

The environment might even be a strong deciding factor in the expression of any genetic predisposition. Predisposition doesn't always mean predetermination.

The environment is a factor that can never be counted out.

.

Abi
02-28-13, 08:38 PM
Amtram,

The fact is all people who have these genes, don't develop a psychiatric condition. There must be more factors, than just having these genes to develop a psychiatric condition?

Surely your not going to label everyone with these genes with a psychiatric condition?

No one disputed that not all people who have those genes develop psych conditions.

No one has labelled everyone with these genes as having psych conditions.

---

If we have a thread discussing the role of unprotected sex in the spread of HIV and AIDS, we are

1. NOT claiming that everyone who has unprotected sex will get HIV and AIDS;

2. NOT claiming that they are not other ways to contract HIV and AIDS

and most importantly

3. NOT interested in how heroin junkies contract HIV and AIDS by sharing needles. We are talking about unprotected sex and AIDS. If you want to talk about shared needles, that is a different discussion.

mildadhd
02-28-13, 08:57 PM
No one disputed that not all people who have those genes develop psych conditions.

No one has labelled everyone with these genes as having psych conditions.

---

If we have a thread discussing the role of unprotected sex in the spread of HIV and AIDS, we are

1. NOT claiming that everyone who has unprotected sex will get HIV and AIDS;

2. NOT claiming that they are not other ways to contract HIV and AIDS

and most importantly

3. NOT interested in how heroin junkies contract HIV and AIDS by sharing needles. We are talking about unprotected sex and AIDS. If you want to talk about shared needles, that is a different discussion.


Abi,

Amtram said in post #22, in a reply to my post.


a group of genes together that are appearing in the DNA only of people who have one of these five conditions.


But my point from the beginning has been that people have these genes that Amtram is referring to, but don't have a psychiatric condition.

It is also well known that the environment can affect a infants brain development both good and bad before birth.



Side note, since your going to throw mud.

Everything I have said in this thread is part of discussing the OP topic.

This is the Science Section threads, , specific to science discussions, I don't mind being wrong.

If I posted information saying that genes where not involved with ADD. (which I am not)

You would have a right to reply,

without me accusing you of derailing the thread.

.

Amtram
02-28-13, 09:06 PM
Peripheral, let me explain why I feel this is so incredibly important. You're a parent, so you should understand as well.

Right now, we wait until a person exhibits symptoms before diagnosing him/her with one of these psychiatric disorders; often, by that point, damage has been done by "the environment" already. Diagnosis may include more than one of these related disorders, and pharmaceutical treatment is often by trial and error because comorbidity complicates prescribing.

Therapeutic options depend on the condition, age at diagnosis, and how much other damage has already been done.

If you had a child, and knew that you or the other parent or either family had a history of any of these disorders, and were able to test prenatally for them, you would be able to prepare a more suitable plan for this child so that he didn't develop the problem, so that his needs would be better met in school, and so that he could cope with and overcome his obstacles, wouldn't that be a better outcome than what we have now? That's one thing finding the genetic basis for these conditions will give us.

If you were seeking treatment for that child, and were able to pick the appropriate medication right from the start that would be most effective and have the fewest side effects, wouldn't that be better than the medication-go-round we have now? Finding better medications and picking the one most likely to work is another thing finding the genetic basis for these conditions will give us.

The issue is that if we can establish a genetic causation, correlation, or even predisposition, we open the door to avoiding many of the problems that aggravate these conditions and treating them more effectively if they are unavoidable.

I see that as a good thing. Whether or not the collection of SNPs guarantees the development of these conditions or merely indicates a statistically significant predisposition for developing them, knowing what they are and what else they do will improve the lives of all the people that carry them.

mildadhd
02-28-13, 09:34 PM
Peripheral, let me explain why I feel this is so incredibly important. You're a parent, so you should understand as well.

Right now, we wait until a person exhibits symptoms before diagnosing him/her with one of these psychiatric disorders; often, by that point, damage has been done by "the environment" already. Diagnosis may include more than one of these related disorders, and pharmaceutical treatment is often by trial and error because comorbidity complicates prescribing.

Therapeutic options depend on the condition, age at diagnosis, and how much other damage has already been done.

If you had a child, and knew that you or the other parent or either family had a history of any of these disorders, and were able to test prenatally for them, you would be able to prepare a more suitable plan for this child so that he didn't develop the problem, so that his needs would be better met in school, and so that he could cope with and overcome his obstacles, wouldn't that be a better outcome than what we have now? That's one thing finding the genetic basis for these conditions will give us.

If you were seeking treatment for that child, and were able to pick the appropriate medication right from the start that would be most effective and have the fewest side effects, wouldn't that be better than the medication-go-round we have now? Finding better medications and picking the one most likely to work is another thing finding the genetic basis for these conditions will give us.

The issue is that if we can establish a genetic causation, correlation, or even predisposition, we open the door to avoiding many of the problems that aggravate these conditions and treating them more effectively if they are unavoidable.

I see that as a good thing. Whether or not the collection of SNPs guarantees the development of these conditions or merely indicates a statistically significant predisposition for developing them, knowing what they are and what else they do will improve the lives of all the people that carry them.


I agree. I am working on understanding the same concept with the primary emotional systems. These groups of genes and molecules your discussing,

may even be involved with the primary emotional systems/pathways? I think it is important to bring up any genetic information, that might be important.

I think it is equally important to bring up any environmental information, that might be important. There is reasons why I keep bringing up these topics.

I think it is wrong to count out environment completely, I agree there may be genetic predispositions. The level of sensitivity is very important to consider.

I just don't think the evidence is strong enough to discredit the environmental factors that may result in expression of any sensitivity, before birth.

Or after birth. I am also coming from a prevention, lessening of severity and treatment view. The discussion may appear to be circular for a reason.







.

TygerSan
02-28-13, 11:01 PM
I know I'm not the most scientific person in the world... in fact, most of it goes right over my head.... but I'm missing the correlation between calcium and newly found genes within a DNA strand. (Granted, I didn't understand much about what was said about calcium.... but I don't see the correlation)


Gotta make this brief as I'm on my phone. Hate typing on this thing.

Genes code for proteins. A lot of our cellular mechanics rely on ion flow through channels which happen to be made of protein. Some of those channels control sodium ions into and out of neurons. Others do the same for calcium, potassium, or chloride. All channels have effects on neurons whether by determining whether or not it fires an action potential to how much neurotransmitter is released at the synapse.

So the genes in question code for some of the proteins that make up the ion channels that regulate calcium flow into and out of neurons (and other cells as well).

meadd823
03-01-13, 02:44 AM
Interesting abet a long read - bare bones high lights

Response variability in Attention-Deficit/Hyperactivity Disorder: a neuronal and glial energetics hypothesis (http://www.behavioralandbrainfunctions.com/content/2/1/30)


Investigation of the prevalence of genetic markers for factors that regulate energy metabolism (lactate, glutamate, glucose transporters, glycogen synthase, glycogen phosphorylase, glycolytic enzymes), release of glutamate from synaptic terminals and glutamate-stimulated lactate production (SNAP25, glutamate receptors, adenosine receptors, neurexins, intracellular Ca2+), as well as astrocyte function (α1, α2 and β-adrenoceptors, dopamine D1 receptors) and myelin synthesis (lactate transporter, Lingo-1, Quaking homolog, leukemia inhibitory factor, and Transferrin).


The hypothesis extends existing theories of ADHD by proposing a physiological basis for specific aspects of the ADHD phenotype – namely frequent, transient and impairing fluctuations in functioning, particularly during performance of speeded, effortful tasks. The immediate effects of deficient ATP production and slow restoration of ionic gradients across membranes of rapidly firing neurons have implications for daily functioning: For individuals with ADHD, performance efficacy would be enhanced if repetitive and lengthy effortful tasks were segmented to reduce concurrent demands for speed and accuracy of response (introduction of breaks into lengthy/effortful activities such as examinations, motorway driving, assembly-line production). Also, variations in task or modality and the use of self- rather than system-paced schedules would be helpful. This would enable energetic demands to be distributed to alternate neural resources, and energy reserves to be re-established.



The genesis of this type of intra-individual performance variability (variability during continual responding to externally-paced stimuli) remains unknown. We propose that it arises from inefficient and inconsistent neuronal transmission of information, due to a deficient energy supply – lactate production – by the major non-neuronal component of the central nervous system (CNS), the astrocyte [11-13]. Astrocytes play a critical role in providing energy via lactate to rapidly firing neurons. Astrocytes can also provide lactate to oligodendrocytes, which is used as a substrate for myelin synthesis by oligodendrocytes [14], and thus enables rapid neurotransmission. The presence of receptors for the major brain neurotransmitters on astrocytes adds to the robust evidence for their direct involvement in neurotransmission [15-18]. Given that performance variability is not unique to ADHD but rather a common and unifying feature of several disorders, such as Traumatic Brain Injury, Schizophrenia, Narcolepsy, Phenylketonuria (PKU), as well as ADHD, we do not propose such variance as a specific marker of ADHD. Rather we argue that intra-individual response variability may be an important index of the efficiency of neural signalling which, in turn, is dependent on neurobiological regulation of brain function (e.g. factors that regulate the energy supply to neurons). Also, we suggest that it may account for a substantial proportion of the variance in performance of executive function tasks such that poor task performance may not reflect impaired executive function per se, but rather an admixture of poor neurobiological regulation of the external physiological environment of rapidly firing neurons as well as slowed processing speed arising from inadequately myelinated neurons, particularly those involved in working memory [19].



The present paper addresses this aspect by postulating that reaction time variability and other manifestations of transient fluctuations in performance, which arise in the context of the need for continuous rapid neuronal firing, reflect the effects of transient depletion of neuronal energy on the efficiency of information processing.



According to our hypothesis, the reinforcement contingency is not so much a causal factor in ADHD, as it is an occasion in which the mechanisms we have outlined are likely to be operative. People with ADHD will tend to go "off-task" independent of the reinforcement lost because the effort to remain "on-task" requires energy resources that are no longer available to them.


Investigations of potential therapeutic agents that target the energetic system rather than neurotransmitter function may yield additional improvements in treatment beyond the positive modulation of the energy balance noted for monoaminergic drugs in current use. One aim could be to stimulate creatine kinase function, and thus to increase the availability of phosphocreatine, and the re-synthesis of ATP. Increasing creatine levels would have the additional advantage of being neuroprotective [280]. While there is clearly a need to restore carbohydrate and energy reserves and to ensure an adequate supply of omega fatty acids and other elements essential for myelin synthesis, it is equivocal whether dietary supplementation is capable of delivering the requisites to where they are needed. In the longer term it may prove more feasible to modify the expression of genes demonstrated to be essential in the regulation of astrocyte function, lactate production, glutamate transport and myelin synthesis [261]. Several novel forms of therapeutic agent and delivery system based on the components of the energy cycle and the synthesis of myelin could be tested.


This hopefully ties into the symptoms variation question the Ca+ presentation along with the genetic presentation across various condition initial post topic with a bit about executive function theory limitation thrown in for my personal pleasure. :D

SB_UK
03-01-13, 04:05 AM
Astrocytes

Slow wave transmission in the astrocytes was exactly what we looked at last time.

New Proof for Astrocytes Having L-type Calcium Channels (http://www.bioline.org.br/abstract?zr07074)

&

The calcium waves (https://wiki.brown.edu/confluence/display/BN0193S04/Calcium+Signaling+in+Astrocytes) were proposed to be a kind of long-distance signal as they can travels hundreds of micrometers, possibly signaling to hundreds of cells. These waves travel at 10-20 micrometers/second, an order of magnitude slower than neuronal signaling.

SB_UK
03-01-13, 04:30 AM
The matched stressors of stress (CRH) and depression
-> depress ->
the SCN leading to defects in calcium channel [signalling]

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3125703/
Taken together, these results demonstrate that mitochondrial Ca2+mediates SCN2.2 rhythms in extracellular ATP accumulation and suggest a role for circadian gliotransmission in SCN clock function.

This is interesting.

That paper suggests that it isn't SCN defects ->- lead to ->- calcium channel signalling problems ... ...

- but -

'factor' eg light
->- leads to ->-
poor timing in the ultra-slow astrocytic calcium wave
->- leads to ->-
poor timing in the SCN
->- leads to ->-
poor timing in the eg slow wave (but fast compared to the astrocyte !) of the neurone (delta EEG),

All just a question of health when 'you got riddum' ?

SB_UK
03-01-13, 04:32 AM
'factor' eg light
->- leads to ->-
poor timing in the ultra-slow astrocytic calcium wave

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2573039/
These results suggest multiple roles for melatonin receptors in the regulation of astroglial function, impacting specific brain regions differentially.

Production of melatonin by the pineal gland is inhibited by light to the retina and permitted by darkness

SB_UK
03-01-13, 04:40 AM
http://www.ncbi.nlm.nih.gov/pubmed/1609019
Temporal relationship between melatonin and cortisol [stress, stress, stress!]

It has been shown that, in the rat, physical stress decreases pineal melatonin levels at night ... ...

-*-

All consistent with the idea that 'stress' (particularly caused by having to contravene our highest emergent property of mind ... ... and acting immorally by handling money) ... ... the 'Western' economic system results in the diseases of 'Western' living.

Though the 'Western' economic system and diseases of 'Western' living have both gone global in an entirely bad way.

Human beings are stressing other human beings out by their behaviour - resulting in disease to both those who stress and those who're stressed out ... ... ... for none of that is properly human behaviour aligned with the highest of our prime directives ... of ... conscience.

SB_UK
03-01-13, 04:49 AM
So - this argument places the SCN (light) - pineal gland (dark) as the axis of organization of all subsequent events ... ... whereby disruption of the basic axis (the root of human functioning) results in physiological/psychological downstream disorganization.

http://thebrain.mcgill.ca/flash/d/d_11/d_11_cr/d_11_cr_hor/d_11_cr_hor.html

Second, in experiments where the suprachiasmatic nuclei were destroyed in animals such as hamsters, their cyclical behaviours, such as their sleep/wake cycles, become completely disorganized.

dark -- light
A brief history of time.

SB_UK
03-01-13, 05:00 AM
http://www.cell.com/current-biology/retrieve/pii/S0960982207014911
In mammals, the circadian system is hierarchical — a brain pacemaker located within the suprachiasmatic nucleus (SCN) is responsible for regulating locomotor activity rhythms and for synchronizing peripheral oscillators.
Makes sense ... ... the fundamental level of disorganization leading to disease reflecting stress deflection of the body's key (hierarchically highest) timing function.

So - imagine what'd happen if our electronic calendar was completely scrambled versus one entry shifted backwards by 5 minutes ... ... the hierarchically highest would completely disorganize our lives ... ... whereas perturbing one local peripheral oscillator 'd have relatively little effect.

SB_UK
03-01-13, 05:05 AM
Just checking ... ...


- that idea makes sense :-) , I think.

Lunacie
03-01-13, 10:13 AM
I agree. I am working on understanding the same concept with the primary emotional systems. These groups of genes and molecules your discussing,

may even be involved with the primary emotional systems/pathways? I think it is important to bring up any genetic information, that might be important.

I think it is equally important to bring up any environmental information, that might be important. There is reasons why I keep bringing up these topics.

I think it is wrong to count out environment completely, I agree there may be genetic predispositions. The level of sensitivity is very important to consider.

I just don't think the evidence is strong enough to discredit the environmental factors that may result in expression of any sensitivity, before birth.

Or after birth. I am also coming from a prevention, lessening of severity and treatment view. The discussion may appear to be circular for a reason.

.

Why do you keep making this accusation that posters are "counting out the
environment completely" or "discrediting environmental factors" when no one
has done any of that?

Amtram
03-01-13, 11:27 AM
We're finding more and more that as we understand what genes are responsible for what things, or what groups of genes are responsible for what groups of things, we end up understanding causes and effects in living organisms better.

With the calcium channels - which are connected to a variety of functions and dysfunctions - it's not enough to understand what they do. They do too many things, and while we may know a lot about what happens when they don't work from observing the end results, tracing their development back to the genetic level can give us more information about not only their purposes (which may reach beyond what we know so far) but also what other parts of the brain and body are affected by the same genes.

Going back to the genetic level also is going to allow us treatment specificity that we don't have now. The recent information about the genes behind non-responsiveness to morphine will help countless numbers of pain patients avoid useless treatments. Genetics that drive symptoms will do the same for other patients. Being able to look for SNPs that show responsiveness or non-responsiveness to medications will help a great deal in psychiatric treatment, where it's a guessing game using limited treatment options.

Finally, the genetics will help with diagnosis. This study isn't showing genes that cause every symptom in each of these conditions - it's showing a strong genetic correlation that will help confirm diagnoses. Plenty of studies already have found genetic correlations that don't correspond to ADHD, but do correspond to individual symptoms. One of the studies I recall offhand from among the African studies I was reading was that they found an allele that was not present in all the ADHD subjects, and not present in all the control subjects, but was present in all the subjects who had tested high for impulsivity.

This has tremendous potential in diagnosis and treatment. Correlations between genes and symptomology can better insure that relevant symptoms are being addressed medically and therapeutically, and nonexistent symptoms are not being treated unnecessarily. Medications that treat nonexistent symptoms can exacerbate present symptoms. By knowing what needs treatment and what doesn't, that problem can be solved.

Fuzzy12
03-01-13, 12:02 PM
According to one of the link you provided the underlined is not accurate.

People can have these genes and not develop a psychiatric disorder.

I think, having a gene or a group of genes predisposes you to developing the disorder. You don't necessarily actually have to develop it but there is a chance that you will. What actually triggers the expression of the gene, I don't know. It could be environmental factors.

I think, Amtram's statement is accurate as all it said is that the group of genes in question was found in all the the subjects with a psychiatric disorder but not in any of the control subjects. So it's possible that you need to have this particular group of genes to develop one of these 5 disorders but just having these genes doesn't necessarily mean that you will develop any of them.

EDIT: OH sorry, if that's been said or if my argument has been refuted already with actual science. I didn't read the entire thread. :)

mildadhd
03-01-13, 12:33 PM
I think, having a gene or a group of genes predisposes you to developing the disorder. You don't necessarily actually have to develop it but there is a chance that you will. What actually triggers the expression of the gene, I don't know. It could be environmental factors.

I think, Amtram's statement is accurate as all it said is that the group of genes in question was found in all the the subjects with a psychiatric disorder but not in any of the control subjects. So it's possible that you need to have this particular group of genes to develop one of these 5 disorders but just having these genes doesn't necessarily mean that you will develop any of them.

EDIT: OH sorry, if that's been said or if my argument has been refuted already with actual science. I didn't read the entire thread. :)


I agree.

It is also a very important point that all people that have these genes don't develop the disorder,

this point was not made.

So I posted that.

...

Then Amtram said environment isn't involved before birth, which is not true.

How do we know that environment is not a major factor expressing these genes being discussed?

...

There is lots of interesting topics in this thread. I want to hear discussions on them all.

I would not have made any more posts about the environment, after my first post.

But Abi and Amtram disagreed so I had to reply again, to make my point.

I don't have anything more to say about those posts and am ready to move on and learn more, unless someone brings up those topics.

And if they do I will tell them again why I think the parts they missed are very important.

I spent the night researching calcium-channels and I am learning a lot and really appreciate all members insight in those topics , as well.

mildadhd
03-01-13, 01:06 PM
After mentioning the important fact that not all people with these genes develop a disorder.

I replied to Abi,

Originally Posted by Peripheral
What ever Abi? Environment is part.Then Amtram replied to my reply to Abi,

Reply by Amtram. (post #23)
Not until after the fact. This is about the phase of development when the brain itself is being built, before any chemicals influence methylation or nurturing influences psychology...I disagree, environment can be an influence on gene expression before birth.

How do we know that environment is not a influence in these genes being expressed? I have seen research that says it is possible before birth.

Can we move on now?

mildadhd
03-01-13, 03:26 PM
We're finding more and more that as we understand what genes are responsible for what things, or what groups of genes are responsible for what groups of things, we end up understanding causes and effects in living organisms better.



Amtram,

What do you mean by "responsible"?

There is a big difference between calling genes "responsible"

and saying that similar genes are "involved" in similar pathways in these disorders.

I do I think the OP research information might be valuable for finding new treatments and figuring out similarities between disorders.

But these genes specifically "may only account for a very small part of the risk driving these disorders". (see quote below from the link you provided)

Smoller noted these genetic risk factors may only account for a very small part of the risk driving these disorders, and just how big a share they account for isn't yet known.

http://healthyliving.msn.com/diseases/adhd/shared-genes-may-link-adhd-autism-and-depression

sarek
03-01-13, 04:53 PM
MOD NOTE: lets just keep the personal stuff out of this thread. We are supposed to be debating facts here, not people.

Amtram
03-01-13, 04:59 PM
When I say "responsible," I mean directly involved as a driving force. As I've mentioned elsewhere, there are an incredibly small number of things that are monogenic (and they're mostly bad things) so a "responsible" gene would be one that contributed directly to the formation of the relevant physical structure.

We know lots of genes that are "involved," while still not knowing how many other or which other genes are involved in many complex pieces of anatomy. We know an increasing number of genes that are "responsible" for parts of those pieces - many of the neuroscientists in the MIND and CARTA videos from UC Davis point out "this gene determines the thickness of this part of the cerebral cortex in this area of the brain," and in a case like that, responsibility has been established.

In this way, they're working in what you might think of as a top-down manner. Over the course of many pieces of research, a connection has been made between people who share a symptom and people whose brains share a physical characteristic. A connection has been made between the location of that physical characteristic and the way that it's different. Genetic testing points to possible genes that might cause that part to be built differently. Lab animals are bred to have that gene to see if the difference can be reproduced.

It's working from big to small, from observable to reproducible and repeatable. Then after you have the small piece, you can work back up to how it fits in to the bigger picture, back and forth to make all the connections.

mildadhd
03-01-13, 05:08 PM
When I say "responsible," I mean directly involved as a driving force. As I've mentioned elsewhere, there are an incredibly small number of things that are monogenic (and they're mostly bad things) so a "responsible" gene would be one that contributed directly to the formation of the relevant physical structure.

We know lots of genes that are "involved," while still not knowing how many other or which other genes are involved in many complex pieces of anatomy. We know an increasing number of genes that are "responsible" for parts of those pieces - many of the neuroscientists in the MIND and CARTA videos from UC Davis point out "this gene determines the thickness of this part of the cerebral cortex in this area of the brain," and in a case like that, responsibility has been established.

In this way, they're working in what you might think of as a top-down manner. Over the course of many pieces of research, a connection has been made between people who share a symptom and people whose brains share a physical characteristic. A connection has been made between the location of that physical characteristic and the way that it's different. Genetic testing points to possible genes that might cause that part to be built differently. Lab animals are bred to have that gene to see if the difference can be reproduced.

It's working from big to small, from observable to reproducible and repeatable. Then after you have the small piece, you can work back up to how it fits in to the bigger picture, back and forth to make all the connections.

Well the link you provided said,

Smoller noted these genetic risk factors may only account for a very small part of the risk driving these disorders, and just how big a share they account for isn't yet known.

http://healthyliving.msn.com/disease...and-depression

So as far as we know, these linked genes are not determined as " responsible". (meaning not sure if they are directly involved as a driving force).

Lunacie
03-01-13, 08:21 PM
Not all people who carry these genes develop psychiatric disorders. (Same with other genes shown to be related to ADD)

What environmental factors are involved in gene expression,

that might result in a actual psychiatric disorder?

Does the research mention anything about similar environmental factors that might be involved in the actual expression of these genes ?

Why don't all people with these genes develop a disorder?


.

Maybe all people with this set of genes do develop one of these disorders,
but maybe it's missed because it's borderline by that doctor's judgment.

silivrentoliel
03-01-13, 10:23 PM
bit of a bunny trail, but kind of on topic... I hope :D

Wouldn't it be awesome if they could test, prenatally, for things like ADHD, AS, BP, etc and run your specific DNA codes into some spiffy machine and create the perfect medication for what you'd need?

I don't actually see that happening, but it would be cool nonetheless.

mildadhd
03-01-13, 11:14 PM
Maybe all people with this set of genes do develop one of these disorders,
but maybe it's missed because it's borderline by that doctor's judgment.

sorry I replied

Lunacie
03-01-13, 11:27 PM
Why would any conditions be borderline, if things where magically just genetic only? Because conditions are not just genetic only.

Catch the Lucky Charms, they're magically genetic. :rolleyes:

Time for me to go to bed before I write something that will get me into trouble. :mad:

... maybe you should log off too ...

SB_UK
03-02-13, 04:53 AM
I think that the whole point of

find a genetic predisposition -> find a broken protein -> find a chemical agonist which restores function

(all of which is a complete fantasy)

- is to eliminate it as a strategy for combating complex genetic diseases.

It's the easy option - where we need to disprove the easy option (maybe??) before the harder option - of social/environmental change is embraced.

However - there is a possibility (as appears to be happening in the calcium channel story underlying psych. disease) ... ... that the genetics approach 'll unambiguously nail a system which is affected by stress (psych. / phys.) in which case - the impressive body of information accumulated in the molecular sciences can be twisted from taking us the wrong way down a one way street ... ... into pushing us violently in the correct direction (towards societal change).

The sole problem we have- is how hard we're willing to look, before we announce that there's no strong genetic component to complex disorders.

The search need not be called off ... ever ... there's always a more rigorous search in genetics to affect; imagine collecting the entire genome, the entire transcriptome in every accessible cell type under every environmental challenge possible ... ... and so it continues ... ... the mol. genetic approach has no natural end-point ... ... can continue and continue.

The numbers involved in current genetic case-control studies are huge (hundreds of thousands to millions of people studied in the last 2 studies looked at with Lunacie)
- at which point do people put their hands up and announce that not only are complex disorders very much less 'genetic' than monogenic disorders

- but we can't do anything about the far simpler monogenic disorders anyway (apart from in very, very rare cases - for vast amounts of money) ... ... and so why did we ever pursue this approach in the first place (see above) ... ... and when have we travelled sufficiently far down the route of disproving a paradigm - to call it a day ?

I wonder whether current medical research will begin funding NASA in order to find complex disorders on other planets as replication dataset - having run out of sick people on this planet to study, have we.

SB_UK
03-02-13, 05:06 AM
Now ... rewinding 10 years back on site -
there's a desperate nature to those types of study

There certainly is.

No scientific study should ever turn into an ever more desperate fishing expedition - at the end of each and every properly scientific study - we should be better off - not drowning ever further in masses of inconclusive data.

As it happens though - I'm pretty sure that we can down tools now - and synthesize all currently available data into a story which'll permit us to prevent complex human disease.

To eliminate human suffering using the data which we've accumulated to date.

Problem is - is that with an eradication of human disease - comes unemployment to disease specialists.

The same is true in any discipline - prevent the need (empower other people) - and you are rendered unemployed.

The nature of the economic system encourages forcing dependence on other people - and not setting other people free; this environmental motivation (which reflects a primitive internal motivation) is what we're required to combat, in order, so we shall see
- and thankfully - to render ALL people (all workplace assignments) simultaneously excess to requirement in a properly social organism.

I'm trying to suggest that we're confounded from making a better (STRESS-LESS) world in an external environment (monetary based economy which forces the ownership (of stuff and knowledge) paradigm) which prevents an internal motivation (to compete against other people and beat them) from being transcended.

It's this internal motvation (to compete against other people and beat them)which we're seeking to transcend which results in stress, which results in the common, complex disorders which we're seeking to solve.

SB_UK
03-02-13, 05:15 AM
It's this internal motvation which results in stress, which we're seeking to transcend.

All of which is impossible in a monetary-based economy which prevents the internal motivation from being transcended - by reward-reinforcing its maintenance (strengthening its hold over us) ... ... driving its control over our behaviour ... ... and not (as we require) ... ... supporting its loss.

SB_UK
03-02-13, 05:31 AM
Disease as human beings are forced out of the physiological state/space.

Severe disease as human beings are subject to chronic stress - keeping people (chronically) out of the physiological space.

There's only one chronic stressor which we need to consider - the stress from having to earn an immoral construct (money) for an immoral task (everything done in the workplace - as explained above)
- because it contravenes our highest defining property (mind/conscience) and is completely impossible for the average human being to escape from.

That's all there is to it.

Chronic stress -> leads to -> the diseases of Western living (which fire off in gestation (maternal stress elevating foetal stress in utero, post-natal depression in mother) ... ... at each and every stage in life - from fast catch-up growth in Syndrome X (baby growing too fast) ... asthma/ADHD in early childhood - through acne at puberty into diabesity turns into auto-immune disease courts cancer (stress hormone connection) - with Alzheimer's (informally renamed Type III diabetes) disease waiting to greet us in the twilight years
... ... if we're 'lucky' ???? enough to make it that far.

And all because of an inhuman (immoral) environmental societal infrastructure which human beings have no choice other than to adhere to.

Earn money or die.

SB_UK
03-02-13, 05:44 AM
It's just that stress is physiology's way of optimising itself (of putting the individual into a 'happy' place) - if 'stressed' tben strive to minimise stress ... ... as physiology's approach to ensuring happy survival of the organism.
... ...jus' that physiology of the organism didn't reckon on a stressor in existence - which the individual (alone) was completely incapable of eliminating exposure to alone.

Eliminating money (and settling into a properly social/moral societal infrastructure) from the planet is the solution to human disease - ALL of them.

Amtram
03-02-13, 11:23 AM
Actually, I think the biggest moral issue in tracking down the genetic bases of whatever condition it is is something we've already seen in places where testing for gender has been popular.

Forget about the money, forget about the post-birth societal and emotional environment.

The moral issue about finding the genetic basis for a condition is that it opens the doors to reproductive prohibitions on people who carry the relevant genes, and either the option to or compulsion to have fetal genetic testing done and eliminate the carriers of the genes in question before they can be born.

TygerSan
03-02-13, 12:23 PM
SB, have you read any of the default mode network stuff about ADHD?

There's been talk about very slow oscillatory activity in these attentional networks being linked to the response variability seen in the disorder:

http://www.plosone.org/article/info:doi/10.1371/journal.pone.0017325

And the more general search: http://www.ncbi.nlm.nih.gov/pubmed/?term=low+frequency+oscillations+ADHD

It's honestly been a while since I've followed this literature, but one thing that dopamine seems to do is to prevent such low frequency waves from spreading (i.e., if you damage dopamine neurons in the motor circuits of the basal ganglia, you get propogation of these low-frequency signals throughout the circuit in a way that doesn't happen when dopamine is present)

http://www.ncbi.nlm.nih.gov/pubmed/17112675

So, there is vast possibility for oscillatory activity 1) determining and correlating with symptoms 2) this activity is at least somewhat regulated by dopamine status (though the relationships between the two are complex).

http://onlinelibrary.wiley.com/doi/10.1002/mds.10358/abstract;jsessionid=20F30B7BCA8A4497BBC87515927967 56.d03t04?deniedAccessCustomisedMessage=&userIsAuthenticated=false

SB_UK
03-03-13, 10:45 AM
The moral issue about finding the genetic basis for a condition is that it opens the doors to reproductive prohibitions on people who carry the relevant genes, and either the option to or compulsion to have fetal genetic testing done and eliminate the carriers of the genes in question before they can be born.

Is an issue - but we'll find that the research community - in the more common diseases - won't come up with a small list of genes which lead to disease - and so we don't really need to consider the issue.

If there were 1 disease gene which carried a 'death' sentence to chronic disease (per disease) then we'd absolutely need to consider the GATTACA type problem of mandatory testing and sterilization of those who're unfortunate enough to carry such a variant ... ... just though that - that story won't ever come to pass - enough genetic studies have been conducted in all the common diseases - to know that that we've safely passed that scenario.

SB_UK
03-03-13, 11:06 AM
SB, have you read any of the default mode network stuff about ADHD?

There's been talk about very slow oscillatory activity in these attentional networks being linked to the response variability seen in the disorder:

http://www.plosone.org/article/info:doi/10.1371/journal.pone.0017325

And the more general search: http://www.ncbi.nlm.nih.gov/pubmed/?term=low+frequency+oscillations+ADHD

It's honestly been a while since I've followed this literature, but one thing that dopamine seems to do is to prevent such low frequency waves from spreading (i.e., if you damage dopamine neurons in the motor circuits of the basal ganglia, you get propogation of these low-frequency signals throughout the circuit in a way that doesn't happen when dopamine is present)

http://www.ncbi.nlm.nih.gov/pubmed/17112675

So, there is vast possibility for oscillatory activity 1) determining and correlating with symptoms 2) this activity is at least somewhat regulated by dopamine status (though the relationships between the two are complex).

http://onlinelibrary.wiley.com/doi/10.1002/mds.10358/abstract;jsessionid=20F30B7BCA8A4497BBC87515927967 56.d03t04?deniedAccessCustomisedMessage=&userIsAuthenticated=false

Excellent stuff.
That's exactly what I've just been thinking about - the theme of dissociation.

from this point:
http://www.addforums.com/forums/showpost.php?p=1452892&postcount=31

into http://en.wikipedia.org/wiki/Default_network
"The default network is an interconnected and anatomically defined brain system that preferentially activates when individuals engage in internal tasks such as daydreaming, envisioning the future, retrieving memories, and gauging others' perspectives. It is negatively correlated with brain systems that focus on external visual signals."

-*-

Dissociation from the external world - as happens in daydream, deep concentration/writing ... ... associating with the production of dissociativws - whcih make us feel happy.

Dissociatives driving on an empty highway versus loss of dissociative in a traffic jam (road rage).

Personally - I'm only happy in the dissociative state - be it thinking at the computer, robotically acting, daydreaming ... ... ... hate speaking - hate thinking about anything which isn't worth considering (eg how to make money a fair system when it's by definition unfair ... ... ie thinking up solutions to problems which cannot be solved).

Amtram
03-03-13, 11:23 AM
However. . .there is also a moral issue in not trying to find the genetic basis for conditions, illnesses, and susceptibility to them. That moral issue is that not trying to find a treatment that will improve longevity and quality of life for people who already have these conditions and predispositions until you can figure out some way of addressing them without getting into treatment options, you are causing unnecessary human suffering.

Except in most cases of communicable diseases, the susceptibility at the very least is going to have some genetic component. When there is an environmental factor that would trigger or activate a condition, knowing that the genetic predisposition exists allows preventive interventions that may not be appropriate or necessary for the population at large. Exploring the genetics not only gives us good information for the overall study of all the life sciences, but also gives us the potential to discover the most effective interventions for specific individuals, whether those are pharmaceutical, cognitive, behavioral, or risk avoidance.

SB_UK
03-03-13, 12:51 PM
However. . .there is also a moral issue in not trying to find the genetic basis for conditions, illnesses, and susceptibility to them. That moral issue is that not trying to find a treatment that will improve longevity and quality of life for people who already have these conditions and predispositions until you can figure out some way of addressing them without getting into treatment options, you are causing unnecessary human suffering.

Except in most cases of communicable diseases, the susceptibility at the very least is going to have some genetic component. When there is an environmental factor that would trigger or activate a condition, knowing that the genetic predisposition exists allows preventive interventions that may not be appropriate or necessary for the population at large. Exploring the genetics not only gives us good information for the overall study of all the life sciences, but also gives us the potential to discover the most effective interventions for specific individuals, whether those are pharmaceutical, cognitive, behavioral, or risk avoidance.


... ... is the theory ... ... but not how it works out in practice.

In practice - a phenomenal amount of money is spent trying (and failing) to find the smallest contributors to disease - whilst preventative schemes are pushed to one side.

One researcher into the genetics of infectious disease susceptibility volunteered the information that if all of the money being spent on genetics was to be pushed into setting up safer habitats - that actual (as opposed to more) good 'd be done.

The entire molecular genetics paradigm is being pushed because we can and not because we should.

Because we can, because many people have developed an expertise in these areas, because when all you have is a hammer - everything's a nail.

It's time for the new 'omics to recover itself by making it clear that there are no clear genes underlying major disease - and that there's an alternative and attractive other explanation for the alarming rise in Western disorders - which is in line with all available (including molecular genetic) data
- with that being the stress of our collective existence in a monetary/materialist based economy/world.

At its root - the stress of existence in a monetary based economy will wipe out nonADDers and ADDers alike - but ADDers more so.

Amtram
03-03-13, 02:17 PM
What explains the presence of these illnesses in populations that don't have a monetary-based economy? What explains the presence of stress in populations that don't have monetary-based economies? What explains these "Western" disorders and ongoing stressors in decidedly non-Western populations with non-western diets and non-western social systems and non-western views of materialism?

It being the case that stress and illness and developmental disorders exist in all social structures all around the world, there is a stronger case for genetic correlation for population-wide conditions than there is for societal correlation.

mildadhd
03-03-13, 07:47 PM
What explains the presence of these illnesses in populations that don't have a monetary-based economy? What explains the presence of stress in populations that don't have monetary-based economies? What explains these "Western" disorders and ongoing stressors in decidedly non-Western populations with non-western diets and non-western social systems and non-western views of materialism?

It being the case that stress and illness and developmental disorders exist in all social structures all around the world, there is a stronger case for genetic correlation for population-wide conditions than there is for societal correlation.

None of these thoughts, rule out stress, population wide.

None of these thoughts make a stronger case for genetic correlation, population wide.

Stress is a major factor in gene expression.

Stress can make it more likely.

Predisposition can make it more likely.

It is both (or more)

It could be argued that stress is a decisive factor,

because people don't need to have a genetic predisposition to express the genes involved with ADD.

Also if we are discussing treatment, we can't change the genes, we can change the environment.(stress)

I think it is more than very fair to say both (or more) when including all ADDers, in a general discussion.

Because I am a Bothist.

Bothism (or more) 50 : 50 when discussing all ADDers in general.

50 : 50 doesn't point fingers/blame,

and is consistent with the facts.


.

Amtram
03-03-13, 08:47 PM
Psychologists have, for years, used scaling methods to rate stress levels (http://www.mindtools.com/pages/article/newTCS_82.htm), and a good deal of what goes into those ratings depends upon what the stress inducer is. The stress of having a terminal illness is not the same as the stress of caring for someone with a terminal illness, for example. The stress of being socially unacceptable because of being overweight is different from the stress of being socially unacceptable because of a severe facial deformity.

So as long as you're using such a broad term as "stress," you might as well be saying "stuff" instead.

I've expressed multiple times that neither nature nor nurture operates in a vacuum. One may bear more responsibility than the other in a particular case, but each case is different enough that using general rather than specific terms does not clarify things, but instead muddies the waters of understanding.

You can say that "germs" cause a disease, but that's of no help at all in diagnosing or treating the disease. You need to be specific - is it a virus, or a bacterium, or maybe a parasite? Is it one that is killed by antibiotics? What area of the body does it attack? Did you get it from touching something, or breathing something, or did it have to get directly into your bloodstream?

This, and this alone, is why I raise objections when the topic of "stress" comes up. Is it long-term, or short term? Is it related to a physical, mental, or social cause? Does it originate from one particular area of life, such as work, school, or family, or somewhere else? Is it impacted by too many available choices, or too few? Does it involve other people, or is it primarily internal?

If you look at the scale I linked above, you'll see that at the top is "death of a spouse," with a rating of 100. At the bottom of the scale are "Christmas," with a rating of 12, and "minor violations of the law," with a rating of 11. If you don't distinguish what you mean by "stress," then what you're essentially saying is that "christmas shopping and traffic tickets can cause this thing," which is clearly not true.

And with such a wide variance in "stress," and the complexity of not only the human genome but human biological diversity, nothing is a nice, easy split down the middle. Each condition, and to an extent each individual, is going to have some fluctuation as to what factors have the most impact.

mildadhd
03-03-13, 11:03 PM
Psychologists have, for years, used scaling methods to rate stress levels (http://www.mindtools.com/pages/article/newTCS_82.htm), and a good deal of what goes into those ratings depends upon what the stress inducer is. The stress of having a terminal illness is not the same as the stress of caring for someone with a terminal illness, for example. The stress of being socially unacceptable because of being overweight is different from the stress of being socially unacceptable because of a severe facial deformity.

So as long as you're using such a broad term as "stress," you might as well be saying "stuff" instead.

I've expressed multiple times that neither nature nor nurture operates in a vacuum. One may bear more responsibility than the other in a particular case, but each case is different enough that using general rather than specific terms does not clarify things, but instead muddies the waters of understanding.

You can say that "germs" cause a disease, but that's of no help at all in diagnosing or treating the disease. You need to be specific - is it a virus, or a bacterium, or maybe a parasite? Is it one that is killed by antibiotics? What area of the body does it attack? Did you get it from touching something, or breathing something, or did it have to get directly into your bloodstream?

This, and this alone, is why I raise objections when the topic of "stress" comes up. Is it long-term, or short term? Is it related to a physical, mental, or social cause? Does it originate from one particular area of life, such as work, school, or family, or somewhere else? Is it impacted by too many available choices, or too few? Does it involve other people, or is it primarily internal?

If you look at the scale I linked above, you'll see that at the top is "death of a spouse," with a rating of 100. At the bottom of the scale are "Christmas," with a rating of 12, and "minor violations of the law," with a rating of 11. If you don't distinguish what you mean by "stress," then what you're essentially saying is that "christmas shopping and traffic tickets can cause this thing," which is clearly not true.

And with such a wide variance in "stress," and the complexity of not only the human genome but human biological diversity, nothing is a nice, easy split down the middle. Each condition, and to an extent each individual, is going to have some fluctuation as to what factors have the most impact.

Considering "stuff" (stress) during the time of early development is very important.

ADD is developed very early in life, when specifically humans infants are very sensitive in general and very influenced/shaped by both good and bad experiences.

As we grow older we are less influenced by experience.

I recommend you research Dr.Bruce Perry's work,

he has a lot of good information on the topic of early life experience and the influence of experiences on early brain development.

Amtram
03-04-13, 11:37 AM
I do consider stress. And chemicals. And diet. And sleep. However, each of these is both qualitative and quantitative, and can't be grouped together in a single category and measured on a single continuous scale.

I have read Dr. Perry. The kind of stress he is talking about is traumatic and postnatal.

He is not talking about maternal prenatal stress that would activate the endocrine system and put hormones into the fetal bloodstream that would affect gene expression.

He is not talking about maternal dietary stress, which would include food scarcity that would induce ketosis, which would influence the chemistry of fetal blood, or overconsumption of chemicals in food or beverage that might enter the fetal bloodstream, or obesity that would affect glucose levels and affect fetal glucose levels.

I could go on, but the point is that if we are talking about something genetic, whether it's gene-determined or gene-influenced or gene-predisposed, then it's extremely important that we keep in mind that it's the chemicals that influence gene expression.

Not all genes will be affected by all chemicals. Not all chemical exposures will hit the right place and the right time to influence the vulnerable genes. Not all chemicals are ingested, inhaled, or otherwise absorbed into the system. And not all stress produces chemicals that affect gene expression.

So it is vital to be specific. It is essential to differentiate stressors and environmental factors and social factors and emotional factors and so on, because they each have unique effects that disappear in a poof of statistics if they're lumped together in a single category.

mildadhd
03-04-13, 02:20 PM
I do consider stress. And chemicals. And diet. And sleep. However, each of these is both qualitative and quantitative, and can't be grouped together in a single category and measured on a single continuous scale.

I have read Dr. Perry. The kind of stress he is talking about is traumatic and postnatal.

He is not talking about maternal prenatal stress that would activate the endocrine system and put hormones into the fetal bloodstream that would affect gene expression.

He is not talking about maternal dietary stress, which would include food scarcity that would induce ketosis, which would influence the chemistry of fetal blood, or overconsumption of chemicals in food or beverage that might enter the fetal bloodstream, or obesity that would affect glucose levels and affect fetal glucose levels.

I could go on, but the point is that if we are talking about something genetic, whether it's gene-determined or gene-influenced or gene-predisposed, then it's extremely important that we keep in mind that it's the chemicals that influence gene expression.

Not all genes will be affected by all chemicals. Not all chemical exposures will hit the right place and the right time to influence the vulnerable genes. Not all chemicals are ingested, inhaled, or otherwise absorbed into the system. And not all stress produces chemicals that affect gene expression.

So it is vital to be specific. It is essential to differentiate stressors and environmental factors and social factors and emotional factors and so on, because they each have unique effects that disappear in a poof of statistics if they're lumped together in a single category.


The quote below simply is not true.(more specifics upon request)


He is not talking about maternal prenatal stress that would activate the endocrine system and put hormones into the fetal bloodstream that would affect gene expression.


Why is everything else but genetics just a "poof" to you.

There is so much research, that I and others have posted here at the forums,

discussing these same topics.

But you ignore it all, so I'm not going to keep posting the research information in this thread unless you or some asks about specifically.

In my opinion you have already made up your mind, that environment isn't a factor.

Which is totally your right.

But this thread was posted to explore new ways measuring/understanding and new treatment.

I think that would be done best by looking at the whole picture.


I don't deny the genetic factors you can present.

I am not sure why you deny the environmental factors?

And I would like to request from you specific evidence that ADD is totally genetic and rules out environment?


I have never seen any. Has anyone else?



If anyone wants to see specific research on any of these topics I would be happy post some on request.


i!i