Adderall and HPPD?

[qhqhzn]

I did a quick search on your disorder and it is referred to as a "disinhibition of visual processing related to loss of serotonin receptors on inhibitory neurons". I think that amphetimines in general have MAOI action, so there should be an increase of serotonin.

Where did you find the quote above? It's somewhat inline with current medical thinking, not that that advances much. The usual thinking is that the above neurons which Dr Abraham calls the "inhibitory GABA circuit in the visual pathway" are 5ht2a on one end and GABA on the other, that LSD (usually) damages the 5ht2a bit, but you can still stimulate the neurons with GABAergic drugs, so they offer some relief. Even Dr. Abraham is skeptical that actual "brain damage" has been done though, since there's no way of imaging HPPD except a minor difference in qEEG.

My knowledge ends there, sort of. LSD and risperidone both stimulate postsynaptic 5 ht2 receptors, possibly on the same neurons that the GABA drugs work on, if indeed they have receptors for both, except that LSD and risperidone both make HPPD wose. I don't understand why stimulating the same neurons with GABA makes HPPD better, but maybe someone with a better understanding of neuroscience would. It might explain why amphetamines seem to temporarily help.

 

[seep]

My knowledge ends there, sort of. LSD and risperidone both stimulate postsynaptic 5 ht2 receptors, possibly on the same neurons that the GABA drugs work on, if indeed they have receptors for both, except that LSD and risperidone both make HPPD wose. I don't understand why stimulating the same neurons with GABA makes HPPD better, but maybe someone with a better understanding of neuroscience would. It might explain why amphetamines seem to temporarily help.

The GABAa receptor has a benzodiazepine site; when a benzo molecule binds to the site it rearranges the receptor so that it has a higher affinity to GABA. GABA then binds to its site on the receptor and opens the ion channel. Skipping the complicated electrochemical details, lets just say that the opening of this channel inhibits 5-HT2a activity (je crois).

Wait. What's there to be said about aripiprazole? It's a D2 partial agonist and a 5-HT2a antagonist. Wouldn't this be ideal for HPPD? It has zero abuse potential.

 

[Sykoknot]

But this the very definition of Low Latent Inhibition. LLI has 2 major causes: psychosis and/or dopamine agonism. This is what I meant by counterintuitive.

Oh BTW, I meant do you get phosphenes while on amp?

No sleep deprivation, excessive daytime sleepiness, cataplexy, anterograde amnesia, delusion, dissociative episodes, depersonalization, paranoid ideation?

No noticed phosphenes during the duration of the amp.
Yes, mild sleep dep, daytime sleepiness, dissociative episodes, paranoid ideation. I have struggled with insomnia my whole life though, though the symptom has been worsened by hppd, and more recently parnoid looping due to a LSD trip. see this http://www.bluelight.ru/vb/showthread.php?t=462916
I belive LLI and HPPD are extremely related. HPPD being a catalyst for LLI maybe?
Had the thought, also, that HPPD, like a drug, manifests differently in different people. Therefor drugs will effect your HPPD on a personal psychological level.

If what i am saying seems irrelevant let me know.
My knowledge in pharmacology of stimulants is low.
My thoughts come from intuition rather than fact.

 

[Gormur]

Gormur: 296.64

well to be clear, i was formerly diagnosed with borderline personality disorder, schizotypal personality w/thought disorder, bipolar II. then separately with ADD and dyslexia (the latter recently, the former when starting pre- school followed by years of cognitive therapy

obviously a lot of this shit overlaps so all i can really do is explain my experiences and go from there. i'm sure when it comes down to it, i as well as many others here have symptoms that meet some but not all requirements for HPPD or PTSD, so i think it's kind of relative the way these terms get thrown around.... yes i have persistent visual/aural distortions, but dissociation, mood and anxiety that may or may not accompany them could be called bipolar or schizo symptoms as well

in any case, i'd venture to say a lot of people who use psychedelics are different from the norm and indeed many have psychological isssues they seek to resolve with alterative methods- psychedelics. nothing wrong with that.

- i'd say people who are unusually talented or smart in certain areas may benefit more from drug treatment than therapy... few people can relate to them, and this feeling of misunderstanding and isolation is where things like dissociation and perceived rejection come in

trying to escape reality through dissociation is problematic if it's the main goal of someone, in any case, in the long-run... but obviously lsd isn't the only substance people use for such

it has its purposes, tho i don't think that it's for everyone..

peace

 

[seep]

well to be clear, i was formerly diagnosed with borderline personality disorder, schizotypal personality w/thought disorder, bipolar II. then separately with ADD and dyslexia (the latter recently, the former when starting pre- school followed by years of cognitive therapy

ADD and dyslexia are beside the point. Also, unless you're under 18, the personality disorders are appended and subordinate to the underlying condition. The value of 296.64 is that it accounts for the symptoms collectively (as a syndrome) instead of piecemeal.

I don't think bipolar II accommodates psychotic features well because the fifth digit is fixed as a 9. Also, BP-II must be ruled out if there has ever been a manic episode (the difference between mania and hypomania is anything but subtle).

Schizoaffective disorder is also often conflated with BP-I, but is way over-diagnosed IMHO. I've always thought of it as a clinician's way of covering his ass in case tardive dyskinesia ensues from elephant doses of antipsychotics. Also, about this HPPD business: it cannot be diagnosed if the symptoms are better accounted for by another mental disorder.

Think of DSM as an extremely rigorous flowchart, not a surrogate for objective reality.

To the OP: LLI is a symptom, not a syndrome.

 

[ShaolinBomber]

The current consensus for the theory of HPPD amongst the researchers at Harvard medical is that theres been a loss of 5-ht2a receptor subtypes on GABAergic inhibitory neurons. Normally, when serotonin binds to these GABAergc neurons, it releases GABA. GABA output=inhibition=calm.

Without this necessary negative feedback loop between the serotonergic and GABAergic systems, you have a disruption in the key process of GABA release in the neocortex (specifically the visual cortex of course) and you have excess exctitation where one's brain with HPPD cannot calm down excitatory currents as quickly/easily/normally than before. So you're left with visual disturbances that linger because the brain cannot shut off what its just seen as quickly as before. This is why afterimages, trails, etc. are cookie cutter disturbances with HPPD.

LSD binds to 5-ht2a receptors and excites them. MDMa binds to 5-ht2a receptors. Psilocybin binds to 5-ht2a receptors. Each have their own unique way of interacting with neurons, BUT its SIMILAR. You have to look at how all Lowest common denominator (drugs that cause HPPD) operate, and then observe what the problem is. Well, since all these drugs interact at the same parts of the synaptic cleft, then you have to assume that this is where the problem lies.

Dr. A was the first to recognize this and thats where he began his research.

Anyways, to the OP. Strong stimulants usually are reported to increase visuals with HPPD. I have not yet tried a strong stimulant, and now that i think about it, i've never done any kind of amph in my life,except for MDMA, so i cant give my opinion for you. If i ever do decide to try adderall i will let you know how it goes.

What i can tell you is that when i take an opiate, my visuals calm down quite a bit. Now granted, im on klonopin when i take opiates, BUT i already know what kind of relief i get from klonopin so i can distinguish between the 2.

 

[seep]

The current consensus for the theory of HPPD amongst the researchers at Harvard medical is that theres been a loss of 5-ht2a receptor subtypes on GABAergic inhibitory neurons. Normally, when serotonin binds to these GABAergc neurons, it releases GABA. GABA output=inhibition=calm.

I was under the impression that 5-HT2a activity was inversely proportional to the activity of the ion channel: hence the efficacy of 5-HT2a antagonists in treating benzo withdrawal.

LSD binds to 5-ht2a receptors and excites them. MDMa binds to 5-ht2a receptors. Psilocybin binds to 5-ht2a receptors. Each have their own unique way of interacting with neurons, BUT its SIMILAR. You have to look at how all Lowest common denominator (drugs that cause HPPD) operate, and then observe what the problem is. Well, since all these drugs interact at the same parts of the synaptic cleft, then you have to assume that this is where the problem lies.

Doesn't this contradict your 1st 2 paragraphs? How does the same process that enables geometric hallucinations and hypervigilance also ameliorate these symptoms? Not debating you, just curious.

What i can tell you is that when i take an opiate, my visuals calm down quite a bit. Now granted, im on klonopin when i take opiates, BUT i already know what kind of relief i get from klonopin so i can distinguish between the 2.

Now I'm debating. You realize there's serious synergy between the two? I found this out the hard way many years ago. Also, when you take the opioid by itself, you will get pretty elaborate hallucinations so long as you don't pass out. I mention this because of the possibility of daytime parahypnogogia or some permutation of narcolepsy exacerbating the HPPD symptoms. Thus the efficacy of the amp would be due to it's antisoporific qualities.

 

[permastoned]

Weird.. my HPPD is always augmented, rather than dissipated, by amphetamine.

http://www.bluelight.ru/vb/showthread.php?t=446372

 

[qhqhzn]

The GABAa receptor has a benzodiazepine site; when a benzo molecule binds to the site it rearranges the receptor so that it has a higher affinity to GABA. GABA then binds to its site on the receptor and opens the ion channel. Skipping the complicated electrochemical details, lets just say that the opening of this channel inhibits 5-HT2a activity (je crois).

Wait. What's there to be said about aripiprazole? It's a D2 partial agonist and a 5-HT2a antagonist. Wouldn't this be ideal for HPPD? It has zero abuse potential.

Thanks for this. Regarding aripiprazole, some have reported success on another forum, (though a lot of HPPDers are adverse to antipsychotics because of the stigma and the side effects, as well as the LSD-mimicking risperidone experience some of us had...).

What i can tell you is that when i take an opiate, my visuals calm down quite a bit. Now granted, im on klonopin when i take opiates, BUT i already know what kind of relief i get from klonopin so i can distinguish between the 2.

Opiates tend to increase my visuals a little bit, especially when trying to sleep afterwards. Then again, so does going on aeroplanes, again, afterwards (!?!). The psychological factors are so big, I don't think I've ever noticed a drug that increased visuals more than the brain was capable of doing on its own semi-randomly, nor unfortunately, reducing them.

 

[seep]

Tangent:

What is BMS-820836? Is this one of the TRIs that BMS has in its pipeline?

 

[ShaolinBomber]

I was under the impression that 5-HT2a activity was inversely proportional to the activity of the ion channel: hence the efficacy of 5-HT2a antagonists in treating benzo withdrawal.



Doesn't this contradict your 1st 2 paragraphs? How does the same process that enables geometric hallucinations and hypervigilance also ameliorate these symptoms? Not debating you, just curious.


Now I'm debating. You realize there's serious synergy between the two? I found this out the hard way many years ago. Also, when you take the opioid by itself, you will get pretty elaborate hallucinations so long as you don't pass out. I mention this because of the possibility of daytime parahypnogogia or some permutation of narcolepsy exacerbating the HPPD symptoms. Thus the efficacy of the amp would be due to it's antisoporific qualities.

Binding of neurotransmitters opens the ion channels. This is the chemical reactions of all neurotransmiter binding. This is what makes the plasma membrane of the neuron more excitable or less excitable.

I'm not sure what the question is here, but i will answer it as i have interpreted it. 5-ht2a/c serotonin receptors are mainly located upon post-synaptic GABAergic cells. When serotonin or a serotonin agonist binds them, they excite it. If you're referring to taking serotonin supplements or whatever to ameliorate symptoms, its totally off. Yet, when you take medications that slow down neurotransmitter communication and increase GABA efficiacy in inhibitoy GABAergic cells, you induce a synthetical state of calmness. There is no help from serotonin with benzodiazepine drugs are administered.

i am aware that opiate act upon dopamenergic cells and both OC and klonopin calm nerve impulses in their different ways. I did not however realize how much they would actually work well with eachother. I still have experimenting and obviously i lil reading i need to do.


Please respond back with any questions.

 

[Bell Ringer]

Do you take anything else regularly?

My initial impression is that Adderall would increase your HPPD, but after thinking things over....

Well, let's assume that Adderall does decrease your preception of HPPD's symptoms. It could be due to an increase in norepinephrine. Adderall is a norepinephrine agonist. It is also a dopamine agonist. Some dopamine degrades (wrong word but I'm tired) norepinephrine. Norepinephrine increases one's fight or flight response which would distract you from less essential things such as your HPPD.

take this with a grain of salt. This was written off the top of my head.

Long term I predict that the adderall may actually increase the severtity of HPPD.

BTW I had HPPD for years. I enjoyed it and actually miss it.

 

[seep]

Binding of neurotransmitters opens the ion channels. This is the chemical reactions of all neurotransmiter binding. This is what makes the plasma membrane of the neuron more excitable or less excitable...I'm not sure what the question is here, but i will answer it as i have interpreted it. 5-ht2a/c serotonin receptors are mainly located upon post-synaptic GABAergic cells. When serotonin or a serotonin agonist binds them, they excite it. If you're referring to taking serotonin supplements or whatever to ameliorate symptoms, its totally off. Yet, when you take medications that slow down neurotransmitter communication and increase GABA efficiacy in inhibitoy GABAergic cells, you induce a synthetical state of calmness. There is no help from serotonin with benzodiazepine drugs are administered...i am aware that opiate act upon dopamenergic cells and both OC and klonopin calm nerve impulses in their different ways. I did not however realize how much they would actually work well with eachother. I still have experimenting and obviously i lil reading i need to do.

Before I say anything else, what I meant by "learned this the hard way" was flatlining after trying to boost 120 mg of IV heroin with 6 mg of alprazolam. Be careful.

In post 25 you give a detailed explanation of the set of neurological events that cause HPPD. Summary of what you say: 5-HT2a receptor density diminishes in the visual cortex after chronic hallucinogen use. Since activation of this receptor is necessary for the production of GABA molecules, synaptic GABA levels decrease and the GABAa receptor is unable to open.

I'm simply rephrasing this: if fewer 5-HT2a receptors are present, fewer extracellular chloride ions are needed (I wasn't talking about all ion channels, just GABAa). So then how is it that the messenger that enables the positive symptoms of HPPD be absent and active at the same time?

Maybe we're looking at this from opposite frames of reference.

 

[permastoned]

Opiates also increase my HPPD.

 

[Sykoknot]

I smoke weed daily, which i know boosts my HPPD.
So maybe the amph gets rid of the boost from cannabis, and its own boost is much weaker.
?

 

[ShaolinBomber]

Before I say anything else, what I meant by "learned this the hard way" was flatlining after trying to boost 120 mg of IV heroin with 6 mg of alprazolam. Be careful.

In post 25 you give a detailed explanation of the set of neurological events that cause HPPD. Summary of what you say: 5-HT2a receptor density diminishes in the visual cortex after chronic hallucinogen use. Since activation of this receptor is necessary for the production of GABA molecules, synaptic GABA levels decrease and the GABAa receptor is unable to open.

I'm simply rephrasing this: if fewer 5-HT2a receptors are present, fewer extracellular chloride ions are needed (I wasn't talking about all ion channels, just GABAa). So then how is it that the messenger that enables the positive symptoms of HPPD be absent and active at the same time?

Maybe we're looking at this from opposite frames of reference.

By positive symptoms i'm guessing you're referring to the symptoms that are listed under the DSM as HPPD symptoms, and by messenger im guessing you're referring to GABA. The theory of the loss of 5-ht2 receptor sites being a cause of the problem would be problematic because there would be less binding of serotonin to GABAergic cells and this would decrease GABA output. Serotonin usually acts as an excitatory neurotransmitter. However, in the case of the feedbackloop between the serotonergic and GABAegic cells, it assumes an inhibitory role. Serotonin does excite GABAergic cells to my understand but this excitation is a millioneth of a second and all reactions after that are inhibitory.

Serotonin is not the problem here. Its the binding sites that are the problem. You have to have a receptor for a neurotransmitter to bind to. Normally, when 5-ht2 receptors are bound to and opened on GABAergic cells, it causes the release of GABA to calm the excitatory current. This is the negative feedback loop between the serotonergic and GABAergic system.

The theory=less 5-ht2 subtypes=less seronergic binding opportunities=less GABA output=widespread occipital, temporal, and parietal disinhibtion=somatosensory problems(possibly an explanation for dissociation symptoms in some HPPD patients) and visual distortions among other problems that have been reported by HPPD sufferers.

 

[seep]

Yo.

By positive symptoms i'm guessing you're referring to the symptoms that are listed under the DSM as HPPD symptoms, and by messenger im guessing you're referring to GABA.

Positive symptoms is simply the antonym for Negative Symptoms. A negative symptom involves "the loss or absence of normal traits or abilities. Here, PS include geometrical hallucinations, peripheral illusions, aberrations in chromatic perception, trails, phosphenes, positive (in the photographic sense) afterimages, nimbii, macropsia and micropsia (and a buttload of others the current DSM doesn't list). NS here would be the consequent "clinically significant distress or impairment in social/occupational/etc. functioning." As well as the loss of baseline latent inhibition.

By messenger I meant the serotonin and 5-HT2a receptor pathways that are implicated in the manifestation of the aforementioned positive symptoms.

The theory of the loss of 5-ht2 receptor sites being a cause of the problem would be problematic because there would be less binding of serotonin to GABAergic cells and this would decrease GABA output. Serotonin usually acts as an excitatory neurotransmitter. However, in the case of the feedbackloop between the serotonergic and GABAegic cells, it assumes an inhibitory role. Serotonin does excite GABAergic cells to my understand but this excitation is a millioneth of a second and all reactions after that are inhibitory.

Yeah we are looking at this from different frames of reference. I was fixated on 5HT2a pathways that enable the phantasmagoric effects, while you were focusing on diminished production of GABA. Thanks for that millionth of a second inflection.

Serotonin is not the problem here. Its the binding sites that are the problem. You have to have a receptor for a neurotransmitter to bind to. Normally, when 5-ht2 receptors are bound to and opened on GABAergic cells, it causes the release of GABA to calm the excitatory current. This is the negative feedback loop between the serotonergic and GABAergic system.

So the claim is that 5HT2a activity is a significant catalyst for GABA release. I misread you. I thought you were saying that 5-HT2a binded to the GABAa receptor and changed its conformation so the channel could be opened and the membrane hyperpolarized.

The theory=less 5-ht2 subtypes=less seronergic binding opportunities=less GABA output=widespread occipital, temporal, and parietal disinhibtion=somatosensory problems(possibly an explanation for dissociation symptoms in some HPPD patients) and visual distortions among other problems that have been reported by HPPD sufferers.

Here's where I start to get confused. I'll try to say this without ambiguity. Some premises:

1) Serotonergic 5HT2a channel activity is implicated as the principal mechanism that produces psychedelic sensory distortions.

2)Hallucinogens cause permanent attenuation of 5-HT2a receptors in the associative portions of the visual cortex.

This leads me to conclude that:

3) The mechanism that produces the relevant perceptual disturbances is therefore incapacitated.

and the rejoinder:

4) How then do these perceptual disturbances persist?

Peace.

 

[ShaolinBomber]

Yo.



Positive symptoms is simply the antonym for Negative Symptoms. A negative symptom involves "the loss or absence of normal traits or abilities. Here, PS include geometrical hallucinations, peripheral illusions, aberrations in chromatic perception, trails, phosphenes, positive (in the photographic sense) afterimages, nimbii, macropsia and micropsia (and a buttload of others the current DSM doesn't list). NS here would be the consequent "clinically significant distress or impairment in social/occupational/etc. functioning." As well as the loss of baseline latent inhibition.

By messenger I meant the serotonin and 5-HT2a receptor pathways that are implicated in the manifestation of the aforementioned positive symptoms.



Yeah we are looking at this from different frames of reference. I was fixated on 5HT2a pathways that enable the phantasmagoric effects, while you were focusing on diminished production of GABA. Thanks for that millionth of a second inflection.



So the claim is that 5HT2a activity is a significant catalyst for GABA release. I misread you. I thought you were saying that 5-HT2a binded to the GABAa receptor and changed its conformation so the channel could be opened and the membrane hyperpolarized.



Here's where I start to get confused. I'll try to say this without ambiguity. Some premises:

1) Serotonergic 5HT2a channel activity is implicated as the principal mechanism that produces psychedelic sensory distortions.

2)Hallucinogens cause permanent attenuation of 5-HT2a receptors in the associative portions of the visual cortex.

This leads me to conclude that:

3) The mechanism that produces the relevant perceptual disturbances is therefore incapacitated.

and the rejoinder:

4) How then do these perceptual disturbances persist?
Peace.

Without GABAergic neuron stimulation from 5-ht2a binding from serotonin, you have less GABA output. Without GABA, you have excess excitation. This excess excitation(disinhibtion) causes the visual disturbances as well as the other problems reported by HPPD patients. So its not the serotonin or its receptors causing the visual disturbances exactly, its the lack of GABA output to stop the exctitatory currents BECAUSE theres been losses of 5-ht2a receptors on post-synaptic inhibitory neurons.

Basically an HPPD'ers brain is in a constant state of overexcitation, and things that should be filtered out in the field of vision are not, simulating a SIMILAR state of psychedelia, but not the same like if you were on LSD.

So again HPPD=less GABA output in the visual cortex=less filtered visual information=visual disturbances.

The psychological symptoms like dissociation etc. could be effected by this constant state of disinhibtioh as well.

 

[seep]

Shaolin, I'll be happy to put on a dunce cap and strum my lips while making semi-mammalian noises in a very public place and then post the video on you tube if we can break out of the circularity here.

Perhaps if I can see the Abraham paper, or any paper (whether it comes from Harvard or from the North Korean Ministry of Defense or from some guy named O-Dog) anything that explains or attempts to explain the pathophysiology of HPPD.

I'll go first, simply using Offerman's Encyclopedia of Molecular Pharmacology:

First the obvious:

The most widespread extraclinically
used psychostimulant is ecstasy (3,4-methylenedioxymethamphetamin;
MDMA), which also exhibits perceptual
distortions due to 5-HT2A-receptor agonism like
lysergic acid diethylamide (LSD).

So then, your (or Abraham's) claim is that hallucinogens damage this selfsame 5-HT2A pathway by permanently eliminating many of those receptors in specific areas of the visual cortex. This immediately prompts the question, "If the primary pathway is cut off, how can the hallucinogens' symptoms recur?"

So then, the claim is that the hallucinations et al of HPPD are not caused by the 5HT2a pathway, but rather by a critical lack of GABA molecules in the relevant synapses and the consequent hyper-exitation. It is also claimed that benzodiazepine drugs (especially clonazepam) ameliorate the symptoms of HPPD. This sets up a contradiction:

At a given concentration
of GABA in a synapse, the chloride current will be
increased. Benzodiazepines have no action in the absence
of GABA (use-dependence) and cannot increase
maximal physiological stimulation by a high concentration
of GABA, i.e. their action is self-limiting, which
most likely contributes to the safety of these drugs with
respect to overdoses.

Also, it's claimed that the reason there's a decreased GABA concentration in the synapse is that since the 5HT2A's are decimated, pre-synaptic GABA release is insufficiently stimulated. This assumes that one of the principal catalysts of presynaptic GABA release is serotonin activity, principally at the 5-HT2A receptor. I don't know enough about triggers for GABA release, but I assume the triggering has something to do with all exitatory transmitters; if so, the hypervigilance and anxiety which accompany flashbacks (to call a steer a steer) are necessarily the products exitatory transmitters and depolarization. So then, given all that's been said about GABA release, there seems to no dearth of triggers. This is speculation on my part. Offerman only gives me this:

GABA...is synthesized in
presynaptic terminals from glutamate by the action of
the enzyme glutamic acid decarboxylase, stored in
vesicles and released upon the arrival of an action
potential.

One or two of us is oversimplifying or overlooking key aspects of the process. Either that or the 5HT2A-receptor-attenuation theory is incomplete. I'd really like to see that Abraham paper.

I'm keeping this up because I honestly want to know, not because I think you're wrong.

 

[Bell Ringer]

fight or flight |dopamine +norepinephrine

I did a quick search on your disorder and it is referred to as a "disinhibition of visual processing related to loss of serotonin receptors on inhibitory neurons". I think that amphetimines in general have MAOI action, so there should be an increase of serotonin.

I also thought about how some antipsychotics can cause parkinsons-like symptoms because they are dopamine receptor antagonists, and I think dopamine is related to "disinhibition" of motor neurons in your brain. Maybe increasing the dopamine reduces disinhibition in your visual system somehow?

Yes!
Dopamine and norepinephrine are key IMO. I am sure most of you know that some dopamine is converted to norepinephrine. Gaba probabaly should be considered IMO but probably plays a minor role. I think serotonin is being way overempisized. The role of the CNS and PNS has been researched extenivly.
By dis-inhibation do you mean figt or flight? Non essental systems are certinly inhibated in such situations, so that the mind may function on a more primitive level.

Amphepmens do inhibit MAO-A and MAO-B but not much.

If I understand OP's question he is asking why he precieves less symptms of HPPD on adderal.

Who ever suggested that this thread is full of circular logic, I could not agree more.

If anyone needs/wants any full articals feel free to ask (PM) and I will make them available. I'd give out my password to access them but that would get me in trouble.

I will do some actual research and then get back to you guys