Trouble

>FOUND IT INSULIN ACTIVATES THE DELTA 9 SATURASE AND CONVERTS STEARIC ACID TO OLEIC ACID !! In summary, 1) the activities of enterocyte microsomal membrane delta-5, delta-6 and delta-9-desaturases are independently influenced by dietary fatty acids or cholesterol, or by diabetes; 2) changes in dietary fatty acids, cholesterol and diabetes are associated with alterations in the fatty acyl constituents of brush border membrane phosphatidylcholine and phosphatidylethanolamine, but these fatty acyl changes are not explained on the basis of variations in the activities of the microsomal desaturases....

And you probably have both screwed up. Isn't coconut oil enriched in stearic and acids? Can't remember, trivia. Anyway, like I said, without the right desaturases, you won't store fat.

Thats why you need the proper combination of both PUFA and MUFAs (middle chain length unsatuated fatty acids. And that, you obtain from olive oil.

>i am taking vitamin C ester C due to preventing more acidicity at 500 mgs 5-6 times a day. I took 1000 mgs of vitamin C ester and blood sugar went through the roof. There is that insulin again needed to transport C in to the cell.

Small amounts then, you'er even more sensitive than I presumed.

Yes ph is fucked up urine and salvia or pure acid, but during day time they are fine. My problem is i have trouble reducing acids when I sleep. My blood test did show elevated anion gap HINT INT slight metabolic acidosis prehapes

>Since my insulin is not working efficently could the nutrient be backing up in the blood and enter the kreb cycle but at a reduced amount then 100%.

Yes, and thats why you should guardedly be trying acetate and citrate, along with the BCAAs, to push start TCA and also feed energy for protein synthesis.

>Is lectithan a good source of choline or will it add more insult to injury.

Choline is cheap, buy it in bulk. Add lethicin later.

>I can pretty much guarantee my acetylcholine is low due concidering on it is a parasympathetic neurotransmitters which I could definitely use. Since its the parasympathetic system that does seem to be out of balances and is responsible for releasing insulin, and gastric secretions, gut molity.

PI is screwed up, and we're going to use that to help drive adrenal recovery, remember? Its needed for muscle cell growth, triggers AR as well, when you have the right training stimulus.

>Every since eating all those eggs lady me had me eating my tongue starting to turn white again. Now knowing that saturated fats cause inflammation and weaken immune system this explains why. So instead of shoveling 8 whole eggs a day to raise AA. It would have been more productive to correct the under lying deficeincy by insulin management. This could have been successful in possible helping issues at different levels. It not candida either i tested negative in candidisphere test, metabolic testing blood antibodies, stool sample as well..

Correcto mundo. I told you it wasn't candida. Sure a lot of people buy into that explanation though.

>You mentioned about BCAAS between meals, like 1/2 tsp is good 2500 mgs per serving good?

Hard to get into solution - use a drink blender (cup sized one). Sip it.

You feeling more confident of where we are going now? I'd like you to tell your story, eventually, in another forum, as an example, if you please. You're not the first to go down this road, and you won't be the last. May help other bbers who have run into similar issues figure their way out of tough spot.

First though, we need to see your test results for insulin sufficiency.

Another good post.

hardasnails1973

Very confident i kept telling drs about glucose abnormalities, thyroid and other factors on blood test, but since i was in norma range they would not do a damn thing and ignored it
Yes you may use my thread as a reference if it an help some one else from going through bullshit I have use it

i think you are right about the choline
Hepatic steatosis and fat malabsorption are common in CF. Choline deficiency results in decreased phosphatidylcholine synthesis (through the cytidine diphosphocholine-choline pathway) and in hepatic steatosis, and it also results in increased synthesis of phosphatidylcholine (from phosphatidylethanolamine using methyl groups from S-adenosylmethionine

ok if there are no triglycerides, cholesterol, lipids in the blood is it possible that they are being stored and not released from the liver due to lack of choline >

Its a good methydonor which I can use.

Here is a possible reason why homocysteine is not getting mylenated back to the methionne, In the liver, but not in peripheral tissues, remethylation of homocysteine to methionine by MS is regulated by dietary intake of methionine. High levels of hepatic AdoMet allosterically inhibit MTHFR and the formation of 5-Me-THF and stimulate cystathionine β-synthase (CBS). CBS catalyzes the committing step in the transulfuration pathway in which homocysteine is converted to cysteine.

The onl thing I can find is that aTP can lower the AdoMet which is blocking the MS pathway, but look what I found

and so the insulin story goes LOL
http://www.ncbi.nlm.nih.gov/entrez/q...&dopt=Abstract

A diabetic state also increased the activity of the folate-independent homocysteine remethylation enzyme betaine-homocysteine S-methyltransferase, whereas the activity of the folate-dependent enzyme methionine synthase was diminished 52%. In contrast, RA treatment attenuated the streptozotocin-mediated increase in betaine-homocysteine S-methyltransferase, whereas methionine synthase activity remained diminished

And so this defect in the MS pathway would explain why the elevated serum b-12 and folic acid were never broken down and used or use yet could no enter the cell because of insulin dyfunction !!!

Now question is how to reduce the AdoMeT so it can be diverted to the MS pathway. Load up on methycobalonin to overide it or correct the insuline dysfunction..Hard choice Survey says ..Correct the insulin problem...Here we been chasing this so called mercury theory,,,

Diabetes, which can associate with increased protein degradation, also associates with decreased BCOD kinase activity. Since insulin promotes the activity of the BCOD kinase, it would follow that its lack, as in diabetes, would lead to (decreased activity of the kinase and) increased protein degradation.

So is it safe to hypothsize that due to numerous varaibles I self induced a state of insulin resistace that was not identified and over time this lead in to a insulin deficeincy as well as starvation from not having the glucose entering the cells and resulted in body starvation which altered thyroid function and hypothalamus as well. So if the mitocindrion are just sluggish then feeding them the proper intermediataires and then correcting the insulin deficeincy would allow the nutrient to enter into the kreb cycle so they could be fully utlized. Does this sound feasible explanation to get back to health, plus clearing out the liver and lower renegade fats, increasing methylation

Hypothyroid homocysteie
Summary. We investigated the influence of hypothyroidism on homocysteine metabolism in rats, focusing on a hypothetical deficient synthesis of FAD by riboflavin kinases. Animals were allocated in control group (n=7), thyroidectomized rats (n=6), rats with diet deficient in vitamin B2, B9, B12, choline and methionine (n=7), thyroidectomized rats with deficient diet (n=9). Homocysteine was decreased in operated rats

The hypoventialiation is coming from reaction to gabba at 500 mgs..
There are few if any side effects of GABA. Some users have experienced some mild tingling sensations around the face and neck area after supplementing GABA. Some users also notice a brief and milk change in heart rate or breathing patterns. Does this mean i am allergic to it ?

No gaba no gh LOL extra gh output could be helpful you think ? LOL

Trouble

>i think you are right about the choline

Warning, warning: do not second guess me here.

We are ALSO using choline for a different purpose, one almost never used.
Clever chemistry for gene regulation. The fact that you have choline def in the liver underscores its need. Gee, think they're connected issues??

>ok if there are no triglycerides, cholesterol, lipids in the blood is it possible that they are being stored and not released from the liver due to lack of choline

*sigh* We HAD this conversation already, I told you were storing bile acids.

No need to revisit this stuff, HAN.

>Here is a possible reason why homocysteine is not getting mylenated back to the methionne, In the liver, but not in peripheral tissues, remethylation of homocysteine to methionine by MS is regulated by dietary intake of methionine.

Thats correct, which is why glutathione precursors in whey are important, as is NAC and sam-e.

The onyl thing I can find is that ATP can lower the AdoMet which is blocking the MS pathway, but look what I found

--> make ATP using TCA intermediates, feed the pathway with TMG..betaine.

And so this defect in the MS pathway would explain why the elevated serum b-12 and folic acid were never broken down and used or use yet could no enter the cell because of insulin dyfunction !!!

>Correct the insulin problem...Here we been chasing this so called mercury theory,,,

I told you that I didnt think you had a mercury problem, still don't.

>So is it safe to hypothsize that due to numerous varaibles I self induced a state of insulin resistace that was not identified and over time this lead in to a insulin deficeincy as well as starvation from not having the glucose entering the cells and resulted in body starvation which altered thyroid function and hypothalamus as well. So if the mitocindrion are just sluggish then feeding them the proper intermediataires and then correcting the insulin deficeincy would allow the nutrient to enter into the kreb cycle so they could be fully utlized. Does this sound feasible explanation to get back to health, plus clearing out the liver and lower renegade fats, increasing methylation

Plus directly feeding various pathways to get enzymes induced and feeding the start of the pathways to get genes induced. Plus use of a few smart nuclear receptor agonists.

>The hypoventialiation is coming from reaction to gabba at 500 mgs..
Some users also notice a brief and milk change in heart rate or breathing patterns. Does this mean i am allergic to it ?

No, merely sensitive to it because all you make is locked up in glutamine, and that goes to brain..and that is not good, HAN, not good at all. We will get GABA going again and keep what you make from being converted to NMDA, in spinal column and parts of the brain where it is not being regulated properly, out of balance with GABA and with taurine.

Taurine is one of the keys, along with glutathione.

>No gaba no gh LOL extra gh output could be helpful you think ? LOL

Yes sir, thats why its on your supplements to get list, eh?

Such fun. Now why can you understand me so easily and yet other whine about me being so difficult to understand?

*shrug* What is your background education and training, HAN?

hardasnails1973

Background is exercise science,
Training is self survival. When sick I started researching phyisiology of autism, cancer, AIDS, in a person can understand what is going on bioliolgoically in these cases they can just about understand any thing.

Could large dosages of ALA with caffine, ephederine, low carbs, ALCAR, tyrosine say over a 12 weeks period with large amounts of protein possible put you into a insulin resistant state or increase your chances ?

What I meant about choine was that with out you can not make PC or even acteylcholine which I am in much need of due to sympathetic sysem over load (assuming) and my cell membranes will not heal with out choline (major core problem), but taurine taking should help with that as well.

I was just curious does building up of the NDMA some how effect cholingeric receptors affecting acteylcholine production and binding?
I found this but did not understand how nmda ties in with cholinegeric binding. Does it block it some how ?
http://toxsci.oxfordjournals.org/cgi...2/2/185?ck=nck

and
What I mean by 'metabolic machinery' is that a lack of oxygen, for example, in ischemia, can deplete a cell of ATP. Without ATP, a neuron cannot maintain a voltage difference across the membrane. Without a resting membrane potential, the NMDA channel would be constantly open and allowing for unregulated calcium influx. Calcium is a tricky molecule in that it can initiate a plethora of biochemical pathways. Consequently, its homeostatic balance is necessary to generate the appropriate cellular responses.

is it my understanding tht too much calcium inside the cell causes it to calcify and die (aptosis) ?

I been taking free form amino acids for longest time even before the metabolic testing and then still have not made a change in the urine test. Ammonia was the only thing that was in "normal" range on the urine test and i think if i was on a higher protein diet the I would have been in trouble. MY kidney enyzme on metaboic pannel are actually on the low end of normal meaning protein deficeincy (go figure). Now since everything seems to be digesting and into the blood what is it doing once in there if it is not getting metabolized ? And metabolic testing showed that glyclosis was at a dead halt pretty much as well as protein metabolites, fatty acid metaboites. Could this bottle necking of the krebs cycle so to speak be affecting the ph balance due to the build up of acids in the blood. (probably explained it already)

HERE IS THE answer to above remark
To overcome the lack of glucose, the body begins breaking down protein stores, leading to a negative nitrogen balance. In the continued absolute absence or ineffectiveness of insulin, fat stores are mobilized into free fatty acids (FFAs). In the liver excess amounts of fatty acids cannot enter into the Krebs cycle and instead condense into acetoacetic acid and beta hydroxybutyrate, called ketone bodies, which are acidic. To buffer these acids, the body excretes acidic urine and buffers the blood acidity with bicarbonate and buffer bases reserves. However, continued production and buffering of ketones causes a drop in plasma pH, acidosis, and eventually death if left untreated



urnie test showed
high normal taurine,serine, cystathionine,sarcosine , phosphoserine,
urea cycle is sluggish
conclusion maldigestion, absorption - malabsorption in liver not transporting, not from digestion.
nitrogen insufficeny - No shit
elevated need for b-12, folic acid - MS pathway defect and overload of CBS due to insulin defect.

AS you mentioined just above the glutemine is being locked up and being converted to glutemate and the glutemate is not being converted to the gabba and resulting in excitory activity in the brain NMDA

How can we protect from this if we can not get nutrients to cell to be processed without the insulin?
Time- and dose-dependent neuroprotection against NMDA toxicity by vitamin B2, B9 and B12.

Creatine in urine was not even detected, there is the insulin dyfunction again. Since insulin drive creatine into the cell. Its been pulling it from my muscle to keep homostatis in the blood. Creatine at this time would be useless since I can not enter the cell do you think?

Since i felt good with 30 grams slow releseing carbs should I bump it up to see how I feel with like 50 grams for breakfast with vanadyl?..

if one has hyperglycemia this inhibits NO2 production which then inhibits IGF-1 levels and Igf-1 stimulate MS pathway. So it may be possible that insulin secretions may be indirectly responsible of inducing MS pathway due to the increase of NO2 to IGF-1. My urine also should low dopamine levels as well and tyrosine.

http://www.nature.com/mp/journal/v9/...B797F9C69B6D0E

Other factors known to lower IGF-1 (Ref 2, 3,6) levels include oral estrogen, protein calorie malnutrition, insulin deficiency, liver failure, hypothyroidism, pregnancy, glucocorticoid therapy, renal failure and acute catabolic stress (eg, surgery, trauma, hip fractures and infectious diseases). All of these factors are thought to stress the liver and interfere with IGF-1 production.

"Improved outcomes from insulin administration in critically ill people may be due to favorable alterations in myocardial and skeletal muscle metabolism, oxidative glycolisis, and increased nitric oxide production that results in arterial vasodilatation"


Conclusively it appears that Hypothalamus dyfunction ( hypothyroid, iinsulin insuffiency, liver) are easily the culprits in the MS pathway mystery .

So easy to say I have a sublcimical fatty liver some what?

I think the build up of alot of the fats in RBC namely the dha, epa are due because they are not getting meaboized due to hypometabolism of the kreb cycle or possiblr carnitine deficiency to transport them in. Since I am showing the characteristics of EFA deficeincy..

Come to think about it may be the body lowered the thyroid as a protective measure from eating it self up due to cellular stavation from lack of glucose from insulin resistance at first and now deficiency And by focusing on thyroid and getting that running would be counter productive because you have more need for substrates and if they can not get glucose in the firat place its only going to go after the muscle next. So the insulin insufficency which is highly supported by valid data needs to be addressed first and then
hypothalamus stress will be reduced as well and body can go back to normal.
Does this sound plausible explaination?

This showed show really whats going on in the celll next friday getting white blood cell vitamin , antiixdents (ALA,gluthione, sulfate) so it showed give a more precise picture of what is happening at cellular level..

Hyperglycemia causes protein oxidation (protein not being able to be ulitized for protein synthesis) YIPPE pieces are starting to fit into the puzzle
Thus, insulin deficiency will lead to increased catabolism of protein

hyperglycemia increases muscle catabolism despite an endogenous insulin, which then breaks down muscle to produce acids which over load systems clogging them up .

ITS LACK OF INSULIN I TOOK A PILL OF GLIPSERIDE - insulin and I felt a nice rush of glcose and muscle sweeledd and got vascular...

i think self induced hyperglycemia was hidden for several years leading into inuslin resistance and this time it just it was too much for my body to handle and it took foot and caused hypothalamus dyfunctions, but now I feel so good. No wonder my brain was fucked up it was not getting any glucose and with out insulin tyrptophan can not be taken in either to the brain. Would explain my low serotonin levels yes? Again this is all speculation untill insulin test comes back or Hemoglobin glycination test. Blood sugar imbalance I think were one of the major issues that started this chain reaction..

The cause of constpation is from the hyperglycemia casuing dehydration verified by elevated serum albumin and also elevated anion gap. Another reason is to du lack of energy from the glucose not entering the cell to drive the mechanism AKA my colon to make it move..

Trouble

>Background is exercise science
Degrees. minors, please.

> When sick I started researching phyisiology of autism, cancer

Interesting choice in autism. There is a reason for you choice of this malady. Why autism, HAN?

I think we will now reach into your hardwiring, and it's history for the next clues. Why is your glutamate chemistry is brain skewed? From this next chapter in our long running discussion, comes the behavioral corrections hat must occur for you to get well again.

>Could large dosages of ALA with caffine, ephederine, low carbs, ALCAR, tyrosine say over a 12 weeks period with large amounts of protein possible put you into a insulin resistant state or increase your chances ?

Ceffeine and ephedrine feed the beta-adrenergic release of NE and from it, ACTH, this mediated by glutamate. Carnitine must have its redox couple needs met to be controlled, else it is a power oxidant. Excess cortisol, from NE hyperstimulation, leads to elevated ROS, and that is worsened by carnitine when one is low on antioxidants, eh?

Tyrosine is a potent cell regulator, and yes, its binding is part of the complex picture of cell life regulation, in cell proliferation and apoptosis (cell death).

The link you inquire about here, is that of ACTH and cortisol action that turns insulin on and off from the brain on the top end, and glucogenic amino acids, highly enriced in WPI, inducing insulin spiking, at the organ end.

A dangerous coupled effect, HAN, for the molecularly misbegotten.

>I was just curious does building up of the NDMA some how effect cholingeric receptors affecting acteylcholine production and binding? I found this but did not understand how nmda ties in with cholinegeric binding. Does it block it some how ?

Link didn't work. NMDA is a lot like GABA, its a modulator of secretory function in various organs, and has neurotransmitter functions of its own in brain. Its part of a coupled system of agonist/antagonist = push/pull action.

>What I mean by 'metabolic machinery' is that a lack of oxygen,

Now you get to an important crux of your problem. Oxygen is needed for respiration, to make ATP. Its can get sucked up into other reactions, and it can be reduced in gas pressure (blood gas volume) by autonomic reflexes.

Driven by glutamate and taurine, and taurine mitigates for low oxygen (hypoxic) damage in brain, same as it does for hyperosmotic states.

Too much ion charge, not enough water being shuffled in and out of cells - guess whohelps regulates that?

Insulin.

>Without a resting membrane potential, the NMDA channel would be constantly open and allowing for unregulated calcium influx. Calcium is a tricky molecule in that it can initiate a plethora of biochemical pathways. Consequently, its homeostatic balance is necessary to generate the appropriate cellular responses.

Correcto mundo. And who helps that calcium flux work like it should, so that it doesn't build up tonus (high calcium that can't efflux from organelles like SR)??

Magnesium. Magnesium is a cofactor for Na/K ATPase driven calcium pump (transmembrane proteins that shuttles Ca in and out of cells).

What else does it regulate at the same time? (coupled actions)??

Cellular pH.

See my posts in the thread discussion on pH regulation (lactic acid) in muscle. You'll see what I mean.

Whats the appropriate buffers?

Citrate and phosphate. (thats should be lightbulb time for you)

> it my understanding tht too much calcium inside the cell causes it to calcify and die (aptosis) ?

Its not that simple, but yeah, its at the base of problems like muscle cramping.

Thats why the fix is more likley to be magnesium, than either calcium (duh) or potassium (bananas) for muscle cramps.

Gots to know you chemistry, in order not to be led astray by some of these anecdotate fixes.

I>been taking free form amino acids for longest time even before the metabolic testing and then still have not made a change in the urine test. Ammonia was the only thing that was in "normal" range on the urine test and i think if i was on a higher protein diet the I would have been in trouble. MY kidney enyzme on metaboic pannel are actually on the low end of normal meaning protein deficeincy (go figure).

Aminos you should be taking: lysine, panthothetic acid. B2.

Oh yes, your comments are right on here. You could have been in a world of hurt for kidney tubule disease. Lucky.

>Could this bottle necking of the krebs cycle so to speak be affecting the ph balance due to the build up of acids in the blood. (probably explained it already)

Not only pH, but as I said, water balance. Yes, you can't form glycogen in liver and muscle when osmotic load is too high in the the cytosol.

> In the continued absolute absence or ineffectiveness of insulin, fat stores are mobilized into free fatty acids (FFAs). In the liver excess amounts of fatty acids cannot enter into the Krebs cycle and instead condense into acetoacetic acid and beta hydroxybutyrate, called ketone bodies,

Oh gee, the magic words. The very enzyme I spent years working on. You are singing to the choir here, makes me smile.

You see, this is the point for using HMB. See? I get these fuckchop detractors who have said, "she doesn't know what she is talking about when she tells them to take HMB, it doesn't do shit!"

Oh, contraire. It does this expediting of energy, and then some. Its a key signalling agent for TCA and for translocation of free fatty acids into mito, as well as acting like leucine, in the signalling of protein synthesis.

Mind in my madness, there is.

>AS you mentioined just above the glutemine is being locked up and being converted to glutemate and the glutemate is not being converted to the gabba and resulting in excitory activity in the brain NMDA

Taurine, babe. And avoidance of glutamine metabolic fuckups in liver, by making sure that GABA is being made. That requires methylation, and that means the transulfration station bottlenecks must be addressed.

What comes around, goes around.

>How can we protect from this if we can not get nutrients to cell to be processed without the insulin?
Time- and dose-dependent neuroprotection against NMDA toxicity by vitamin B2, B9 and B12.

More like B6, B12, B1 and 2,. zinc, folate, and vitamin C. In liver.

Creatine in urine was not even detected, there is the insulin dyfunction again.

Yes and no. Creatine doesn't work without GSH. Simple. Use NAC and it will. Otherwise, you get that pH (acidification) effect that shuts it down.

I found and wrote about a MOST elegant description of this from citations I found buried...dating from 2001-2004. God, its glorious old tyme biochemsitry, the way we used to do it...

Anyway, the review article described in terms of the Nernst equations, the role of pH control of creatine metabolism.

I have mentioned several times, but not gone again into the chemistry. Why? It would fly over the heads of 99% of the readers in any forum.

Better just to mention it the bottom line, use the NAC to offset pH drift during respiration that will shut down creatine action.


>Since i felt good with 30 grams slow releseing carbs should I bump it up to see how I feel with like 50 grams for breakfast with vanadyl?..

KRALA is what you want. No sir, slow as she goes, gots to get other cellular action on line first. But yeah, you are going to be using a high load protein approach, once we get insulin going again, to pack muscle on you, bring strength back up.

You'll be visiting another forum to read up on this idea, and for the training you need to go with it.

>if one has hyperglycemia this inhibits NO2 production

It fucks up insulin action on endothelial/vascular NOS, and that has its own repercussions, as does the lack of ROS regulation at ITS CORE - you understrand, a lack of EFAs or ascorbate...of GSH.


>Other factors known to lower IGF-1:
protein calorie malnutrition check
insulin deficiency check
liver issues check
hypothyroidism check
glucocorticoid supression check
acute catabolic stress

>All of these factors are thought to stress the liver and interfere with IGF-1 production.

And hence, the lack of protein synthesis.

Your links are working, HAN,. but no matter, I was able to answer it.

>Conclusively it appears that Hypothalamus dyfunction ( hypothyroid, iinsulin insuffiency, liver) are easily the culprits in the MS pathway mystery .

Yes...but at its core, stress.

Our discussion now, must take a more serious turn, for we need to drill down into sensitive, underlying causatives.

For that you must loop back, and delve into the autism angle.

Read up on it, and do a search on the terms autism and glutamate excitotoxicity. Report back...but before you do so, you will also please read up on a form of high functioning autism.. Aspergers and then tell me what it means to you.

You are unusually good at pattern recognition, the gift of the natural diagnositian (when you are not misdirected by side trips into lala-land notions). Why?

> easy to say I have a sublcimical fatty liver some what?

Nonalcoholic fatty liver. I menionted it back at the beginning of this lengthy dialog, eh?

>I think the build up of alot of the fats in RBC namely the dha, epa are due because they are not getting meaboized due to hypometabolism of the kreb cycle or possiblr carnitine deficiency to transport them in. Since I am showing the characteristics of EFA deficeincy..

A little simplistic, but yes indeed. A valid connection.

> So the insulin insufficency which is highly supported by valid data needs to be addressed first and then hypothalamus stress will be reduced as well and body can go back to normal. Does this sound plausible explaination?

Yes and no. Like I said, we next go into the stress effects and its complex chemistry.

And for that, we need your history, childhood. But first you do the reading I asked for, and then we have this chat.

It is a familiar road we walk down. This is a chronic stress situation which MUST be addressed for positive results to be lasting.

Most illuminating. A classic story.

hardasnails1973

background is kinseiology minor nutrition, dabbled in psychology
John berardi AKA DR now were traning partners for a few years and we were way a head of our time.
through researching autism i looked at patterns and studied neurochemistry of the brain from biological pathways from how food gets digested to enyzmatic reactions how it transfer across the intestinal lining by amino acid carriers on the intestinal wall which where driven by atp. To the reactions of specific amino acids intergreted with nutrients to form neurotransmitters. Then I looked at how once in the blood how does it get into the cell (this was my most major obstacle to convince drs that its not at the blood level but at the tissue level transfers were not taking place). I kept telling drs if you do not provide the proper substrates off course your brain is not going to be balanced properly. It was funny as shit I went to see shrink to appease the drs and when I started to explain the situation he was like HMMM you have a point. Shrink almost pissed his pants when he started to ask me speciific questions about certain things. I said "do you take me for a fool " he said what are you talking about. I told him no I am not schizophrenic or bipolar. i recognized the sequence of questions he was asking to determine diagnosis. It was funny I kind of turned the topic around on him and put him on the spot and dummy never even knew it. Iq never had tested but my one freind is 175 and she can only talk to certain peope and She came out to me on time and ask me if I had an extremly High IQ I never had it tested, but I can make the most complicated problems seem the easiest, but have hardest time figuring out the most simple things. I am not a test taker because my mind is light years ahead of the simplictic problem and tend to over think things too much. Problems with my relationships I would start to analyse everything an it would drive them nuts, but in the end my hypothesis was usualy correct based upon the supporting facts. When there is a problem I do not look at one dimesional but rather from all possible angles and try to recongize a speciic pattern whether it be a behavioral or analytical and then I would break it down piece by piece. I started this behavior when working at clubs I would people watch all night long and people that were going to be trouble would fall into specific pattern or show certain facial expressions and before the problem esculated I would identify it and act according. Thats what I tried to do with OTB tried to find the metabolic blockers and identified we had same patterns even on metabolic testing same liver pathways were not functioning properly, but his psychological issues were becoming to great to reason and was makiing him more aggitated. i knew the general idea, but did not have the bavk ground to fully understand what was happening at the molecular level now I do..

one can suspect with out insulin I am probably having a cellular potassium deficeincy since high insulin drive potassium into the cell and low would cause a deficeincy ..dOes this make sense since people with second stage adrenal faitgue have high insulin levels usually high intracellular potassium amd low sodium levels. You mentioned you had this before..

The ability of insulin to stimulate, and glucagon to inhibit, HMG-CoA reductase activity is consistent with the effects of these hormones on other metabolic pathways. The basic function of these two hormones is to control the availability and delivery of energy to all cells of the body.

Citrate and phosphate. (thats should be lightbulb time for you)
Yes if I remember right phosphates are used to help thyroid from decreasing t-3
could not find the link
J Physiol Pharmacol. 1996 Jun;47(2):373-83. Phosphate supplementation prevents a decrease of triiodothyronine and increases resting metabolic rate during low energy diet. Nazar K, Kaciuba-Uscilko H, Szczepanik J, Zemba AW, Kruk B, Chwalbinska-Moneta J, Titow-Stupnicka E, Bicz B, Krotkiewski M.

But here is the thing I have all this b-6 built up in my blood ?
One hypothesis is that pyri-doxine toxicity is caused by exceeding the liver’s ability to phosphorylate pyridoxine to P5P, yieldinghigh serum levels of pyridoxine which may be directly neurotoxic or may compete with P5P for bind-ing sites, resulting in a relative deficiency. i have functioinal b-6 defciency why glutemate is not converting back to gaba posible because the enzyme is b-6 driven. Sound feasible


So as we can once again see that insulin stilulates HMG-CoA reductase which increase cholesterol synthesis. Now if I remember right stain drugs reduces this enzyme and if this enzyme is reduced it could cause a coenzyme q 10 deficeincy?

Could the insulin dyfunction be acting like a statin drug?
Statins could initiate and/or accelerate malignant growth by a) blocking the production of Coenzyme Q10, which has been shown to have anti-cancer effects; b) stimulating the growth of new blood vessels that malignancies require to promote their propagation; c) decreasing the cytotoxicity of natural killer cells; d) blocking the production of squalene, an intermediate cholesterol metabolite with anti-cancer activities in animal studies and currently used as adjunctive therapy in treating cancer; e) reducing the production of DHEA, which has been shown to have anticancer and immune stimulating effects in experimental studies."...

What about epson salt foot baths to increase sulfate stores. i was taking MSM but I researched and people (autistic) with underfunctioning sulfruation pathways can not convert to sulfate. And my plasms sulfate levels are in the shitter. No sulfate no insulin and low gluthione. looking back on my tests all the subtrates to formi nsulin are depleted.

i see your reasoning for lysine, lysine is needed to make carnitine and also act as an anchor for P5P which i am low in ...hmmm
b2 converts to FAD which is needed in the TCA cycle, and will also lower VLCFA's as well, as well as lower sarcosine
B-5 drives coenzyme A but for some reason I seem to think i have an over production of coenzyme A that is being resistant to enter. B-5 is the only vitamin that is shown as being over ultized in the metabolic testing. Could this becaue of underactive adrenals? i did read some where that excessive coenyzme A can clogg the TCA cycle but I forget how. may be it causes an in balance in NADH/ NADPH. I know if this ratio is skewed dyfunction happens, but not sure what?


i really did not have any problems untll I started to up my sugar intake after the contest this is when I experinced the brunt of the problems. I continued after working out to consume up to 100 -125 grams of dextrose 4-5 days a week After sipping on the drink I would start sweating perfusely and even a few times a got light head driving home and when I go home I would goto sleep for about 30 minutes and then wake up feeling refreshed, but in puddle of sweat. Shit after prejuding I had a baked potatoe with my meal and starting sweating like never before and then passed out in the car after dinner for an hour and then I was fine. So could a radical change from a super low sugar diet to a sudden sugar rush have triggered a biological stress response and excellerated the insulin imbalance and the wheels were set in motion and there was no way to stop them. To add more insult from injury figuring I had candida i went on a high fat ketogenic diet (cocconut oil) which only added to more insulin resistace and when I got my first blood test my cholesterol was 100, hdl where 40 vs 60 an LDL where 40 points higher then usual, triglycerides were in normal range, but dr said i was fine and also t-3 were at low total pole and t-4 where in upper range. So does this help to start to paint the picture.

This should shed some light of things
Plus with in that amount of time 1 weeks time before the shit hit the fan my with excessive sugar intake from holiday foods, holidays lonely brother got diagnosed MS, freind died in car accdent, I was exposed to paint at work it was affecting my job performance as well I would come home light headed, and dizzy in a daze, bull shit from customers at work , plus training like a made man for photo shoot in ca = metabolic stress u think?


DAMN LIGHT BULB JUST CAME ON NOW I SEE YOU METHOD TO YOUR MADNESS

you are preparing the mitochondrion by preparing them with proper intermediatries and also at same time supplying nutrients to build up the antioidents (gluthione, SOD,ect)and clear the liver pathways to rebuild the neurotransmitters. Once these are built up and mitochomdrion are ready you are going to supply them with the fuels (AA, carbs, fats) by manipulating the insulin with cAMP. I have an idea once insulin levels are stabilzed adrenals will return because PGE2 AA production would be increased from the rise of insulin and then ANABOLIC state will be introduced once again and also testosterone should rise, as well thyroid due to the fact that it will be taken out of starvation mood and balacing of adrenals. (this is in a nut shell of course)

I was thinking about going back to nursing school, but what i have goes against what medical professions beleive in and it would be conflict I am sure.

I have all this understanding of chemistry, but what job could I do where I can put it to use helping people and make a living off of it?

i chose autism based upon the fact that the drs were so set on mercury poisoing from all the tuna fish I had consummed over the years and autism parellels alot of things I have been expereincing as well as explains what can go wrong in each biological system at a cellular level.

This is what i believe the future of medicine should be
Find out what nutrients the body requires through cellular testing (whole blood, RBC, metabolic testing) if they are low find out where the metaboic block is (stress digestion, mitochondrion dysfunction, toxins,ect). We could prevent alot of health problem if the GOV't would set new RDA guidelines to higher standards of certain vitamins and design a test to find out what nutrients you are deficienct in and have a company design a supplment based on your testing once ever 3-4 months. Wish ful thinking I know !!

Trouble

HAN, lets try another hint.

We want to go further back in the pathogenesis of this issue of yours and OTBs as well.

Please do a Google search on glutamate and autism.

Then read what you can on it, report back here.

Time to open up some eyes. Then we'll talk some more on the driver for glutamate excitotoxicity in chronic stress. This is really a continuum related disorders, predicated of a central glutmate regulation issue.

On one end the related bipolar and depression neurological diorders, then autistics, then high functioning autistics, then PTSDs, and then the general population, with somatype issues (ecto and endomorphic deviation from standard mesomorphic type) depression, intestinal disorders, hormonal issues, all driven by anxiety and chronic stress loading - with occasional acute episodes that keep natural correction mechanisms from de-silencing genes in the forebrain, hypothalamus, pituitary, and other areas.

What we got is what a friend of mine refers to as a battery problem. Loading on the battery is high, and the ceiling for overload is low. You get burnout and overloading. Thats the crash that you and OTB had.

This is pretty important, or I wouldn't be asking twice.

hardasnails1973

"First, I find that it is critical to remove excitotoxin triggers from the diet. This simply involves reading labels and closely monitoring food and supplement intake to avoid excitotoxins. Foods or supplements that contain excitotoxins include MSG (monosodium glutamate), glutamic acid, glutamine, nutrasweet, aspartate, aspartame, and cysteine. Mercury and aluminum can also serve to trigger glutamate release"

My urine tested high for aluminum and also I use tons of glutemine a day thinking it was good 20 grams for years

The brain requires sufficient levels of oxygen and energy to remove excess glutamate. However, glutamate release leads to the release of insulin, which results in decreased glucose levels. I always had problems handling sugar all my life. I was a sugar feen when I was younger and it made me get me hyperactive and mean..

In fact, conditions of hypoglycemia, or low calorie/starvation conditions induce the release of glutamate and reduce the ability to remove excess levels of glutamate from the brain. (dieting for contest time prime example)

WOW NO SHIT
A central problem in neurological inflammation is the function and health of the liver.

No wonder my body was producing taurine like crazy to help lower the glutemate exocitory toxin to produce for gaba

here is the bile acids coming in !! OTB problem
CCK stimulates the gall bladder to release the bile (made by the liver) into the intestines to neutralize the acid and help digest fats. If, however, the pancreas and the liver are in a weakened state, this ideal situation will not occur. Instead, the HCL is still dumped into the small intestine; however, these three proteins will not be released properly. This results in a situation where the intestinal tract will become more acidic due to lack of released bile, and result in an environment that is more conducive to growth of yeast

now i am seeing things much clearer
Individuals should consider supplements to help to detoxify the excess glutamate in the system. These would include branched chain amino acids, pycnogenol, and grape seed extract. Magnesium is critical as it regulates the excess calcium from flowing into the nerves and killing them. Epsom salt baths (magnesium sulfate) are useful particularly if the bathing water is high in chloride and fluoride. Chloride blocks the action of sulfur in the body. Limited amounts of zinc and calcium are fine, but too much will increase nerve damage.

i was taking zinc like crazy passed 2 years and only adding more insult to injury
Supplements that add energy (oxygen and ATP) to the brain will help it to detoxify the inflammatory reactions caused by excess glutamate and heavy metals, which trigger glutamate release. These supplements include ginkgo, vinpocetine, NADH, CoQ10 and carnitine. Carnitine actually helps to increase the energy in the mitochondria, which are the energy producing organelles inside each cell. Carnitine is also useful in repairing liver damage
Sources of Excitotoxins
Definite Sources of MSG

Could the excessive amount of protein powder I was taking contributed to excess glutemate by having it hidden? or could the amount of sushi i consumed have hidden MSG in it and ended up poisoning. It was after that when I really notice my problems arise. I was thinking it was a bacterial infection, but now could it have been excessive glutemate?

Henry Wrote:

"I have a feeling that the naturally-occurring MSG in seaweed is not so bad (as long as you don't go overboard on eating seaweed or sushi), because the seaweed may have other supporting nutrients which counteract the MSG's effects."



Textured ProteinCarrageenan or Vegetable Gum
Seasonings or Spices
Flavorings or Natural Flavorings
Chicken, Beef, Pork, Smoke Flavorings
Bouillon, Broth or Stock
Barley Malt, Malt Extract, Malt Flavoring
Whey Protein, Whey Protein Isolate or Concentrate
Soy Protein, Soy Protein Isolate or Concentrate
Soy Sauce or Extract

Trouble

Closer, you're getting the links futher down the chain of events.

This citation might be over your head, but try to see if it makes sense in the big picture of stress associated brain chemistry here.

"The mRNA levels of several genes were significantly increased in autism, including excitatory amino acid transporter 1 and glutamate receptor AMPA-1, two members of the glutamate system. Abnormalities in the protein or mRNA levels of several additional molecules in the glutamate system were identified on further analysis, including glutamate receptor binding proteins. AMPA-type glutamate receptor density was decreased in the cerebellum of individuals with autism.

Conclusions: Subjects with autism may have specific abnormalities in the AMPA-type glutamate receptors and glutamate transporters in the cerebellum. These abnormalities may be directly involved in the pathogenesis of the disorder."

Should start to ring bells.

Per glutamate excess. Its a regulated quantity in brain. You synthesize it, but unshielded (no blood brain barrier present) on hypothalamus causes localized glutamine/glutamate excess. High levels of blood glutamine (dietary sources) can also cause changes in transport of glutamine across the BBB, under certain conditions of low GABA concentrations in the brain (which modulates BBB transport).

My point is NMDA. Go review the relationship between NMDA and glutamate, and GABA again.

The unusually high glutamate in brain is due to a buildup, and local excess in key portions of the brain. Glutamate is the second most important energy source in brain, next to glucose. Its also an important neurotransmitter. Polymoprhism of a gene that regulates glutamate dehydrogenase, the enzyme that metabolized glutamine for energy, is fucked up in a chunk of the population. Plus, translocation of neurotransmitter glutamate seems faulty as well.

This is due to gene silencing, cause by low levels methylation and insufficient glutathione production out of liver. Glutathione and sulfur chemistry being dysfunctional in liver...you get this problem in brain...see?? Connections, important ones.

Methylation reactions keep the housekeeping proteins, called histones, that sit on DNA and keep it safe and tidy in the nucleus, in check. You demethylate these histones, they change shape, and they turn off genes. We call this gene silencing (this is pretty new stuff in the literature).

Silenced genes are the bottom line here. How they get silenced: massive stress loads during brain development, and subsequent acute stress events that keep them silent.


PS: quite throwing the kitchen sink into your replies. Keep it simple.

Now go do a search on glutamate and PTSD.

hardasnails1973

The majority of cases of congenital hyperinsulinism appear to be due to defects in insulin secretion by pancreatic cells. Currently, it is thought that mutations in any of four different genes can cause the disorder. One of these genes codes for an enzyme called glutamate dehydrogenase. This enzyme is stimulated by the amino acid leucine, meaning that protein meals that contain leucine lead to activation of glutamate dehydrogenase, which in turn triggers the release of insulin from pancreatic cells.

Could the excess glutemate for all these years be the reason why I kept living in the past so much and keep dwelling on it? All my life i have never been able to let it go. it kept playing back in my head like it was a movie over and over again....

The dysregulation of GABA & glutamatergic pathways is implicated in development and maintenance of
PTSD. These two amino acids (GABA, glutamate) work in tandem to translate experience and stimuli into memory. Extreme stress
can advesely affect these pathways, eventually causing long-term synaptic changes that leads to abnormal, often excessive, encoding
of memory. In essence, memories can become deeply ingrained when these pathways are overstimulated by stress. This mechanism
helps to explain the re-experiencing (e.g, flashbacks) symptoms of PTSD

Usually PTSD sufferers have LOWER than normal cortisol levels - HMMM

i am starting to see where you are going with this now. You are trying to trace back to see what happened in my life that could have caused this imbalance of glutemate. And I will tell you this in college for3 months i comsumed a way protein with aspartame in it at 9 scoops a day and i had such severe brain fogg I had to be under parents superviosin to cook so I would not leave stove on. After month it cleared up as soon as i stopped.

Unless you block the glutamate system, the serotonin will shut down - this sounds all to familar to me.
So stress stimulates glutemate release and it will shut down serotonin production. This just opened my eyes to alot of things !!

So by using the gaba this will preserve the glutamine for other purposes (gluthione, muscle mass, leaky gut) and prevent it from being converted into glutemate?

So stress raises glutemate with cause liver pathway dyfunction because the body will diverting to the CBS pathways to produce taurine and will be diverting from the MS pathway which is needed for production of serotonin and also recycling back to methionne . sound valid ?

Trouble

"The majority of cases of congenital hyperinsulinism appear to be due to defects in insulin secretion by pancreatic cells. Currently, it is thought that mutations in any of four different genes can cause the disorder. One of these genes codes for an enzyme called glutamate dehydrogenase. This enzyme is stimulated by the amino acid leucine, meaning that protein meals that contain leucine lead to activation of glutamate dehydrogenase, which in turn triggers the release of insulin from pancreatic cells."

Wait a minute! You're barking up the wrong tree. Thats when you see obese little kids with immediate insulin problems, not what I'm talking about.

I'm talking about gene silencing from acute or chonic stress effects during childhood. This changes the slice and dice mechanisms of exon/intron action during gene transcription from DNA to RNA. Its delayed...you don't see the effects right way, some not until adulthood, some even later, in the mid30s.

Thats the silencing of genes that keep this splice and dice to the altered product (RNA that is then transcribed into faulty enzyme, GDH2).

Little different scenario than you suggest. A paper published back in I think 2001 used an animal model to induce social stress for a couple weeks during the equivalent time period of childhood in humans. Stress led to a dump in glutathione, and then loss of methylation control of histones.

They tracked the changes in gene regulation to hundreds of factors in brain.

Massive effect..mostly in the areas that process visual information. You read faces to determine intent in social situations. This brain loci was affected, as was striatal loci (home of dopamine control of addiction and reward responses) and also the unique portion of the brain that encodes for learning language and symbolic logic.

These issues and others are seen as a conglomerate of symptoms, we night call a developmental chronic stress disorder.

Your pattern of circular thinking, where you get caught up in ideas - can happen with other processing, aural - songs that repeat in your brain, or more likely short passages...yeah, you see this kinda problem probably associated with these silenced genes and changes in brain function in specific loci.

Thats called big picture logic. Soup to nuts idea of what might be going in these stress driven disorders. Now you're getting the message that there are ways to help shift this big picture of disturbed biochemistry and gene control towards a more healthy, maybe even near normal, functionality.

That clue was published very recently, like one year ago and another last month, and these recports suggest that methylation issues can be reversed in these gene silencing events, if you got the glutathione...and control glucose methabolism (cause that ROS related) and sterss hormone.

Only way to do that - change lifestyle. Diet, exercise, supplements, change in behaviors and attitude, including modulating stress response by stress management, and returning neuroendocrine and liver system function to an approximation of normal status.

Get my drift here, HAN?? Thats the other half of the story. And you can see why I might pinpoint glutamate and glutathione, GABAnergic system and NMDA, then insulin, cortisol and methylation/transsulfuration pathsways screwups.

I'm among the first to propose this linkage, and tie into a plethora of stress driven disorders. Others have hinted at it.

Probably most telling: CDCs recent published study on autism incidence among school children. No pattern emerges whem demographics are analyzed...only that the number of affected children has risen dramatically in the last 3 decades.

Coincident with the current lifestyle problems driving cardiovascular disease, diabetes, obesity, and cancer: stress, poor diet, and lack of exercise.

Thats what brought me to the world of strength training, and to this forum and others. Y'all are perfect functional models of disturbed neurohormonal controls behind this chronic stress syndrome.

hardasnails1973

Your pattern of circular thinking, where you get caught up in ideas - can happen with other processing, aural - songs that repeat in your brain, or more likely short passages...yeah, you see this kinda problem probably associated with these silenced genes and changes in brain function in specific loci.

That above paragraph describes me to a T. If you want to delve into my psyche. My mother was 21 and father was 42 and I was born out of wedlock. Every since I was born I had these feelings of not ever being wanted or being self accepted because my mother was wrestling with the idea of if she wanted to keep me or not These feelings began to get more pronounced as I got older. I was best athlete in school but kids would humilate me and pick me last. I was always thinking in my side "what was so wrong with me" One night my brother sat me down and told me it was not me at all, but other people. i had so much going for me, but nights I come home and start anlayzing what was i did that was so wrong to make other not like me. I would cry to release the anger and hold it all inside untill out on the field during sports. I used to get teased and taunted for no reasons. thats why I started to working out to protect my self. To built this strong outer shell, but inside I was very vulerable but never showed it and over time this built up in time. I did load a gun when I was 15 thinking I could not take it any longer, but something maybe reconcider that there is so much more to life and i am not going to give up that easy. MY mom constantly would yell at my dad for no reason and this scared me to death. i would either go up to my room or get out of the house. Still to this day when a person raises their voice it startles me. Still to this day i can not enjoy 4 th of july or shoot a gun because it bothers my ears. As a child was scared to goto kids parties due to fact of balloons pooping and scaring me. So as you can see it was like pattern recognitioin. i see a gun, ballon I cover my ear run other way. I saw my father get yelled at and that was imprinted on me when some one would yell at me to stand there and take it and to do nothing. All my relationship failed because I would try to hard and be to good to make things right and in the end be taken avantage of and used. Still til this day I hear a song and these visual cues would pop in my head and keep playing over constantly. i had people drill into my head that i was worthless, never aount to anything..This was not my parents but my peers. My parents encourage me to do what i wanted never forced me at all and keep a tight wrap on me, but ruling with iron fist meaning if I got in trouble in school or on the streets there would be no sports for that week. So as you can see patterns you pointed out strong are indicitive of me. So you can see I had my mid life crisis 20 years early so to speak.

In order to try to get healed I have explored several avenues one of these avenues was errie. i went to see a spiritaul healer and she said a curse was placed on me years ago. Thinking back to where it could have been placed I finally pinpointed the source. To check her validity I gave her a list of 10 differnt names of people randomly and during this time she was not wathcing me. I rattled off the name (20 of them) and she stopped at one specific name. Now i figured out she got lucky know I knew the name of the spirit and to test her a gain i gave her 10 different names of spirits and with her eyes closed she picked the specific name. To make things ever more mysterious. I called my freind that I have not talked o in 15 years and just left him a message "hey how you been ect. and to call me back" Next day he called me back first words of of his mouth were "you were calling about him (spirit)" This freaked me out and till this day I can remembered when the transfer took place and he remembers it as if it was yesterday as well. When we were kids we did the blood brother cermemony because we both were in to spiritualism and martial arts. He did the ceremony with 2 other people and one of them mysteriously died and other is crippled for life. My friend who is the source is deabliited for live...He is basically a veggiable and now me ..IS this all too coincidental?

Sometimes I do not feel like i belong here strange to explain, but rather a simple explaination. When I was 7 I nearly drowned and during this occasion I saw and felt things I never til this day have felt. While underwater I could only describe that feeeling of love/acceptence i have always wanting to feel. I had a near death expereince. Every since that time I have been given an ability to sense people and what they are feeling sort of like seeing their aura so to speak. Some times these visons as dreams would come to me and I did not know what they meant. Eventualy i started practice mediation when I got sick and got really good at controlling by body and ablility to relax almost as if leaving my body . I know this may all sound strange, but some inciidence that have happen did freak people out. All I know my work in this life was is not done because technically I should not be here. If a cat had nine lives I have used up half of them all ready.

TRouble did you fall into this same profile as well and what triggered your exploration into this field. We all have a reason for doing things.

Trouble

You ask how I got into this topic of related stress disorders.

Sure, I had/have it as well. A lot of people do - many more than you would suspect.

The animal model on bullying - that rang a bell right away, as did the feelings of being different..and if you dig down, you find as well, the problems with maternal stress (mother has stress during pregnancy) that appears to bear out over and over in similar cases.

Mother/father divorced, mother left, mother extremely nervous/anxious type or has depression/anxiety disorders - all related causatives for early childhood stress. There is theory in the autism research archives that appears to be borne out by neurophysiology studies conducted recently. That maternal stress hormone levels affect developing prenatals - perhaps changes their sensitivity to stressors.

This might set the role for passive aggression in childhood. Children can be surprisingly good at reading body language - and smelling fear. Kids quickly assert dominance and that spreads within childhood peer groups, so that a rank order of dominance is estabilished. The passive aggressive are at the bottom of the pecking order.

That pecking order behavior can go on for years -a low level stress effect that is chronic, and when combined with a home life that maybe lonely, isolated, and also punctuated with periods of parental stress, which kids are pretty sensitive to, you have a scenario that suggests ongoing reinforcement of previous gene silencing and possiblly a worsening of the condition through development (well into puberty).

See? Patterns again. Right now, off the top of my head, I can list a dozen individuals I know personally, who have related very, very similar patterns of childhood stress. I know there are many more out there. BTW, children who have these childhood assocated stressors are exceptionally good at pattern recognition and are often highly intelligent and...different.

Maybe others who have these attributes will stumble onto this thread, and persevere in its lengthy history, to read this post.

They will have much the same types of symptoms that you, I, and others have had. Most came to bodybuilding for the same reasons, Quite a few got into more difficult health circumstances because of the need to get mass up and bodyfat down - depsie metabolic tendencies towards the contrary. They had to use heavy chemical measures and very strict dieting that unfortunately worsened their neurological difficulties with exictotoxic NMDA and glutamate.

So there you have it. Not so much that I had the same issues, more like the same catalytic patterns of stress during key periods of development, reinforced in young adult and later adult years.

This is the story of systematic gene repression from stress and its manyfold effects on health, on wellbeing and on mental attitudes of fitness and fitting in.

My sincere belief, backed by a still new but slowly growing body of scientific evidence, is that its a largely reversible condition.

I guess one of my contributions during this upcoming phase of my life will be to help identify the factors and conditionals that must be met to reverse these stress disorders.

Anecdotal evidence, beyond the science, says that people can function normally or near normally, with Aspergers syndrome, PTSD (types I and 2), and from various neurological disorders - social deficit, panic disorder, phobia and OCD, depression, mild bipolar diorders, epilepsy..many more disorders - all related to the same root causes - that these can be largely corrected or nudged into more naturally controlled chemsitry.

The larger panopoly of related conditions, that are termed autocrine system disorders, run, as I pointed in my last reply, in a continuum, from severe genetic to mostly expressed and superficially controlled maladies.

This chemistry is linked to somatypes that share the same neurological hardwiring. I call these function ectomorphs and endomorphs - again, anectodotal evidence suggests that these pheonotypes can be nudged with diet and training, to become mesomorphs. Thats affords a method of self correction of the underlying excitotoxicity as well.

I believe my ascertion that these maladies need not be considered permanent health burdens is fundamentally true. Knowledge is power, when you can make people aware that there is hope and a common sense approach to resolving the disheartening syndrome and hardwiring problems of chronic stress disorders.

You could say that's a serendipitous reason for me being here. It fell out of a larger goal, an unexpected benefit of being curious.

PS: To answer you question on the so called transference that took place. Nosir, I don't believe it. Its coincidence of happenstance. To the extent that you believe it, it will control you and cause you no end of grief.