Sure. Likewise My first rule in life is to always be learning.
Ok understood I don't dispute the observed effects. So now there is a big mystery for me.
ALCAR is much more blood brain penetratable. Carnitine is very controlled in transport across the BBB. Note to be clear I never said that carnitine is not in the brain nor does it not have any function there but that it could not be the primary source of fuel for the Krebs cycle. Beta oxidation in neurons is normally very low. Hence the emphasis on glucose or ketones.
Here for example is a paper (one of several) that discusses absorption, transport and beta oxidation in the brain involving carnitine.
http://cellial.com/joomla1.5/images/documents/carnitine transport and physiological 2004.pdf
Now maybe there is something special about LCF transport and the brain. Have not been able to track that down. Even then beta oxidation is meant to be only a small percentage of the energy process normally. Maybe even very small amounts of LCF have significant impact on the limbic system. That part of the brain is very complex. Again all I am saying is normal carnitine abundance and transport is carefully controlled in a normal healthy person. Another option is maybe LCF supplies an alternate pathway sometimes with tough startup consequences. Dunno.
Perhaps people who are hypersensitive have a blood brain barrier integrity problem. Blood brain barrier integrity is an often overlooked defect that has major implication to multiple neurological diseases. The irony is I have a very leaky BBB as either or precursor or a result of my rare autoimmune disease. I have had LCF before several years ago when I was at my worst. It did raise anxiety and insomnia but did not flip me out. I will know soon enough for the present when I have an available testing window (too many things going on at work at the moment to throw myself into the fire atm).
Where there is smoke there is fire. If there is damage in the CNS there is inflammation almost guaranteed.
I don't dispute that the MMA-succinyl COA pathway is important for mitochondrial health. But from everything I have researched it is not a primary source of fuel for the Krebs cycle. On the other hand Adb12 clearly has some profound impact on the entire body if one is deficient. I still think the Gorilla in the Room hypothesis could have enormous impact on the CNS just considering that effect alone.
Not sure if this relevant to LCF but I had stumbled onto this a little while ago since my maternal grandmother died from MS and one of my paternal aunts has MS. As an aside I also have two family members who died of ALS and myself with the Stiff Person Syndrome. So studying of neurological diseases, the functions of microglia, astrocytes, neurotransmitters, etc. has been a common topic of research for me for some time now sadly.
http://www.google.com/url?sa=t&rct=j&q=&esrc=s&source=web&cd=2&cad=rja&ved=0CDwQFjAB&url=http://phx.corporate-ir.net/External.File?item=UGFyZW50SUQ9MzUzMDQ3NXxDaGlsZElEPTQwNTk0NnxUeXBlPTI=&t=1&ei=_cEtUZv6H86ajALc5ICoDg&usg=AFQjCNFClvRvPYip9XQdsExDw_d8kTRizw&bvm=bv.42965579,d.cGE
It is a pdf from Biogen Idec about the history of fumarate as a therapeutic and about dimethylfumarate, monomethylfumarate and their protective effect on neurons and then more recent investigational drugs.
Ok fair enough.
I said "Just because there are indications of low B12 in certain neurodegenerative diseases does not in any way prove that neuronal mitochondria make heavy use of the methymalonic pathway as a primary energy source."
I should not have used the word "prove". I apologize. Honestly we can't really prove anything at the moment. There are too many variables and too much complexity. But proof is not required. I should have said
" ... neurodegenerative diseases does NOT have to mean that neuronal mitochondria make heavy use of the methymalonic pathway as a primary energy source". There are other alternate explanations is all I am suggesting.
Understand I am not out to prove any theory. I have no theory. I am by no means Rich Vank. He was a great guy who helped a lot of people. My goal is perhaps self-centered. Like many on here I want to understand what is going on so I can make the best choices in terms of improving my health. If along the way my questions and knowledge help someone else also then that is great.
Unlike many on here I have an extremely rare automimmune disease so I have to be very careful about what changes I make. I am already a living testimonial which is outside the realm of my disease. By all accounts I should be stuck in a wheelchair by now with an intrathecal baclofen pump. On the other hand, eventually my disease will cripple and kill me that is inevitable. But in the mean time I want to have as much quality of life as I can for my wife and children and myself. If that is self centered, then so be it.
Fair enough. Just please realize it was not my intention to attack anything you said. I was simply stating what I know about brain energy metabolic processes. You don't need to convince me about the idiocy rampant in the medical community. I could tell you horror stories (as I suppose many on here could) about a decade worth of misdiagnosis and fighting with doctors to get to someone who could save my life. Not fun.
Misunderstanding is the beginning towards understanding as far as I am concerned. Humanity still knows very little about the natural world including how are bodies work. Even less about the human brain I might add.
Thank you for all the information, hypotheses and experiences you have shared. You have access to some wonderful information that quite frankly does not exist elsewhere.
My emphasis is more on the biophysical modeling of proteins. But I was also at the ground floor for a numbes of years developing algorithms for identifying novel genes during the genome gold rush of the mid 90s.
It is a small world. I almost went to WPI for undergraduate but ended up going to the Univ of Wisconsin-Madison. In hindsight my decline probably started at the end of college, was still not so bad I could not get my PhD in astrophysics but after a decade in biotech startups that was it. Everything was spent and everything collapsed in blinding pain.
That is great to know. I honestly commend your diligence.
Such idiocy is rampant in all scientific fields to one extent or another. The crime in medicine is how it directly harms people's lives. None of us respect health until we lose it. Those of us who have almost completely lost health, value it far beyond any need for pretentions or horse blinders or enormous egos as are otherwise encountered in all walks of life much to my eternal sadness. It is the sad state of our race quite frankly. Never attribute to malice what is otherwise explained by incompetence
Personally what I find attractive is you are talking about a merger between two of the most important biochemical processes in the body namely ATP production (aerobic respiration) and methylation (which affects gene expression among many other things). But I would add that there may be important effects involving the immune system / inflammation and others like blood brain barrier integrity for the CNS. While not as compact as the Deadlock quartet, they may explain some people's differing responses to increasing the flux through these two cycles (three if you add in the folate cycle).
To clarify, when you say "what are the tests", what for? For assessing a methyl b12 supplement?
See my distinction is this. For example, when I read up on numerous research articles about the limits on beta oxidation in neurons in a normal brain, that is no longer theory to me (of course maybe I misinterpreted something, Lord knows that has happened numerous times). Instead that is research information that any theory I might suggest I feel should embrace and encompass. Just like in physics when I was studying black holes and neutron stars. Any hypotheseses had to obey constraints placed on me by other research data.
Hehe understood. Trust me I have never stopped being a physicist regardless of my occupation. We are what we are, nothing more, nothing less.
Not even close. Also why do you never bring up the high levels of microglial activation and inflammation now know to be signatures of most of the CNS diseases you listed. You focus exclusively it seems on the MMA levels. Why not the inflammation? Can't that tie back into adb12 / BH4 and peroxynitite removal and the low MMAs are a correlative finding?
First I am not certain that neurons and glial cells process mitochondrial fuels the same way. I have to check on that. People often focus on the neurons for obvious reasons, but glial cells and microglia are extremely important and being strongly implicated in several neurological disorders.
Second, I am positive that mitochondria in the brain does use the MMA pathway. I never said that they didn't. Just like someone with high glutamate excitotoxicity probably amplifies the AKG input path. But again like I stated before, in a normal brain the primary fuel is glucose via pyruvate with (I am pretty sure) entry into the Krebs cycle via biotin and not via the beta oxidation path involving carnitine and acetyl COA. If someone can correct me on that aspect, I would be much obliged.
If I remember right, the brain consumes roughly 120 grams of glucose or more a day on average for a healthy person. My neuroendocrinologist used to say the brain needs three primary elements: (a) oxygen, (b) glucose, and (c) blood brain barrier integrity; in that order. A simplistic viewpoint but there is merit to it. When any one of those three get disrupted there is *bleep* to pay. I think long term deficiencies in the deadlock quartet and / or other factors like severe inflammation can and do disrupt those three factors causing ultimately terrible havoc for the person who is suffering.
No problem. I apologize for any misunderstanding as well. I probably should have been clearer in what I was writing, something that is hard to do when I am in a rush.
Take care.
Hi Dbkita,
It is a small world. I almost went to WPI for undergraduate but ended up going to the Univ of Wisconsin-Madison. In hindsight my decline probably started at the end of college, was still not so bad I could not get my PhD in astrophysics but after a decade in biotech startups that was it. Everything was spent and everything collapsed in blinding pain.
That is great to know. I honestly commend your diligence.
WPI was amazing. This was back in 1966. Our big new computer (7090) was set for 1967 delivery when the new computer center was to be finished. We had just the most amazing toys. There was a full machine shop for making anything we wanted. There was a warehouse full of military surplus electronic junk that we could glean parts from. My roommate built a kilowatt power supply for his ham radio at a cost of $3 in small parts. He also built an automated maple syrup tap to pour off the hot syrup at exactly the right temperature for their sugarhouse back home. They were working on computer automation of the big turret lathes at the time. We had genuine old German physicists who had worked with Bohr and others who had escaped. The school had the most amazing collection of profs one could hope for. When the old chem building was being cleared out the mechanical analytical balances were going for $5 and a triple beam for $1. The large patch in the brickwork from when Goddard blew up his lab was still visible. He was almost run out of town on a rail at the time after his gasoline powered rockets came down and set cornfields on fire.
Not sure if this relevant to LCF but I had stumbled onto this a little while ago since my maternal grandmother died from MS and one of my paternal aunts has MS. As an aside I also have two family members who died of ALS and myself with the Stiff Person Syndrome. So studying of neurological diseases, the functions of microglia, astrocytes, neurotransmitters, etc. has been a common topic of research for me for some time now sadly.
I’m adding some family history here too. My paternal everything is unknown. My maternal grandfather died at 89 of MS and had regular b12 injections. My mother had colon cancer and survived. My half-sisters have lots of symptoms and one dropped over in the doctor’s office with a heart attack at 45. Being in the hospital was the only thing that saved her life. All my kids carry forward a requirement for the same set of nutrients but in differing ratios and frequencies.
Stiff Person Syndrome is something I came across a lot in my reading, looking by symptoms and b12. In references to SPS there is lots of b12 mention. SACD, like MS has demyelization; does SPS? Death from SACD is usually from paralysis, followed by diaphragm and heart paralysis. It might also be considered terminal exhaustion of the body’s ability to generate the ability to move biochemically. The old PA descriptions, and that would likely but not always be coupled with megaloblastic madness, are contradictory about the interpretation of what is happening in final stages. It’s “not supposed to happen” any more
A similarity between IF and parietal cell antibodies and high MCV and SPS and GAD antibodies. The hypothesis is that IF antibodies cause high MCV via b12 deficiency. Only one problem, high MCV is present long before IF and parietal cell antibodies which tends to show up the longer and worse high MCV is present. The percentage of those lacking GAD and IF/parietal-cell antibodies in their respective situation are about the same. I have no idea if that means anything at all, just something I noticed.
Ok understood I don't dispute the observed effects. So now there is a big mystery for me.
ALCAR is much more blood brain penetratable. Carnitine is very controlled in transport across the BBB. Note to be clear I never said that carnitine is not in the brain nor does it not have any function there but that it could not be the primary source of fuel for the Krebs cycle. Beta oxidation in neurons is normally very low. Hence the emphasis on glucose or ketones.
Endothelial dysfunction? Maybe, in a population without these deficiencies and problems ALCAR response would be different. I have no idea how or why there is so much difference. Also the liquid freebase carnitine from Jarrow (Sigma Tau manufactured) generally works well too. And truly it doesn’t concern me in the least what percentage it accounts for. Maybe that accounts for its very “local” effects as in the limbic system or maybe dorsal horns.
http://en.wikipedia.org/wiki/Astrocyte
Astrocytes in chronic pain sensitization
Under normal conditions, pain conduction begins with some noxious signal followed by an action potential carried by
nociceptive (pain sensing) afferent neurons, which elicit
excitatory postsynaptic potentials (EPSP) in the dorsal horn of the spinal cord. That message is then relayed to the
cerebral cortex, where we translate those EPSPs into "pain". Since the discovery of astrocytic influence, our understanding of the conduction of pain has been dramatically complicated. Pain processing is no longer seen as a repetitive relay of signals from body to brain, but as a complex system that can be up- and down-regulated by a number of different factors. One factor at the forefront of recent research is in the pain-potentiating synapse located in the dorsal horn of the spinal cord and the role of astrocytes in encapsulating these synapses. Garrison and co-workers (Garrison, 1991)[
full citation needed] were the first to suggest association when they found a correlation between astrocyte
hypertrophy in the dorsal horn of the spinal cord and hypersensitivity to pain after peripheral nerve injury, typically considered an indicator of glial activation after injury. Astrocytes detect neuronal activity and can release chemical transmitters, which in turn control synaptic activity (Volters and Meldolesi, 2005; Haydon, 2001; Fellin, et al., 2006). In the past,
hyperalgesia was thought to be modulated by the release of
substance P and excitatory amino acids (EAA), such as
glutamate, from the presynaptic afferent nerve terminals in the spinal cord dorsal horn. Subsequent activation of
AMPA (α-amino-3-hydroxy-5-methyl-4-isoxazole proprionic acid),
NMDA (N-methyl-D-aspartate) and
kainate subtypes of ionotropic
glutamate receptors follows. It is the activation of these receptors that potentiates the pain signal up the spinal cord. This idea, although true, is an oversimplification of pain transduction. A litany of other neurotransmitter and neuromodulators, such as
calcitonin gene-related peptide (CGRP),
adenosine triphosphate (ATP),
brain-derived neurotrophic factor (BDNF),
somatostatin,
vasoactive intestinal peptide (VIP),
galanin, and
vasopressin are all synthesized and released in response to
noxious stimuli. In addition to each of these regulatory factors, several other interactions between pain-transmitting neurons and other neurons in the dorsal horn have added impact on pain pathways.
Two states of persistent pain
After persistent peripheral tissue damage there is a release of several factors from the injured tissue as well as in the spinal dorsal horn. These factors increase the responsiveness of the dorsal horn pain-projection neurons to ensuing stimuli, termed "spinal sensitization," thus amplifying the pain impulse to the brain. Release of glutamate, substance P, and calcitonin gene-related peptide (CGRP) mediates NMDAR activation (originally silent because it is plugged by Mg2+), thus aiding in depolarization of the postsynaptic pain-transmitting neurons (PTN). In addition, activation of IP3 signaling and
MAPKs (mitogen-activated protein kinases) such as
ERK and
JNK, bring about an increase in the synthesis of inflammatory factors that alter glutamate transporter function. ERK also further activates AMPARs and NMDARs in neurons.
Nociception is further sensitized by the association of ATP and substance P with their respective receptors, [[P2X3]], and
neurokinin 1 receptor (NK1R), as well as activation of
metabotropic glutamate receptors and release of BDNF. Persistent presence of glutamate in the synapse eventually results in dysregulation of
GLT1 and
GLAST, crucial transporters of glutamate into astrocytes. Ongoing excitation can also induce ERK and JNK activation, resulting in release of several inflammatory factors.
As noxious pain is sustained, spinal sensitization creates
transcriptional changes in the neurons of the dorsal horn that lead to altered function for extended periods. Mobilization of Ca2+ from internal stores results from persistent synaptic activity and leads to the release of glutamate, ATP, tumor necrosis factor-α (TNF-α), interleukin 1β (
IL-1β), IL-6, nitric oxide (NO), and prostaglandin E2 (PGE2). Activated astrocytes are also a source of
matrix metalloproteinase 2 (
MMP2), which induces
pro-IL-1β cleavage and sustains astrocyte activation. In this chronic signaling pathway, p38 is activated as a result of
IL-1β signaling, and there is a presence of chemokines that trigger their receptors to become active. In response to nerve damage,
heat shock proteins (HSP) are released and can bind to their respective
TLRs, leading to further activation.
ter persistent peripheral tissue damage there is a release of several factors from the injured tissue as well as in the spinal dorsal horn. These factors increase the responsiveness of the dorsal horn pain-projection neurons to ensuing stimuli, termed "spinal sensitization," thus amplifying the pain impulse to the brain. Release of glutamate, substance P, and calcitonin gene-related peptide (CGRP) mediates NMDAR activation (originally silent because it is plugged by Mg2+), thus aiding in depolarization of the postsynaptic pain-transmitting neurons (PTN). In addition, activation of IP3 signaling and
MAPKs (mitogen-activated protein kinases) such as
ERK and
JNK, bring about an increase in the synthesis of inflammatory factors that alter glutamate transporter function. ERK also further activates AMPARs and NMDARs in neurons.
Nociception is further sensitized by the association of ATP and substance P with their respective receptors, [[P2X3]], and
neurokinin 1 receptor (NK1R), as well as activation of
metabotropic glutamate receptors and release of BDNF. Persistent presence of glutamate in the synapse eventually results in dysregulation of
GLT1 and
GLAST, crucial transporters of glutamate into astrocytes. Ongoing excitation can also induce ERK and JNK activation, resulting in release of several inflammatory factors.
As noxious pain is sustained, spinal sensitization creates
transcriptional changes in the neurons of the dorsal horn that lead to altered function for extended periods. Mobilization of Ca2+ from internal stores results from persistent synaptic activity and leads to the release of glutamate, ATP, tumor necrosis factor-α (TNF-α), interleukin 1β (
IL-1β), IL-6, nitric oxide (NO), and prostaglandin E2 (PGE2). Activated astrocytes are also a source of
matrix metalloproteinase 2 (
MMP2), which induces
pro-IL-1β cleavage and sustains astrocyte activation. In this chronic signaling pathway, p38 is activated as a result of
IL-1β signaling, and there is a presence of chemokines that trigger their receptors to become active. In response to nerve damage,
heat shock proteins (HSP) are released and can bind to their respective
TLRs, leading to further activation.
http://en.wikipedia.org/wiki/Endothelial_dysfunction
In human vascular diseases, endothelial dysfunction is a systemic pathological state of the
endothelium (the inner lining of blood vessels) and can be broadly defined as an imbalance between vasodilating and vasoconstricting substances produced by (or acting on) the endothelium.
[1] Normal functions of endothelial cells include mediation of
coagulation, platelet adhesion, immune function and control of
volume and
electrolyte content of the intravascular and extravascular spaces.
Endothelial dysfunction can result from and/or contribute to several disease processes, as occurs in
hypertension,
hypercholesterolaemia,
diabetes,
septic shock,
Behcet's disease, and it can also result from environmental factors, such as from smoking tobacco products and exposure to air pollution.
[2] Endothelial dysfunction is more prevalent in shift workers, a group known to have a higher risk for cardiovascular diseases.
[3] Endothelial dysfunction is a major physiopathological mechanism that leads towards
coronary artery disease, and other atherosclerotic diseases.
[4]
As far as I can tell, Deadlock Quartet blockage can cause endothelial dysfunction and inflammation. Have you ever heard of Robert Rinse and the “Rinse diet”? In the original articles in PREVENTION as well as peer review journals, he described the three forms of cholesterol. He is a physical chemist. The three forms he described was a hard melting point 300 deg C, a 100 deg C melting point form and a blood temperature liquid crystal form. The form being determined by the fatty acids in the body, i.e. lecithin, polyunsaturated fats, Vit C, b-complex and a few things. I have met several people for whom it worked exactly as described. That was what put me onto the fatty acids. His hypothesis is that the liquid crystal form literally protected the endothelial tissues in the blood vessels from eroding and damage and also the fatty acids and vitamins would convert the surface of the hard deposits to liquid form and they could melt away in 6 months, if you had all the right factors.
http://www.quackwatch.org/13Hx/dr_rinse/brochure.pdf
Now I had all those chronic pain problems. I still take 180mg of morphine daily for pain attendant to car wreck damage. I used to take Dilantin for the neurological pain and it worked very well. I used to take 2400mg of ibuprofen a day for inflammation. Both became totally unneeded in 1 year
I had direct damage to the dorsal horns from hyper-extension back in 1972 down the left side of my back. There is a pronounced asymmetry in my back and shoulder muscles
http://circ.ahajournals.org/content/early/2012/10/25/CIRCULATIONAHA.112.134304.abstract
Background—Tissue edema and endothelial barrier dysfunction as observed in sepsis and acute lung injury carry high morbidity and mortality, but currently lack specific therapy. In a recent case-report, we described fast resolution of pulmonary edema upon treatment with the tyrosine kinase inhibitor imatinib through an unknown mechanism. Here, we explored the effect of imatinib on endothelial barrier dysfunction and edema formation.
Methods and Results—We evaluated the effect of imatinib on endothelial barrier function in vitro and in vivo. In human macro- and microvascular endothelial monolayers, imatinib attenuated endothelial barrier dysfunction induced by thrombin and histamine. siRNA knock-downs of the imatinib-sensitive kinases revealed that imatinib attenuates endothelial barrier dysfunction via inhibition of Abl-Related Gene kinase (Arg/Abl2), a previously unknown mediator of endothelial barrier dysfunction. Indeed, Arg was activated by endothelial stimulation with thrombin, histamine and VEGF. Imatinib limited Arg-mediated endothelial barrier dysfunction by enhancing Rac1 activity and enforcing adhesion of endothelial cells to the extra-cellular matrix. Using mouse models of vascular leakage as proof-of-concept, we found that pretreatment with imatinib protected against VEGF-induced vascular leakage in the skin, and effectively prevented edema formation in the lungs. In a murine model of sepsis imatinib treatment (6h and 18h after induction of sepsis) attenuated vascular leakage in the kidneys and the lungs (24h after induction of sepsis).
Histamine, and edema, appears to result from severe folate insufficiency/deficiency at least in the situations we have been discussing.
To clarify, when you say "what are the tests", what for? For assessing a methyl b12 supplement?
I and others can identify a really good MeCbl in the first injection of 7.5mg or more subcutaneously. It can take a week to identify a slightly lesser quality MeCbl and a month to identify the barely acceptable by in vivo trials. I am hoping that it is indeed a difference in the form of MeCbl by various bacterial cultures as some report as “known”. Other researchers think it is a mix of MeCbl and various others caused by errors in the refining and concentration process. The pharmacy uindependent analysis that is done for every batch from the compounding pharmacy I use says 100% MeCbl. There are tremendous differences from batch to batch. Preparing my own it is absolutely rock steady from prep batch to prep batch. But it isn’t good enough. I used 5 star mecbl for almost a year. I think a mass spec and an NMR could show us the differences. Maybe some other tests could be useful. If we could get an NMR signature of human CNS effective batches it would provide a way of testing for the best batches to buy.
why do you never bring up the high levels of microglial activation and inflammation now know to be signatures of most of the CNS diseases you listed. You focus exclusively it seems on the MMA levels. Why not the inflammation? Can't that tie back into adb12 / BH4 and peroxynitite removal and the low MMAs are a correlative finding?
First I am not certain that neurons and glial cells process mitochondrial fuels the same way. I have to check on that. People often focus on the neurons for obvious reasons, but glial cells and microglia are extremely important and being strongly implicated in several neurological disorders.
Sounds good to me. I didn’t know about them.
Just like in physics when I was studying black holes and neutron stars. Any hypotheseses had to obey constraints placed on me by other research data.
Hehe understood. Trust me I have never stopped being a physicist regardless of my occupation. We are what we are, nothing more, nothing less.
Black holes and neutron stars, you have to love them. You can’t leave them. After all what can reach through a General Products hull? I did a financial model that I named Black Hole back about 82-87. What it did was to model the conditions that would lead to a possibly worldwide bank collapse triggered by a real estate bubble collapsing or something similar. At the time I wrote it I thought it would be the Japanese real estate collapse. Who would believe such a thing could happen in this modern day of regulation. Ridiculous program. That one went down the black hole of no longer supported floppy formats. I do understand working within constraints unless you can show how they don’t apply.
" ... neurodegenerative diseases does NOT have to mean that neuronal mitochondria make heavy use of the methymalonic pathway as a primary energy source". There are other alternate explanations is all I am suggesting.
There are all sorts of ANDs involved and other explanations. I don’t really care and never claimed as a PRIMARY energy source and never even used that word. If I implied such, it was not intentional. I was just trying to get agreement that it wasn’t 100% glucose and that AdoCbl and LCF COULD make a difference unmatched by HyCbl, and that at least a part of that was ATP related. This is the first time the discussion has gone beyond that.
Personally what I find attractive is you are talking about a merger between two of the most important biochemical processes in the body namely ATP production (aerobic respiration) and methylation (which affects gene expression among many other things). But I would add that there may be important effects involving the immune system / inflammation and others like blood brain barrier integrity for the CNS. While not as compact as the Deadlock quartet, they may explain some people's differing responses to increasing the flux through these two cycles (three if you add in the folate cycle).
The immune system is strongly affected by folate and b12s. Almost all of it appears to correct over some number of years. Actual existing autoimmune damage doesn’t appear to be affected. Methyltrap appears to turn on the hyper responses of many kind;, asthma, allergies, MCS, and lack of resistance to viruses and bacteria. I’ve got to get that symptoms/nutrient analysis up.
Fair enough. Just please realize it was not my intention to attack anything you said. I was simply stating what I know about brain energy metabolic processes. You don't need to convince me about the idiocy rampant in the medical community. I could tell you horror stories (as I suppose many on here could) about a decade worth of misdiagnosis and fighting with doctors to get to someone who could save my life. Not fun.
Not fun at all. I know exactly what that is like. And so do a sizable percentage know the frustration. I found the emotional elevator of expectations and hopes and dreams always being crashed too much to deal with.