Carol in PA
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posted
quote: Laboratory research has revealed that in the progressive, debilitating disease ALS, one of the many processes involved in disease progression appears to be damage of nerve cells by accumulation of glutamate.
posted
The keets kill neurons and the treatment kills neurons because it triggers inflammation. I have posted this before, guess you didn't see it. So, basically, if you are one of those who are damaged by the inflammation (not everyone is who has muscle wasting), then you are damned if you treat, and damned if you don't treat.
I repeat: not everyone with muscle wasting gets worse with treatment. Some people do fine.
Here is an article that explains some of the mechanism for inflammatory damage. There is also a citation in Dr. Fallon's recent paper that deals with peripheral neuropathy being transmitted to the CNS and staying at a high level even after the periphery has decreased its inflammatory atmosphere.
Microglia Are Mediators of Borrelia burgdorferi-Induced Apoptosis in SH-SY5Y Neuronal Cells
Tereance A. Myers, Deepak Kaushal, Mario T. Philipp*
Division of Bacteriology & Parasitology, Tulane National Primate Research Center, Tulane University Health Sciences Center, Louisiana, United States of America
Abstract
Inflammation has long been implicated as a contributor to pathogenesis in many CNS illnesses, including Lyme neuroborreliosis. Borrelia burgdorferi is the spirochete that causes Lyme disease and it is known to potently induce the production of inflammatory mediators in a variety of cells.
In experiments where B. burgdorferi was co-cultured in vitro with primary microglia, we observed robust expression and release of IL-6 and IL-8, CCL2 (MCP-1), CCL3 (MIP-1?), CCL4 (MIP-1?) and CCL5 (RANTES), but we detected no induction of microglial apoptosis. In contrast, SH-SY5Y (SY) neuroblastoma cells co-cultured with B. burgdorferi expressed negligible amounts of inflammatory mediators and also remained resistant to apoptosis. When SY cells were co-cultured with microglia and B. burgdorferi, significant neuronal apoptosis consistently occurred. Confocal microscopy imaging of these cell cultures stained for apoptosis and with cell type-specific markers confirmed that it was predominantly the SY cells that were dying.
Microarray analysis demonstrated an intense microglia-mediated inflammatory response to B. burgdorferi including up-regulation in gene transcripts for TLR-2 and NF??. Surprisingly, a pathway that exhibited profound changes in regard to inflammatory signaling was triggering receptor expressed on myeloid cells-1 (TREM1). Significant transcript alterations in essential p53 pathway genes also occurred in SY cells cultured in the presence of microglia and B. burgdorferi, which indicated a shift from cell survival to preparation for apoptosis when compared to SY cells cultured in the presence of B. burgdorferi alone.
Taken together, these findings indicate that B. burgdorferi is not directly toxic to SY cells; rather, these cells become distressed and die in the inflammatory surroundings generated by microglia through a bystander effect. If, as we hypothesized, neuronal apoptosis is the key pathogenic event in Lyme neuroborreliosis, then targeting microglial responses may be a significant therapeutic approach for the treatment of this form of Lyme disease.
Author Summary
Lyme disease, which is transmitted to humans through the bite of a tick, is currently the most frequently reported vector-borne illness in the northern hemisphere. Borrelia burgdorferi is the bacterium that causes Lyme disease and it is known to readily induce inflammation within a variety of infected tissues.
Many of the neurological signs and symptoms that may affect patients with Lyme disease have been associated with B. burgdorferi-induced inflammation in the central nervous system (CNS). In this report we investigated which of the primary cell types residing in the CNS might be functioning to create the inflammatory environment that, in addition to helping clear the pathogen, could simultaneously be harming nearby neurons.
We report findings that implicate microglia, a macrophage cell type in the CNS, as the key responders to infection with B. burgdorferi. We also present evidence indicating that this organism is not directly toxic to neurons; rather, a bystander effect is generated whereby the inflammatory surroundings created by microglia in response to B. burgdorferi may themselves be toxic to neuronal cells.
Citation: Myers TA, Kaushal D, Philipp MT (2009) Microglia Are Mediators of Borrelia burgdorferi-Induced Apoptosis in SH-SY5Y Neuronal Cells. PLoS Pathog 5(11): e1000659. doi:10.1371/journal.ppat.1000659
Editor: Jenifer Coburn, Medical College of Wisconsin, United States of America
Received: May 11, 2009; Accepted: October 19, 2009; Published: November 13, 2009
Copyright: � 2009 Myers et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Funding: This work was supported by grants NS048952 and RR00164 from the National Institutes of Health. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.
Competing interests: The authors have declared that no competing interests exist.
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karenl
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I have heard that ALS is pseudomonas pseudomallei. The biofilm test from frylabs can detect it. I think it is not lyme. At the moment I have nothing in writing to prove ,so take it as a memo and get the test done.
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What good is another test if there is no treatment for it?
And my personal opinion is that "ALS" is the endpoint that is reached from a number of paths, lyme being one of them.
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Pocono Lyme
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I can only give you my experience.
I was extremely weak and had lost so much muscle mass I couldn't do IM injections per LLMD.
My muscle mass came back with Babesia treatment.
When I relapse the extreme weakness returns.
-------------------- 2 Corinthians 12:9-11
9 But he said to me, �My grace is sufficient for you, for my power is made perfect in weakness.� Therefore I will boast all the more gladly about my weaknesses, so that Christ�s power may rest on me. Posts: 1445 | From Poconos, PA | Registered: Jul 2004
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GiGi
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posted
It all starts with T O X I N . That is where the unraveling should start and on time before adding more and more and before it is too late.
Take care.
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Marnie
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At the outset of lyme (according to the Romanian abstract) Mg levels drop "significantly".
The % drop just happens to equal that
in our muscle.
We have a lot of Mg-ATP in our muscles 'cause we gotta MOVE and that takes a lot of energy. ATP is our energy carrier. (Men have more muscle and this is to their advantage i.e., more available Mg at the outset.)
(The drop in Mg levels at the outset of lyme is about 33% if my math serves me correctly).
(Why all the Mg-ATP in our liver doesn't "help out" maybe due to an immediate increase in the cytokines, TNF alpha and IL 6. In other words, our liver is impacted negatively from the get-go...immediately. TNF alpha and IL 6 prevent the liver from converting caprylic acid to a helpful ketone called BHB.)
Mg is attached to ATP as Mg-ATP and helps to transfer phosphate groups onto proteins.
If insufficient glucose is available to feed our cells to *make ATP* which binds strongly and first to Mg -> Mg-ATP, we will follow other routes to make ATP:
gluconeogenesis OR ketogenesis.
VERY simply stated: ATP -> ADP -> ATP.
In reality it takes TWO phosphates for that to happen.
With insufficient glucose, we breakdown fats first and finally proteins into various amino acids to supply energy and to make other proteins, etc.
There is the muscle wasting.
Caprylic acid -> BHB (in the liver) if TNF a and IL 6 are NOT present)-> "extra" nutrients which enter the citric acid cycle -> citrates - which inactivate PFK and ATP is increased which also binds to available Mg as Mg-ATP to transfer phosphate groups onto proteins.
Mg is an anti-inflammatory, anti-histamine (important to prevent IgE from kicking in), and *inactivates* HMG CoA reductase.
Bb maybe using Mg (export?)as one nutrient to build his biofilm.
Bb inhibits phosphate transfer. I think Bb's PKC inhibitor is PKCB2.
Protein kinase Cβ 2 is involved in a glucose-sensitive, Ca2+-dependent signalling pathway, which is possibly involved in the regulation of glucose transport
in skeletal muscle.
Look at what happens if PKCB2 is INHIBITED:
Inhibition of PKCb2 activation with the specific inhibitor, LY379196, attenuated (diminished) ***serine phosphorylation of core 2 GlcNAc-T (β-1,6-acetylglucosaminyltransferase)*** and prevented increased leukocyte-endothelial cell adhesion.
Bb is PPi-PFK dependent. PPi= pyrophosphate. TWO phosphates. PFK is phosphofructokinase. It is the "rate limiting" enzyme for glycolysis.
Bb follows the "anaerobic glycolytic mode of ATP generation" which
leads ultimately to *lactate.*
Which is re-used.
The increased lactate produced can be removed in a number of ways including conversion to glucose via gluconeogenesis in the liver and release back into the circulation (Cori cycle).
Glucose and gluconeogenesis are "on" to help Bb make his ATP. That leaves ketogenesis, but one ketone cannot be made when TNF alpha and IL 6 are present i.e., BHB.
ICHT in Italy and infrared in Germany goal was to increase ATP.
In the U.S., a "medicinal food" called Axona (for Alzheimer's) contains caprylic acid. The idea is...caprylic acid -> BHB (in the liver) -> more ATP (BHB = a ketone can cross the BBB).
However, keep in mind...caprylic acid cannot convert to BHB in the liver IF there is too friggin much inflammation going on (TNF alpha and IL 6).
ONGOING INFLAMMATION IS BAD. IT BLOCKS US FROM HEALING. And the free radicals that oxidize LDL also can damage our DNA. Hello cancer.
Some believe the ketone, BHB is incapable of anaplerosis. But I think it can work IF we tame down the inflammatory cytokines ALSO.
Anaplerosis = "rescue" the cells depleted of very specific nutrients.
The transport of *lactate*, pyruvate, and BHB across cellular plasma membranes uses the same family of monocarboxylate transporter proteins. (Bb looks to use the first two.)
The citric acid cycle -> citrate which inactivates PFK.
Nerve connection: we need cholesterol to build the myelin sheath (the insulation around our nerves).
In a jam, with a severe infection, cholesterol levels will plummet. The amino acids in fats and proteins needed to make other proteins, enzymes, hormones, etc. will be shuffled off.
LDL = low density LIPO PROTEINS.
Prolactin, used in mice engineered to have MS, spontaneously restored the myelin sheath. Melatonin is its "counter".
Bb follows the "cholesterol pathway" to build "his" cell walls. HMG CoA is being REDUCED.
Melatonin is high because our #1 anti-oxidant, glutathione plummets.
Balance...this is all about balance...oxidative stress vs. control of excessive "free radicals".
The body will try hard to figure out how to prolong life.
Both Bbu and Tpa are expected to derive energy primarily from anaerobic sugar metabolism via the Embden-Meyerhof-Parnas glycolytic pathway.
Find a picture of that pathway and watch for pyruvate and lactate.
Then remember BHB, pyruvate and lactate use the same transport proteins.
I know this is a lot to understand and is "scattered", but so much is happening simultaneously that it is hard to put it in sequence.
But perhaps the following may help you to understand (I've posted this elsewhere too.)
Bb first expresses OspA which triggers ROS (reactive oxygen species) -> oxLDL (oxidized low density lipoproteins) via macrophage (a white blood cell) activation of CB1.
OxLDL -> caspase 9 and then capase 3.
Caspase 3 cleaves MAGI-1 which is required for Rap 1 activation.
But CB2 Rap1 is needed to inhibit CB1 stimulated ROS production.
When Bb's OspA is oxidized, Bb changes his outer cell wall to OspB and the cell sends to the surface, a receptor called CB2 which works the opposite.
Agonists (helpers) of the CB2 receptor STOP INFLAMMATION. It is a call for help.
But by then our own antibody to CB2 is damaged (mAB CB2).(Mg and Ca can restore.)
Bb was counting on that to survive. It needed to buy time.
Your LLMD will understand this:
Macrophage CB1, not CB2, induced phosphorylation of p38-mitogen-activated protein kinase.
p 38 MAPK.
Kinases transfer phosphate groups.
Then Bb's toxin cleaves the phosphates off proteins.
PPi-PFK.
The cure is 2-fold:
Get inflammation down (TNF alpha, IL6 and ILB) AND hit Bb.
Look very closely at the omega 3, EPA.
Google: Tamoxifen EPA (tamoxifen CITRATE is a man-made PKC inhibitor)
Google: EPA multiple myeloma
The ligand for the CB receptors (both) looks to be 2 AG. 2-Arachidonoylglycerol
Omega 6 - Omega 3 balance is way off.
OUR TOXIN!
Protein generated from this cloned Bb gene was examined biochemically and found to have characteristics similar to that of botulinum, the toxin of Clostridium botulinum,
a zinc endoproteinase.
Borrelia burgdorferi-Induced Expression of Matrix Metalloproteinases from Human Chondrocytes Requires Mitogen-Activated Protein Kinase and Janus Kinase/Signal Transducer and Activator of Transcription Signaling Pathways
(MAPK and JAK/STAT signalling pathway -> MMPs.)
MMPs are *zinc endopeptidases* involved in the degradation of extracellular matrix.
oxLDL triggers MMPs.
"oxLDL induced MMP9..."
Caspase 9 has been linked to the mitochondrial death pathway.
Following death...reconstruction.
MMPs = tissue remodeling
BTW...
Doxycycline, at subantimicrobial doses, inhibits MMP activity. It also contains ketones: The presence of adjacent ketone groups gives tetracyclines the ability to chelate divalent metals.
" Doxycycline, a member of the tetracycline family, not only inhibits MMP synthesis but also chelates Zn2+ (required by MMPs) and thus suppresses the activity of MMP-2 and MMP-9"
posted
If what Marnie just said was that the toxins created by the lyme disease interfers with the electrical impulse sent from one nerve cell to another by docking with nerve cell. As more toxins dock with more nerve cells the condition becomes worse. When you kill the disease, the toxins are eliminated from the body, a la botox, in about a year. Botulism kills by toxins docking on to nerve cells in the chest area. It happens quickly so toxin removal isn't effective. In ALS, toxins first attack those nerve cells that it can match up with. Over time more cells dock.
The easy way to determine if it is a toxin and not something else is it attacks one side of the body and usually a hand or foot first. If it were a true case of ALS, it would attack equally as it by definition, before the anterior horn of the spinal column.
This was the simple explanation given to me by our doctor after my wife had been dx with ALS and while being examined for the posibility of lyme instead. I was convienced he knew what he was talking about when her breathing become difficult and he changed her ABX to Rochephin. With hours, her breathing became normal.
For some reason, Rochephin is good for infection near or in the chest area. It killed the lyme there and did it quickly preventing a build up of toxins in that area.
Posts: 219 | From Aubur,Al. USA | Registered: Oct 2004
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Marnie
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Member # 773
posted
I edited the above while you were typing too.
If we don't turn off oxidizing LDL, MMP9 will continue to be upregulated.
MMPs are zinc endopeptidases. This is a toxin WE make.
Once again, the abx. HELP, but the cure is 2-fold:
GET THE INFLAMMATION DOWN AND hit the pathogen.
I can't show the downward arrow, but all these -> are downward:
was specifically inhibited by protein kinase C (PKC)- inhibitor (Rottlerin), but not PKC-B2 inhibitor indicating the possible involvement of
PKCd in HG (high glucose) signaling
Tamoxifen may downregulate PKCd and upregulate the PKCe.
"The team from Garvan's Diabetes Signalling Unit, led by Associate Professor Trevor Biden and Dr Carsten Schmitz-Peiffer, has identified an enzyme known as
"PKCepsilon" (PKCe) that is active during diabetes and blocks the availability of insulin.
Their findings are published in the journal Cell Metabolism."
Insulin Activates PFK. Bb is PFK dependent. IL1 B tries to control.
ONGOING elevation of TNF alpha and IL 1 B will destroy pancreatic cells.
BTW...if you are diabetic, curing lyme will be a lot harder, but researchers in Canada have discovered a protein to...get this...regrow pancreatic beta cells. It is called Exsulin and is in test mode at Mayo's and in Canada.
IME, ALS is not Lyme, but the toxins from Lyme may trigger ALS. Abx did not help me.
I believe I am turning a corner, thanks to Allergie-Immun therapy, liver supporting herbs and ASEA.
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Marnie
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CB1 and CB2 receptors and glutamate:
2-arachidonoylglycerol (2-AG)
It is an ester formed from the ***omega-6*** fatty acid arachidonic acid and glycerol
``2-AG then *activates* presynaptic CB1 receptors, which reduces glutamate releases and tempers excitotoxicity (11-13).
2-AG will also activate CB1 receptors expressed by blood vessels, which will
decrease cerebral blood flow
and reduce edema expansion (14).
Finally, 2-AG will activate CB2 receptors expressed by microglial cells and invading immune cells, which inhibits their ability to release cytotoxic agents (42).
Even small amounts of insulin can turn off *ketoacid* formation.
In addition, several cytokines such as IL1, IL6 and TNF alpha antagonise the effects of insulin.
However, hyperglycaemia also stimulates the production of advanced glycosylated end products, enhances the polyol pathway and activates protein kinase C. These conditions may lead to
posted
As usual I don't understand a bit of the biochem or have a clue what to do about this. I am already taking a lot of Mg. No lyme doc is going to prescribe tamoxifen for ALS/Lyme.
Unless there is a way to use this information, I see no point in reading it.
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posted
Marnie, In a nutshell, what would is your bottom line recommendation to take down inflammation?
-------------------- When we are no longer able to change a situation---we are challenged to change ourselves. (Viktor Frankl- Holocaust survivor) Posts: 460 | From Maine | Registered: Apr 2009
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Marnie
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Member # 773
posted
Read my answer again and see I never really answered your main question. Doc said muscle athrophy, if any, was due to not using the muscle, not any kind of nerve cell death or muscle injury.
In my wife's case she could stand if pulled up, but not lift herself. That meant some muscles worked right next to those that didn't.
After 7 months of Abx she was just beginning to get volunteer movement back in her arms.
Posts: 219 | From Aubur,Al. USA | Registered: Oct 2004
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Marnie
Frequent Contributor (5K+ posts)
Member # 773
posted
Nutshell...OmegaBrite (and I have no ties to it) to help reduce TNFa, IL 6 and ILB.
It is avail. over the internet and children's doses are also avail.
TNF alpha and IL6 look to inhibit the liver from making BHB from caprylic acid (which IS in our diets).
AND (!) Look closely at Capryl (a supplement).
NORMALLY caprylic acid -> BHB in the liver IF inflammation is not present.
BHB -> increased ATP because it supplies missing nutrients that enter the citric acid cycle-> citrate.
Citrates inactivate PFK.
Bb is dependent on PFK...PPi-PFK.
AND increased ATP opens K channels. Bb doesn't like K (Cl), it will slow it down, but not destroy it.
Hyperglycemia can cause hypokalemia -> muscle weakness.
This is why "Coke" is so bad for us.
"The BBC reports that drinking ***excessive amounts*** of cola can lead to muscle weakness and possibly even muscle paralysis.
This information is from a study published in the International Journal of Clinical Practice, and shows that the ingredients within soda
***can cause blood potassium levels to plummet.***
The study finds that when the three main ingredients commonly found in soda -- glucose, fructose, and caffeine -- are consumed in large quantities, it can lead to "caffeine intoxication" and
***"dangerously low" blood potassium levels.***
Even caffeine-free cola can be dangerous, researchers noted, because it still contains fructose.
Mg is attached to our ATP as Mg-ATP. ATP is our cells' energy transporter.
CONCLUSION: Low levels of Mg-ATP and free Mg(2+) are concordant with weakness and fatigue observed in DM and JDM patients. Immunosuppressive therapy alleviates, in part, the magnesium deficits in the diseased muscles. Therefore, Mg-ATP and free Mg(2+) may play a significant role in the pathophysiology of these diseases.
PMID: 11840451
ATP drives Mg back into the cell where it binds to ATP (very strongly) as Mg-ATP.
Do NOT use steroids!!! We know they make lyme WORSE. It has to do with Na channels.
P.S. Lyme patients can have hyperkalemia at the outset of lyme, but eventually, hypokalemia can happen. That is a very tricky and dangerous electrolyte to balance!
posted
Mom and my cousin (her niece) both died of ALS. It is very scary for me to observe symptoms in myself that Mom had. But my LLMD said that my treatment will keep me from progressing so rapidly as she did.
She had terrible arthritis which involved a hip replacement. What do you think they gave her in great quantities? Steroids, of course! When her speech became slurred, they didn't connect the dots. She trembled, had trouble swallowing, etc.
My cousin was a chain smoker, heavy drinker and was an investment broker... lots of stress. She was probably the most toxic person I knew. She wound up completely paralized in a wheelchair until she died.
I truly believe that both of them could have been saved...by a different lifestyle and intelligent medical care. And I intend to prove that I'm right by getting better myself! So there!
-------------------- DOCTOR: "I don't think you are sick." PATIENT: "We are all entitled to our opinions. I don't think you are a doctor." Posts: 697 | From Northern California | Registered: Jul 2009
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Marnie
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Member # 773
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Review and then some added information:
Bb first expresses OspA which triggers ROS (reactive oxygen species) -> oxLDL (oxidized low density lipoproteins) via macrophage (a white blood cell) activation of CB1.
OxLDL -> caspase 9 and then caspase 3. (Remember the word "caspase" for later too.)
Caspase 3 cleaves MAGI-1 which is required for Rap 1 activation. No Rap1 activation happens.
But CB2 Rap1 is needed to
inhibit CB1 stimulated ROS production.
When Bb's OspA is oxidized, Bb changes his outer cell wall to OspB and the cell sends to the surface, a receptor called CB2 which works the opposite.
Agonists (helpers) of the CB2 receptor STOP INFLAMMATION. It is a call for help.
But by then our own antibody to CB2 is damaged (mAB CB2).(Mg and Ca can restore that antibody i.e., mAB CB2.)
Bb was counting on that to survive. It needed to buy time.
The caspase-dependent apoptosis (cell death) cascade is initiated, causing cells to "commit suicide." (Remember I said to keep the word, caspase, in mind.)
If the cell dies through necrosis, it releases glutamate and toxic chemicals into the environment around it. Toxins poison nearby neurons, and glutamate can overexcite them."
Is this the "herx" response? Are we killing off infected defense cells?
What happens to Bb?
Wouldn't it be better to SUPPORT the infected DEFENSE cells that are being starved of nutrients? Knock off Bb
and then, if needed (DNA damage) let the cells die...slowly.
How?
Increasing BHB (a ketone) which goes into the citric acid cycle -> more citrate -> increased ATP and inactivate PFK. (This is how the AD "medicinal food" called Axona works i.e. caprylic acid -> BHB -> ATP.)
Bb is PPi-PFK dependent.
(BHB does not look to supply citric acid "intermediates".)
"Inhibition of the TCA cycle (citric acid cycle)and fatty acid oxidation due to ***increased TCA cycle intermediate concentrations*** and reduced mitochondrial red-ox state lead to the development of steatosis."
Steatosis here(basically the abnormal retention of lipids within a cell):
The liver cannot convert caprylic acid to the helpful ketone, BHB, when TNFa and IL6 are present. So getting the inflammatory cytokines down is paramount.
It appears we need to get the inflammatory cytokines DOWN (bigtime). They include TNFa, IL6 and IL1 B.
We can make ATP 3 ways: glycolysis, gluconeogenesis and ketogenesis.
It appears the first 2 are "on". While the 3rd route maybe the key...esp. the ketone (BHB), not all of the ketones, just that one.
Because ketogenic diets can be/ARE very dangerous esp. kidney wise, it is important to know what BHB might do to the kidneys:
"Fish oil is no snake oil" (Discover Magazine March, 2010 pg. 14) Quoting:
(The Omega 3 fatty acids: "Slow the formation of plaques. Lower blood pressure. Improved insulin sensitivity (reduced risk of diabetes). May raise intelligence scores.
EPA converts to DHA which converts to resolvin D2 which prevents neutrophils from sticking to the walls of blood vessels and initiating an inflammation response.
In mice with sepsis, resolvin D2 reduced the widespread swelling that usually accompanies the condition WITHOUT IMPAIRING THE IMMUNE SYSTEM'S ABILITY TO FIGHT THE UNDERLYING INFECTION."
How important is PPARy?
Very.
Taken together, our results suggest that activation of PPARγ may represent a novel approach for the treatment of pancreatic cancer by increasing PTEN levels and inhibiting PI3K activity.
Tame down the inflammation AND hit the pathogen (or support our own antibodies via increasing Mg levels because Mg and Ca are needed to MAKE healthy antibodies).
Mg INactivates HMG CoA reductase, and is an anti-inflammatory and (important) and anti-histamine (vital if IgE kicks in - allergic reaction when histidine converts to histamine).
It appears very high levels of EPA are needed.
OmegaBrite.
Doses and timing?
Shelly, glutamate is glutamic acid (sort of). Think of it as the brain's "accelerator". GABA comes FROM glutamate. It is the brain's "brakes". First acceleration and then the brakes. These 2 are known as the "workhorses" of the brain.
[ 04-10-2010, 10:52 AM: Message edited by: Marnie ]
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