Hi Interrupted,
Well done on the exam. Smart and beautiful is a good combination.
JCV obviously means no immunosuppressive agents for you. A strong immune system is going to be critical.
If you google "JCV tonsils" guess what pops ups up? It also loves B cells so it may be affected by your use of Valtrex. Who knows? Clearly the researchers don't.
It appears 80% of the population have JCV which is annoying when you consider how little testing is done before drugs are used.
It might be worth asking Buhner on his website if he has a strategy for JCV. http://www.buhnerhealinglyme.com/contact/ or your local lyme people. I suspect they will not reply quickly.
LyndaCarol, we are now jumping into fatty acids and amino acids! We might get lost but its probably the right place to look.
Maybe a ketogenic diet with a coconut core might help, Coconut is also alkaline. Maybe a very alkaline diet may help.
Now we are guessing.
Regards
Beyond Avonex and Valtrex
Re: Beyond Avonex and Valtrex
Many people think of coconut water as a health food. However, one 11 ounce serving contains 15 g of sugar. That's about 3.75 teaspoons worth.lyndacarol wrote:Coconut Milk
Coconut milk is made from the expressed juice of grated coconut meat and water. About 50 percent of the fat in coconut oil is lauric acid, which is rarely found in nature. Your body converts lauric acid into monolaurin, a monoglyceride that can actually destroy lipid-coated viruses such as HIV and herpes, influenza, measles, gram-negative bacteria, and protozoa such as Giardia lamblia.
Lauric acid is a type of medium chain fatty acid (MCFAs), which is easily digested and readily crosses cell membranes. MCFAs are immediately converted by your liver into energy rather than being stored as fat.
Edited to add: Coconut begins to sound like the "cure for all diseases." Consider the source: Coconut Research Center http://www.coconutresearchcenter.org/
Fun Science Facts from the Library of Congress: http://www.loc.gov/rr/scitech/mysteries/coconut.html
Coconut Oil and Alzheimer's Disease (I first heard of Mary Newport, M.D., a few years ago.): http://www.anh-usa.org/coconut-oil-and- ... s-disease/
The intravenous use of coconut water (January 2000): http://www.ncbi.nlm.nih.gov/pubmed/10674546
Re: Beyond Avonex and Valtrex
Hi NHE,
Is there a distinction between the water, the milk and the cream ion terms of sugar?
Regards
Is there a distinction between the water, the milk and the cream ion terms of sugar?
Regards
Re: Beyond Avonex and Valtrex
Yes. Coconut oil is sugar free. I don't know how this differs from coconut cream, but it's likely similar. Read the label though as some brands have added sugar. Coconut milk will vary by brand depending on what's added to it. Essentially, shredded coconut is soaked in water and then squeezed and strained. One brand I looked at only had 1 g of sugar per 8 oz serving.Scott1 wrote:Is there a distinction between the water, the milk and the cream in terms of sugar?
Re: Beyond Avonex and Valtrex
A scientific summary of the activation of Toll Receptor 2 and Toll receptor 4 in the inflammatory phase of demyelination -
Although this summation comes from an Iranian journal it draws heavily on well recognised sources and makes a cogent summation of what I described during my attack. (see- http://iji.sums.ac.ir/june2014/2ndiji_v ... 2_2014.pdf )
“Our study showed that TLR-2 and TLR-4 on PBMCs correlate with MS neurodegeneration. We have identified TLR-2 and TLR-4 overexpression on PBMC of MS patients in comparison with healthy controls. Bystander activation and molecular mimicry are the suggested mechanisms for triggering autoimmune responses in the CNS by pathogenes, which are likely to be mediated by TLRs. Tissue damage can unmask myelin antigens, resulting in epitope spread and expansion of autoimmunity.
TLR-2 is a ligand for Gram-positive bacteria such as Staphylococcus aureus and
Streptococcus pneumoniae. Cell wall of these bacteria contains molecules such as peptidoglycan (PGN), which act as PAMPs and can activate TLR-2. Some viral molecules can also activate immune system via TLR-2 or TLR-4 as seen in Herpes simplex virus 1.
Our study shows the relation between expression of TLR-2, TLR-4, and neuronal damage in the CNS in NC patients with MS.”
I also found this interesting note (see- https://collab.itc.virginia.edu/access/ ... _TLR4.html )
“Toll-Like Receptor 4's extracellular domain can bind and recognize many different bacterial components of LPS including n-acetyl-d-glucosamine (Nag) pocket, lauric acid, 3-hydroxy-tetradecanoic acid, and L-glycero-D-Manno-Heptopyranose in addition to microbe-derived ligands, TLR4 recognizes various endogenous ligands including heat shock proteins HSP60, HSP70 and gp96, Alpha-defensin, Tamm-Horsfall protein, biglycan , fibrinogen, surfactant protein, low-molecular weight oligosaccharide fragments of hyaluronan, fibronectin, and heparansulfate [10]. Hence, the TLRmediated immune response can be activated in the absence of foreign microbes. Prosthetic groups of TLR4 include magnesium and phosphate ions, which serve to arbitrate receptor functionality. Important post-translational modifications defining functionality of TLR4 include glycosylation of Asn residues and di-sulfide bond formation between Cys residues.”
So we can see from this that a component of peptidoglycan (my friend N-acetyl-d-glucosamine) can bind to Toll-like receptor 4 without the presence of a microbe. The previous document points out that viral molecules and bacterial molecules can activate TLR2 and TLR4 creating a cytokine storm. This is possibly the mechanism for our demyelinating phases. Hence something that binds and blocks those receptors is required to prevent a demyelinating attack. It tends to support the view that this mechanism is separate from the peroxynitrite/iNOS/ADMA mechanisms described earlier but there is probably an important link still obscured.
There are lymphocytes antigens required to bind the Toll-like receptors to the peptidoglycans. Perhaps they arise through the other mechanism.
Regards
Although this summation comes from an Iranian journal it draws heavily on well recognised sources and makes a cogent summation of what I described during my attack. (see- http://iji.sums.ac.ir/june2014/2ndiji_v ... 2_2014.pdf )
“Our study showed that TLR-2 and TLR-4 on PBMCs correlate with MS neurodegeneration. We have identified TLR-2 and TLR-4 overexpression on PBMC of MS patients in comparison with healthy controls. Bystander activation and molecular mimicry are the suggested mechanisms for triggering autoimmune responses in the CNS by pathogenes, which are likely to be mediated by TLRs. Tissue damage can unmask myelin antigens, resulting in epitope spread and expansion of autoimmunity.
TLR-2 is a ligand for Gram-positive bacteria such as Staphylococcus aureus and
Streptococcus pneumoniae. Cell wall of these bacteria contains molecules such as peptidoglycan (PGN), which act as PAMPs and can activate TLR-2. Some viral molecules can also activate immune system via TLR-2 or TLR-4 as seen in Herpes simplex virus 1.
Our study shows the relation between expression of TLR-2, TLR-4, and neuronal damage in the CNS in NC patients with MS.”
I also found this interesting note (see- https://collab.itc.virginia.edu/access/ ... _TLR4.html )
“Toll-Like Receptor 4's extracellular domain can bind and recognize many different bacterial components of LPS including n-acetyl-d-glucosamine (Nag) pocket, lauric acid, 3-hydroxy-tetradecanoic acid, and L-glycero-D-Manno-Heptopyranose in addition to microbe-derived ligands, TLR4 recognizes various endogenous ligands including heat shock proteins HSP60, HSP70 and gp96, Alpha-defensin, Tamm-Horsfall protein, biglycan , fibrinogen, surfactant protein, low-molecular weight oligosaccharide fragments of hyaluronan, fibronectin, and heparansulfate [10]. Hence, the TLRmediated immune response can be activated in the absence of foreign microbes. Prosthetic groups of TLR4 include magnesium and phosphate ions, which serve to arbitrate receptor functionality. Important post-translational modifications defining functionality of TLR4 include glycosylation of Asn residues and di-sulfide bond formation between Cys residues.”
So we can see from this that a component of peptidoglycan (my friend N-acetyl-d-glucosamine) can bind to Toll-like receptor 4 without the presence of a microbe. The previous document points out that viral molecules and bacterial molecules can activate TLR2 and TLR4 creating a cytokine storm. This is possibly the mechanism for our demyelinating phases. Hence something that binds and blocks those receptors is required to prevent a demyelinating attack. It tends to support the view that this mechanism is separate from the peroxynitrite/iNOS/ADMA mechanisms described earlier but there is probably an important link still obscured.
There are lymphocytes antigens required to bind the Toll-like receptors to the peptidoglycans. Perhaps they arise through the other mechanism.
Regards
Re: Beyond Avonex and Valtrex
PAMPS and DAMPS
PAMPS (Pathogen-associated molecular patterns) "are molecules associated with groups of pathogens, that are recognized by cells of the innate immune system. These molecules can be referred to as small molecular motifs conserved within a class of microbes. They are recognized by Toll-like receptors (TLRs) and other pattern recognition receptors (PRRs) in both plants and animals.”
(http://en.wikipedia.org/wiki/Pathogen-a ... ar_pattern)
“They activate innate immune responses, protecting the host from infection, by identifying some conserved non-self molecules. Bacterial lipopolysaccharide (LPS), an endotoxin found on the bacterial cell membrane of a bacterium, is considered to be the prototypical PAMP. LPS is specifically recognised by TLR 4, a recognition receptor of the innate immune system. Other PAMPs include bacterial flagellin (recognized by TLR 5), lipoteichoic acid from Gram positive bacteria, peptidoglycan, and nucleic acid variants normally associated with viruses, such as double-stranded RNA (dsRNA), recognized by TLR 3 or unmethylated CpG motifs, recognized by TLR 9.”
“DAMPS (Damage-associated molecular pattern molecules or danger-associated molecular pattern molecules ) are molecules that can initiate and perpetuate immune response in the noninfectious inflammatory response.”
(http://en.wikipedia.org/wiki/DAMPs)
This distinction is important as immune responses are clearly not always dependent on an infection.
“DAMPs vary greatly depending on the type of cell (epithelial or mesenchymal) and injured tissue. Protein DAMPs include intracellular proteins, such as heat-shock proteins or HMGB1(high-mobility group box 1), and proteins derived from the extracellular matrix that are generated following tissue injury, such as hyaluronan fragments.[9] Examples of non-protein DAMPs include ATP, uric acid, heparin sulfate and DNA.”
So things that can arise from fighting infection successfully can create their own problems.
Let us look at ATP
Normally, we think of ATP as being intracellular, What happens if it arises in abundance outside the cell?
I quote now from -
Adenosine 5′-triphosphate and adenosine as endogenous signalling molecules in immunity and inflammation by M.J.L. Bours a,⁎, E.L.R. Swennen a,b, F. Di Virgilio c, B.N. Cronstein d, P.C. Dagnelie (you will have to buy it from science Direct www.sciencedirect.com for around USD$35 There are many cross references so I urge you to support the scientists and buy a copy)
“The naturally occurring nucleotide adenosine 5’-triphosphate (ATP) and its metabolite adenosine (Ado) probably constitute an intrinsic part of this extensive immunological network through purinergic signaling by their cognate receptors, which are widely expressed throughout the body.”
“The overwhelming evidence indicates that ATP and Ado (Adenosine) are important endogenous signalling molecules in immunity and inflammation.”
“ATP in the extracellular compartment is thought to contribute to the regulation of a variety of other biological processes, including cardiac function, neurotransmission, muscle contraction, vasodilatation, bone metabolism, liver glycogen metabolism and inflammation”
“Whereas intracellular concentrations of ATP are very high, its extracellular concentrations are considerably lower. Physiological ATP concentrations in plasma are normally submicromolar”
“Compared to ATP, plasma concentrations of Ado are usually about 10-fold lower”
“Concentrations of ATP and Ado in the extracellular compartment are controlled by enzymes catalyzing their conversion.”
“These so-called ecto-enzymes are located on cell surfaces or may be found in soluble form in the interstitial medium or in body fluids.”
A review of this work shows the large family of membrane-bound receptors which mediate cell
signaling by ATP and Ado. receptors cover just about everything we look at in immune cell distribution: Neutrophils, monocytes, macrophages; dendritic cells, T lymphocytes and B lymphocytes.
Inflammation can cause ATP to be released outside the cell-
“Neutrophils are the body's first line of defence against pathogens and are critical effectors in both innate and humoral immunity.” “neutrophils are capable of releasing both ATP and Ado following inflammatory activation.”
Stephen Harrod Buhner makes the following observation in his book “Healing Lyme disease coinfections”;
“Extreme ATP signalling is severely deleterious to the oliogodendrocyctes that form the myelin sheaths for axons in the brain and spinal cord…ATP also impairs white-matter function in the brain. ATP functions as an excitatory neurotransmitter in the brain, spinal cord, and peripheral nerve terminals; it’s a potent transmitter of astrocytic calcium signalling, as a mediator of axo-oligodendroglial communication and is a potent immunomodulator affecting microglia recruitment and activation. ATP signalling is a major factor in neuroinflammation. Excess ATP release results in neurodegeneration- in severe cases even to the destruction of the spinal cord.”
Buhner makes the point that ATP stimulates P2X7 receptors which leads to oligodendrocyte death, myelin damage and axon dysfunction. There are an abundance of these receptors in oligodendrocytes and myelin.
As Buhner says” Preventing P2X7 activation has been shown to reduce or even eliminate this”
Wikipedia (http://en.wikipedia.org/wiki/P2RX7) says “The P2X7 receptor current can be blocked by zinc, calcium, magnesium, and copper “
Perhaps this is the basis for these supplements being useful. Buhner points the finger at mycoplasmas as the root cause so the effectiveness of these treatments would be prophylactic not curative as the infection itself would be unharmed .
What does all this tell us ?
When ATP is extracellular it can mediate cell signalling. It can be neurotoxic when the P2X7 receptor is activated. This activation can be modulated by Zinc, Calcium, Magnesium and Copper. Those minerals may be uninvolved in the liberation of extracellular ATP which, as Buhner and the other paper both argue is likely to be triggered by bacteria.
Nonetheless, suppressing P2X7 is very important. More importantly, dealing with infection becomes paramount. None of this invalidates the EBV/iNOS/Peroxynitrite argument at all. It tends to support it as we are weakened by that earlier mechanism before this mechanism takes hold.
Better go get some minerals.
Regards
PAMPS (Pathogen-associated molecular patterns) "are molecules associated with groups of pathogens, that are recognized by cells of the innate immune system. These molecules can be referred to as small molecular motifs conserved within a class of microbes. They are recognized by Toll-like receptors (TLRs) and other pattern recognition receptors (PRRs) in both plants and animals.”
(http://en.wikipedia.org/wiki/Pathogen-a ... ar_pattern)
“They activate innate immune responses, protecting the host from infection, by identifying some conserved non-self molecules. Bacterial lipopolysaccharide (LPS), an endotoxin found on the bacterial cell membrane of a bacterium, is considered to be the prototypical PAMP. LPS is specifically recognised by TLR 4, a recognition receptor of the innate immune system. Other PAMPs include bacterial flagellin (recognized by TLR 5), lipoteichoic acid from Gram positive bacteria, peptidoglycan, and nucleic acid variants normally associated with viruses, such as double-stranded RNA (dsRNA), recognized by TLR 3 or unmethylated CpG motifs, recognized by TLR 9.”
“DAMPS (Damage-associated molecular pattern molecules or danger-associated molecular pattern molecules ) are molecules that can initiate and perpetuate immune response in the noninfectious inflammatory response.”
(http://en.wikipedia.org/wiki/DAMPs)
This distinction is important as immune responses are clearly not always dependent on an infection.
“DAMPs vary greatly depending on the type of cell (epithelial or mesenchymal) and injured tissue. Protein DAMPs include intracellular proteins, such as heat-shock proteins or HMGB1(high-mobility group box 1), and proteins derived from the extracellular matrix that are generated following tissue injury, such as hyaluronan fragments.[9] Examples of non-protein DAMPs include ATP, uric acid, heparin sulfate and DNA.”
So things that can arise from fighting infection successfully can create their own problems.
Let us look at ATP
Normally, we think of ATP as being intracellular, What happens if it arises in abundance outside the cell?
I quote now from -
Adenosine 5′-triphosphate and adenosine as endogenous signalling molecules in immunity and inflammation by M.J.L. Bours a,⁎, E.L.R. Swennen a,b, F. Di Virgilio c, B.N. Cronstein d, P.C. Dagnelie (you will have to buy it from science Direct www.sciencedirect.com for around USD$35 There are many cross references so I urge you to support the scientists and buy a copy)
“The naturally occurring nucleotide adenosine 5’-triphosphate (ATP) and its metabolite adenosine (Ado) probably constitute an intrinsic part of this extensive immunological network through purinergic signaling by their cognate receptors, which are widely expressed throughout the body.”
“The overwhelming evidence indicates that ATP and Ado (Adenosine) are important endogenous signalling molecules in immunity and inflammation.”
“ATP in the extracellular compartment is thought to contribute to the regulation of a variety of other biological processes, including cardiac function, neurotransmission, muscle contraction, vasodilatation, bone metabolism, liver glycogen metabolism and inflammation”
“Whereas intracellular concentrations of ATP are very high, its extracellular concentrations are considerably lower. Physiological ATP concentrations in plasma are normally submicromolar”
“Compared to ATP, plasma concentrations of Ado are usually about 10-fold lower”
“Concentrations of ATP and Ado in the extracellular compartment are controlled by enzymes catalyzing their conversion.”
“These so-called ecto-enzymes are located on cell surfaces or may be found in soluble form in the interstitial medium or in body fluids.”
A review of this work shows the large family of membrane-bound receptors which mediate cell
signaling by ATP and Ado. receptors cover just about everything we look at in immune cell distribution: Neutrophils, monocytes, macrophages; dendritic cells, T lymphocytes and B lymphocytes.
Inflammation can cause ATP to be released outside the cell-
“Neutrophils are the body's first line of defence against pathogens and are critical effectors in both innate and humoral immunity.” “neutrophils are capable of releasing both ATP and Ado following inflammatory activation.”
Stephen Harrod Buhner makes the following observation in his book “Healing Lyme disease coinfections”;
“Extreme ATP signalling is severely deleterious to the oliogodendrocyctes that form the myelin sheaths for axons in the brain and spinal cord…ATP also impairs white-matter function in the brain. ATP functions as an excitatory neurotransmitter in the brain, spinal cord, and peripheral nerve terminals; it’s a potent transmitter of astrocytic calcium signalling, as a mediator of axo-oligodendroglial communication and is a potent immunomodulator affecting microglia recruitment and activation. ATP signalling is a major factor in neuroinflammation. Excess ATP release results in neurodegeneration- in severe cases even to the destruction of the spinal cord.”
Buhner makes the point that ATP stimulates P2X7 receptors which leads to oligodendrocyte death, myelin damage and axon dysfunction. There are an abundance of these receptors in oligodendrocytes and myelin.
As Buhner says” Preventing P2X7 activation has been shown to reduce or even eliminate this”
Wikipedia (http://en.wikipedia.org/wiki/P2RX7) says “The P2X7 receptor current can be blocked by zinc, calcium, magnesium, and copper “
Perhaps this is the basis for these supplements being useful. Buhner points the finger at mycoplasmas as the root cause so the effectiveness of these treatments would be prophylactic not curative as the infection itself would be unharmed .
What does all this tell us ?
When ATP is extracellular it can mediate cell signalling. It can be neurotoxic when the P2X7 receptor is activated. This activation can be modulated by Zinc, Calcium, Magnesium and Copper. Those minerals may be uninvolved in the liberation of extracellular ATP which, as Buhner and the other paper both argue is likely to be triggered by bacteria.
Nonetheless, suppressing P2X7 is very important. More importantly, dealing with infection becomes paramount. None of this invalidates the EBV/iNOS/Peroxynitrite argument at all. It tends to support it as we are weakened by that earlier mechanism before this mechanism takes hold.
Better go get some minerals.
Regards
-
Positivenelly
- Getting to Know You...
- Posts: 12
- Joined: Thu Nov 06, 2014 2:48 pm
Re: Beyond Avonex and Valtrex
Thank you for this post. It's a lot to take in so I'm going to read it piece by piece. Meanwhile, I started coq10 yesterday to see if it helps with fatigue. I'm sleeping around 13/14 hours a day right now (currently undiagnosed with a brain MRI coming up soon).
Last edited by Positivenelly on Sun Nov 09, 2014 8:36 am, edited 1 time in total.
Re: Beyond Avonex and Valtrex
Thank you for the nice feed back. It is a bit of a dogs breakfast.
The Q10 can help with the fatigue but, if you can find the other things that influence your sleeping, it will help. Other symptoms can help identify those things.
I do think we need to look for infections but metabolic issues can be a big part of it and everything can overlap. I'll try and help if I can but sometimes others have better ideas.
Regards
The Q10 can help with the fatigue but, if you can find the other things that influence your sleeping, it will help. Other symptoms can help identify those things.
I do think we need to look for infections but metabolic issues can be a big part of it and everything can overlap. I'll try and help if I can but sometimes others have better ideas.
Regards
-
Positivenelly
- Getting to Know You...
- Posts: 12
- Joined: Thu Nov 06, 2014 2:48 pm
Re: Beyond Avonex and Valtrex
Question: why take the coq10 at night? Any particular reason?
I also have to schedule a sleep study and because of the transcranial Doppler results, also need a carotid ultrasound (that isn't until December).
I currently stand at "possible MS"....
I also have to schedule a sleep study and because of the transcranial Doppler results, also need a carotid ultrasound (that isn't until December).
I currently stand at "possible MS"....
Re: Beyond Avonex and Valtrex
Hi,
The reasoning was fairly basic. The question I asked myself is "why do we sleep?" and came up with the primary school answer -"to help us make energy".
The exchange of sodium and potassium through the cell is where our energy comes from. The ATP is the agent that opens and closes the gate in the cell wall. Without ATP the exchange doesn't happen.
To make ATP we need glyceralderhyde-3-phosphate as a link to allow ADP to add a molecule of phosphate to become ATP. We know from work by Szabo and others that peroxynitrite disables the glyceralderhyde-3-phosphate. The Q10 substitutes for this. It will take time to become bioavailable and every cell in your body wants to respire properly so the greater your load of peroxynitrite the more Q10 you need and the more time it takes to properly influence your whole system.
Think of your cells as a battery. Somehow it's gone flat. If it was your car you would get a new battery or call road side assist and get them to give you a kick start. Sometimes it won't recharge because it can't pull a current from the moving car and it runs down again. The Q10 is a daily kick start. Other things can affect whether you can recharge yourself.
So why take it before sleep? Sleep is the time the body repairs itself. Its the time when your call on the stored energy in your body should be lowest. This is the time to charge that battery on a slow charge. It will only happen if the exchange of sodium and potassium continues whilst you sleep.The Q10 has time to diffuse through the body continuously influencing resting cells. Now you will make more energy than expend.
If you take it in the morning, you start your day with a flat battery and keep pulling on it before you have given it a chance to recharge. You will struggle to make energy faster than you expend it and you are already in deficit. You will always feel fatigued. Your cells will be under stress.
This means you have do a few things;
1) Always go to bed at the same time. Whether you sleep is secondary. Your are training your body that it should expect to rest at this time
2)Discover the dose that makes a difference. Start at 150mg and increase by that amount every second night. I'm on 750mg but I think that's a high dose. 450-600mg should be plenty for most. 50mg is useless. If you can't handle it then something else is very wrong.
3)Address what is causing your problem. Check for EBV in particular. It will definitely not be the only thing but its a good place to start.
4) Check the other things I said to look for. Look for other infections. Look at your nutrition. Are you the only thing eating what you eat?
I hope this helps. There is a lot of stuff in this post. It's not exhaustive but it might give you a framework.
Regards
The reasoning was fairly basic. The question I asked myself is "why do we sleep?" and came up with the primary school answer -"to help us make energy".
The exchange of sodium and potassium through the cell is where our energy comes from. The ATP is the agent that opens and closes the gate in the cell wall. Without ATP the exchange doesn't happen.
To make ATP we need glyceralderhyde-3-phosphate as a link to allow ADP to add a molecule of phosphate to become ATP. We know from work by Szabo and others that peroxynitrite disables the glyceralderhyde-3-phosphate. The Q10 substitutes for this. It will take time to become bioavailable and every cell in your body wants to respire properly so the greater your load of peroxynitrite the more Q10 you need and the more time it takes to properly influence your whole system.
Think of your cells as a battery. Somehow it's gone flat. If it was your car you would get a new battery or call road side assist and get them to give you a kick start. Sometimes it won't recharge because it can't pull a current from the moving car and it runs down again. The Q10 is a daily kick start. Other things can affect whether you can recharge yourself.
So why take it before sleep? Sleep is the time the body repairs itself. Its the time when your call on the stored energy in your body should be lowest. This is the time to charge that battery on a slow charge. It will only happen if the exchange of sodium and potassium continues whilst you sleep.The Q10 has time to diffuse through the body continuously influencing resting cells. Now you will make more energy than expend.
If you take it in the morning, you start your day with a flat battery and keep pulling on it before you have given it a chance to recharge. You will struggle to make energy faster than you expend it and you are already in deficit. You will always feel fatigued. Your cells will be under stress.
This means you have do a few things;
1) Always go to bed at the same time. Whether you sleep is secondary. Your are training your body that it should expect to rest at this time
2)Discover the dose that makes a difference. Start at 150mg and increase by that amount every second night. I'm on 750mg but I think that's a high dose. 450-600mg should be plenty for most. 50mg is useless. If you can't handle it then something else is very wrong.
3)Address what is causing your problem. Check for EBV in particular. It will definitely not be the only thing but its a good place to start.
4) Check the other things I said to look for. Look for other infections. Look at your nutrition. Are you the only thing eating what you eat?
I hope this helps. There is a lot of stuff in this post. It's not exhaustive but it might give you a framework.
Regards
-
Positivenelly
- Getting to Know You...
- Posts: 12
- Joined: Thu Nov 06, 2014 2:48 pm
Re: Beyond Avonex and Valtrex
Thanks. I took the third 200 mg dose last night and his morning was the first morning I felt rested after sleeping. I have excellent sleep habits... Sleep is important to me. I do have a few food intolerances and I have a holistic nutritionist. I'll keep you posted.
Re: Beyond Avonex and Valtrex
Hi,
I'm glad you got some benefit. Remember more is not always better so I'd stay on a dose that derives a benefit rather than chase a chance of something better. It took me a while to decide to increase mine again once I found a level.
Underlying it all is something is affecting you. I would go looking for obvious infections like EBV and for measures of nutritional deficiencies like amino acid studies. Obviously avoid the things you have intolerances to.
The mantra should always be look don't guess. Perhaps I should have done that a few times myself but at least you can read about it here.
If the Q10 worked it was offsetting a shortage of glyceraldehyde-3-phosphate. That implies peroxynitrite as a possible cause and that implies excess superoxide and iNOS. (all covered earlier).
Have fun.
I'm glad you got some benefit. Remember more is not always better so I'd stay on a dose that derives a benefit rather than chase a chance of something better. It took me a while to decide to increase mine again once I found a level.
Underlying it all is something is affecting you. I would go looking for obvious infections like EBV and for measures of nutritional deficiencies like amino acid studies. Obviously avoid the things you have intolerances to.
The mantra should always be look don't guess. Perhaps I should have done that a few times myself but at least you can read about it here.
If the Q10 worked it was offsetting a shortage of glyceraldehyde-3-phosphate. That implies peroxynitrite as a possible cause and that implies excess superoxide and iNOS. (all covered earlier).
Have fun.
-
Interrupted
- Family Elder
- Posts: 240
- Joined: Sun Jan 14, 2007 3:00 pm
- Location: UK
- Contact:
Re: Beyond Avonex and Valtrex
Reporting in... 
I've been quiet for a while because my body has literally just been collapsing. Things going wrong all over the show and picking myself up off the floor a few times; not through limb issues severe enough to do that but through sheer weakness, lack of strength, dizziness and breathing troubles. It's been a riot. Consequently I only took the Valtrex for two days, completed the penicillin and then took NOTHING. It was still happening, so not the pills, this was just happening regardless. Obviously not atypical MS so no point calling the nurses. Have to ride this out solo.
I really have never felt so awful for so long. I don't know if anybody has ever experienced it, it's happened to me a few times for maybe a day or so but this was two weeks solid (so far)... it's being so drained, unable to move and weak that there is some kind of chemical change that happens in your brain/thought processes that puts you in a black mental hell. Everything become bleak, dire, negative, deathly and to be blunt, truly frightening. It's 100% not a conscious mental shift, it's a chemical reaction to what the body and brain is going through. It's rather a nasty thing because that happening is obviously just going to cause further stress and anxiety which is absolutely the opposite of what the poor body needs! So yeah, I don't really understand it.
On top of the weakness and mental torture, everything else has degenerated a bit more again, cognition, eyes and limbs included. I so miss my little short daily walks with the dog, i'm hoping to anything that they aren't out of the picture for good (as is the dog!)
I had few options to think down really, so went back to the ATP and mitochondrial failure route. I need to produce energy and strength from somewhere to get out of this and well, hey, the theory makes sense, let's run with it...
http://www.drmyhill.co.uk/wiki/CFS_-_Th ... al_Failure
"Mitochondria are the miniscule engines that burn fuel (acetate groups from fat and sugar) in the presence of oxygen to provide energy for every living cell in the body. We have published three studies showing that mitochondria running slowly is the central cause of fatigue in CFS/ME. Mitochondria go slow for two common reasons - either they are deficient in micronutrients so the enzymes do not work well, or they are blocked by toxins. The third paper we published showed that the nutritional deficiencies are corrected reliably well with all or a combination of micronutrient supplements and this is paralleled by clinical and biochemical improvement.
A typical regime, if the gut works perfectly, would include magnesium 300mgs by mouth (but ideally magnesium by injection), co enzyme Q 10 200mgs, acetyl L carnitine 2 grams, D-ribose 15 gms, niacinamide 1500 mgs and vitamin B12 1mg by mouth (ideally by injection). These should be taken in addition to [a basic everyday set of supplements] and, where tests indicate, extra anti-oxidants.
If gut function is impaired by allergy and/or fermenting gut then injections become more important (only available on prescription). If injections are not available then transdermal nutrients may be helpful."
Hence I now have a lot more supplements to add to my daily rattling. If I can get myself back to any kind of stable state, I will most definitely be trying to take the valtrex again, if viruses are causing the dysfunction, they need to go! Will report back x
I've been quiet for a while because my body has literally just been collapsing. Things going wrong all over the show and picking myself up off the floor a few times; not through limb issues severe enough to do that but through sheer weakness, lack of strength, dizziness and breathing troubles. It's been a riot. Consequently I only took the Valtrex for two days, completed the penicillin and then took NOTHING. It was still happening, so not the pills, this was just happening regardless. Obviously not atypical MS so no point calling the nurses. Have to ride this out solo.
I really have never felt so awful for so long. I don't know if anybody has ever experienced it, it's happened to me a few times for maybe a day or so but this was two weeks solid (so far)... it's being so drained, unable to move and weak that there is some kind of chemical change that happens in your brain/thought processes that puts you in a black mental hell. Everything become bleak, dire, negative, deathly and to be blunt, truly frightening. It's 100% not a conscious mental shift, it's a chemical reaction to what the body and brain is going through. It's rather a nasty thing because that happening is obviously just going to cause further stress and anxiety which is absolutely the opposite of what the poor body needs! So yeah, I don't really understand it.
On top of the weakness and mental torture, everything else has degenerated a bit more again, cognition, eyes and limbs included. I so miss my little short daily walks with the dog, i'm hoping to anything that they aren't out of the picture for good (as is the dog!)
I had few options to think down really, so went back to the ATP and mitochondrial failure route. I need to produce energy and strength from somewhere to get out of this and well, hey, the theory makes sense, let's run with it...
http://www.drmyhill.co.uk/wiki/CFS_-_Th ... al_Failure
"Mitochondria are the miniscule engines that burn fuel (acetate groups from fat and sugar) in the presence of oxygen to provide energy for every living cell in the body. We have published three studies showing that mitochondria running slowly is the central cause of fatigue in CFS/ME. Mitochondria go slow for two common reasons - either they are deficient in micronutrients so the enzymes do not work well, or they are blocked by toxins. The third paper we published showed that the nutritional deficiencies are corrected reliably well with all or a combination of micronutrient supplements and this is paralleled by clinical and biochemical improvement.
A typical regime, if the gut works perfectly, would include magnesium 300mgs by mouth (but ideally magnesium by injection), co enzyme Q 10 200mgs, acetyl L carnitine 2 grams, D-ribose 15 gms, niacinamide 1500 mgs and vitamin B12 1mg by mouth (ideally by injection). These should be taken in addition to [a basic everyday set of supplements] and, where tests indicate, extra anti-oxidants.
If gut function is impaired by allergy and/or fermenting gut then injections become more important (only available on prescription). If injections are not available then transdermal nutrients may be helpful."
Hence I now have a lot more supplements to add to my daily rattling. If I can get myself back to any kind of stable state, I will most definitely be trying to take the valtrex again, if viruses are causing the dysfunction, they need to go! Will report back x
28/07/10, 04/10/10, 16/11/10 - CCSVi Dopplers x3 ** 12/10/10 - Poland procedure. Symptoms worsened. No improvement.
13/02/12 - Wheldon ABX protocol for 1.5yrs. Fairly stable but no improvement. Unable to source alternate ABX needed.
13/02/12 - Wheldon ABX protocol for 1.5yrs. Fairly stable but no improvement. Unable to source alternate ABX needed.
Re: Beyond Avonex and Valtrex
I wondered how you were.
I think you are making the same mistake I was. I want you to go straight to the out patients of a hospital and say "I am several weeks into a bad MS attack and I think I need some help".
I probably haven't made it clear enough but I think there are two paths that can be activated in MS. The first is the mitochrodrial dysfunction that is initiated by the viral/iNOS/superoxide/Peroxynitrite path. You probably have this but it's not the major concern right now.
The second is the violent path. Your Th1 cells are highly activated and recruiting the other arms of your immune system. In particular, your lymphatic system is in overdrive pushing lympth into the glands faster than it can be reabsorbed. Your bodies reaction is to further engage the immune response because it thinks there's war on. You need to reverse this cycle. You need a hospital right now. Let them do the conventional things to slow the attack.
You used the word "alone". We all know we are alone but in this instance, reach out to trained professionals. They will give you a bed for rest, food, monitoring and specifically target the current situation.
In my own case, I did what you are doing for too long and ended up with the top two chambers of my heart stopping. It was purely an electrical problem, not a plumbing issue. I was literally one heartbeat from throwing a series of clots out of my heart and just dropping dead. The issue is- I didn't know it and couldn't tell.
Go to a hospital and say "I need some help".
Take your laptop and we can talk when you're there.
Regards
I think you are making the same mistake I was. I want you to go straight to the out patients of a hospital and say "I am several weeks into a bad MS attack and I think I need some help".
I probably haven't made it clear enough but I think there are two paths that can be activated in MS. The first is the mitochrodrial dysfunction that is initiated by the viral/iNOS/superoxide/Peroxynitrite path. You probably have this but it's not the major concern right now.
The second is the violent path. Your Th1 cells are highly activated and recruiting the other arms of your immune system. In particular, your lymphatic system is in overdrive pushing lympth into the glands faster than it can be reabsorbed. Your bodies reaction is to further engage the immune response because it thinks there's war on. You need to reverse this cycle. You need a hospital right now. Let them do the conventional things to slow the attack.
You used the word "alone". We all know we are alone but in this instance, reach out to trained professionals. They will give you a bed for rest, food, monitoring and specifically target the current situation.
In my own case, I did what you are doing for too long and ended up with the top two chambers of my heart stopping. It was purely an electrical problem, not a plumbing issue. I was literally one heartbeat from throwing a series of clots out of my heart and just dropping dead. The issue is- I didn't know it and couldn't tell.
Go to a hospital and say "I need some help".
Take your laptop and we can talk when you're there.
Regards
Last edited by Scott1 on Fri Nov 14, 2014 11:15 pm, edited 1 time in total.
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Re: Beyond Avonex and Valtrex
Thank you Scott, I mean, well, i'm a little freaked out now at the mention of heart problems and clots but you know, if I say this to a doctor i'll get the raving looney woman look. I understand, but if I go to hospital they will do my obs, tell me i'm fine (and to rest) and send me home with (at a guess) a drama queen A&E timewaster mark on my files. There is no way they would keep me in or think anything is really wrong.
I have an appointment to see my neuro' (at last) on Tuesday - this is, I guess, my opportunity to beg for help so I need to understand what to say and how to put it to him. I think you're right, I think it is different and worse but I really don't know if he'll even absorb the theory. I can only try...
I have an appointment to see my neuro' (at last) on Tuesday - this is, I guess, my opportunity to beg for help so I need to understand what to say and how to put it to him. I think you're right, I think it is different and worse but I really don't know if he'll even absorb the theory. I can only try...
28/07/10, 04/10/10, 16/11/10 - CCSVi Dopplers x3 ** 12/10/10 - Poland procedure. Symptoms worsened. No improvement.
13/02/12 - Wheldon ABX protocol for 1.5yrs. Fairly stable but no improvement. Unable to source alternate ABX needed.
13/02/12 - Wheldon ABX protocol for 1.5yrs. Fairly stable but no improvement. Unable to source alternate ABX needed.