MS Seminar Notes from 4/30
These are the seminar notes that I took on Saturday.
Dr. Barry Arnason was one of the speakers. He has worked on a lot of studies & trials for MS. If you google him, you'll find a lot of great information about his background.
I was bombarded with a lot of new (to me) information and I'd like to share it with everyone. I took a ton of notes and it was kind of hard for me to put this all in a format that could be understood by others. Sorry! I wish I had brought a tape recorder. If I had known that I was going to come away with so much new knowledge, I would have! I've gone to 3 other MS seminars, and they were all redundant. This DEFINITELY was not!
~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~
Etymology
We must look for a prevention to MS, not the cure. The cure for MS will be a vaccination – elimination like Polio. The only established trigger for MS is a viral infections illness.
There is an increased rate of MS in Japan, the Middle East and in Mexico. Environment may also be a trigger because genes have not changed.
Severity of MS does not depend totally on genes. There must be more than one susceptibility gene. We may be able to manipulate the genes in the course of MS.
We also have to work on strategies to deal with the problem of walking/weakness because there are currently no meds. (This is an issue that has gone on too long for us MSers!)
Mono/Epstein-Barr
Mono is increased 4x in MS which is lab proven. The general population tests positive for mono, even if it never shows up as symptoms. The Epstein-Barr Virus (mono) can reactivate during MS attacks. If EBV sets MS in motion, than a vaccination to eradicate MS becomes a consideration.
Depression
15% of general population experience depression
55% of MS patients will have depression at some point in their illness
Depression is 3x – 6x more common and it lasts longer – why? – it is not just stress of having the illness. Anxiety and panic attacks are also all too common in MS. Depression may also precede the onset of MS. Depression is associated with disease activity and attacks.
Anti-depressants correct the over activity of the hypothalamic-pituitary adrenal axis which causes an increase in cortisone levels. Increased cortisol is hard on nerve cells.
** Steroids are cortisone. Over long periods of time they may have a worse effect on MS because of the increased cortisol levels.
A/Ds may be used to treat MS! Not just depression. A/Ds reduce the levels of INF and TNF, which contribute to demyelination. A/Ds increase BDNF (brain derived neurotrophic factor) which protects nerve cells. BDNF protects both motor nerves and motor function (walking!) which is very important in progressive MS.
SSRIs and Tricyclic anti-depressants are immunosuppressive drugs. They also readily enter the CNS. Any of the SSRIs & tricyclic A/Ds work. Like Prozac, Paxil, Zoloft, Celexa and Luvox (SSRIs) and Elavil, Tofranil, etc. (tricyclics) but he said that Wellbutrin wouldn't because it's not an SSRI or tricyclic.
Depression is higher in RRMS than PPMS or SPMS. T-cells have little to no effect on progression. Disability progression occurs because of events that occur in plaques that already exist.
IL-12 p40 is a pro-inflammatory and it’s “bad”. Neuronal damage depends on the balance between neurotrophins/BDNF “good” and pro-inflammatory cytokines/IL-12 “bad”. In a remission, the “bad” is decreased and the “good” is increased. In a relapse, the “bad” AND the “good” are increased. In PPMS, the “bad” is increased and the “good” is decreased – substantially, even more so in very progressive forms.
We must find drugs that attach to the microphages to turn them OFF – they will regulate the production of BDNF and decrease the production of INF. A/Ds correct BDNF levels in non-MS and are being looked at for MS patients. In a study, knocking down the “bad” made patients with an attack feel better by 90% within 24 hours.
**Dr. Arnason made it very clear – he does not advocate the use of anti-depressants in MS for BDNF production because it is not in the FDA guidelines for A/D use … but it can be loosely interpreted! Wink-Wink.
Memory
Short-term memory and being easily destracted in MS is because brain oxygen consumption is reduced in MS. BDNF is not involved in memory. Memory doesn’t depend on demyelination – it must depend on something else.
Oxygen consumption rises with Betaseron treatment but only after a delay of 9 months to a year. There is no change in consumption until after 9 months! Memory itself improves between 1-3 years after starting Betaseron. A different mechanism must be involved but it does eventually get better with Betaseron treatment. (Dr. Arnason was involved in this study and he believes that Betaseron, oxygen consumption & memory are related)
Comparison of CRABs
Head to head, Betaseron is 2x better than Avonex. (Dr. Arnason worked on this study and worked for Idec)
Head to head, Rebif is stronger than Avonex. So it’s not necessarily the med itself, it’s the frequency.
In the re-evaluation of the participants of the original Betaseron trial (16-17 years later – 65% have been re-evaluated so far) – 14 in the placebo group have passed away and 5 in the treated group have passed away. What does that mean? Starting treatment as soon as possible may have an effect.
Stem Cells
How are we going to get the stem cells to the right place of demyelination? In the mouse studies, the mice were mutants and they had no myelin to begin with. Of course there is going to be remyelination anywhere and everywhere because they didn’t have any!
Also, naked axons become capable of nerve impulses!
Test
Unfortunately, there is no test available to show the current levels of BDNF or IL-12 in people.
~~~~~~~~~~~~~~~~~~~~~~~~
Comments from Lori (on the Board):
* I've seen a lot of literature that says there's a connection between EBV and MS. Also, I recently read some info on CEBV (Chronic Epstein-Barr Virus). The symptoms sound a lot like MS.
* I've also read that AD meds can treat MS. If I remember right (I haven't checked to be sure), I read that in Brain Longevity: The Breakthrough Medical Program that Improves Your Mind and Memory by Dharma Singh Khalsa, M.D. with Cameron Stauth.
* The book I just mentioned has a lot of great info on memory, including some good tips on recognizing the three types of memory: auditory, visual, and kinesthetic.
* I've also read that steroids can actually increase the possibility of exacerbations, especially ON.
Dr. Barry Arnason was one of the speakers. He has worked on a lot of studies & trials for MS. If you google him, you'll find a lot of great information about his background.
I was bombarded with a lot of new (to me) information and I'd like to share it with everyone. I took a ton of notes and it was kind of hard for me to put this all in a format that could be understood by others. Sorry! I wish I had brought a tape recorder. If I had known that I was going to come away with so much new knowledge, I would have! I've gone to 3 other MS seminars, and they were all redundant. This DEFINITELY was not!
~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~
Etymology
We must look for a prevention to MS, not the cure. The cure for MS will be a vaccination – elimination like Polio. The only established trigger for MS is a viral infections illness.
There is an increased rate of MS in Japan, the Middle East and in Mexico. Environment may also be a trigger because genes have not changed.
Severity of MS does not depend totally on genes. There must be more than one susceptibility gene. We may be able to manipulate the genes in the course of MS.
We also have to work on strategies to deal with the problem of walking/weakness because there are currently no meds. (This is an issue that has gone on too long for us MSers!)
Mono/Epstein-Barr
Mono is increased 4x in MS which is lab proven. The general population tests positive for mono, even if it never shows up as symptoms. The Epstein-Barr Virus (mono) can reactivate during MS attacks. If EBV sets MS in motion, than a vaccination to eradicate MS becomes a consideration.
Depression
15% of general population experience depression
55% of MS patients will have depression at some point in their illness
Depression is 3x – 6x more common and it lasts longer – why? – it is not just stress of having the illness. Anxiety and panic attacks are also all too common in MS. Depression may also precede the onset of MS. Depression is associated with disease activity and attacks.
Anti-depressants correct the over activity of the hypothalamic-pituitary adrenal axis which causes an increase in cortisone levels. Increased cortisol is hard on nerve cells.
** Steroids are cortisone. Over long periods of time they may have a worse effect on MS because of the increased cortisol levels.
A/Ds may be used to treat MS! Not just depression. A/Ds reduce the levels of INF and TNF, which contribute to demyelination. A/Ds increase BDNF (brain derived neurotrophic factor) which protects nerve cells. BDNF protects both motor nerves and motor function (walking!) which is very important in progressive MS.
SSRIs and Tricyclic anti-depressants are immunosuppressive drugs. They also readily enter the CNS. Any of the SSRIs & tricyclic A/Ds work. Like Prozac, Paxil, Zoloft, Celexa and Luvox (SSRIs) and Elavil, Tofranil, etc. (tricyclics) but he said that Wellbutrin wouldn't because it's not an SSRI or tricyclic.
Depression is higher in RRMS than PPMS or SPMS. T-cells have little to no effect on progression. Disability progression occurs because of events that occur in plaques that already exist.
IL-12 p40 is a pro-inflammatory and it’s “bad”. Neuronal damage depends on the balance between neurotrophins/BDNF “good” and pro-inflammatory cytokines/IL-12 “bad”. In a remission, the “bad” is decreased and the “good” is increased. In a relapse, the “bad” AND the “good” are increased. In PPMS, the “bad” is increased and the “good” is decreased – substantially, even more so in very progressive forms.
We must find drugs that attach to the microphages to turn them OFF – they will regulate the production of BDNF and decrease the production of INF. A/Ds correct BDNF levels in non-MS and are being looked at for MS patients. In a study, knocking down the “bad” made patients with an attack feel better by 90% within 24 hours.
**Dr. Arnason made it very clear – he does not advocate the use of anti-depressants in MS for BDNF production because it is not in the FDA guidelines for A/D use … but it can be loosely interpreted! Wink-Wink.
Memory
Short-term memory and being easily destracted in MS is because brain oxygen consumption is reduced in MS. BDNF is not involved in memory. Memory doesn’t depend on demyelination – it must depend on something else.
Oxygen consumption rises with Betaseron treatment but only after a delay of 9 months to a year. There is no change in consumption until after 9 months! Memory itself improves between 1-3 years after starting Betaseron. A different mechanism must be involved but it does eventually get better with Betaseron treatment. (Dr. Arnason was involved in this study and he believes that Betaseron, oxygen consumption & memory are related)
Comparison of CRABs
Head to head, Betaseron is 2x better than Avonex. (Dr. Arnason worked on this study and worked for Idec)
Head to head, Rebif is stronger than Avonex. So it’s not necessarily the med itself, it’s the frequency.
In the re-evaluation of the participants of the original Betaseron trial (16-17 years later – 65% have been re-evaluated so far) – 14 in the placebo group have passed away and 5 in the treated group have passed away. What does that mean? Starting treatment as soon as possible may have an effect.
Stem Cells
How are we going to get the stem cells to the right place of demyelination? In the mouse studies, the mice were mutants and they had no myelin to begin with. Of course there is going to be remyelination anywhere and everywhere because they didn’t have any!
Also, naked axons become capable of nerve impulses!
Test
Unfortunately, there is no test available to show the current levels of BDNF or IL-12 in people.
~~~~~~~~~~~~~~~~~~~~~~~~
Comments from Lori (on the Board):
* I've seen a lot of literature that says there's a connection between EBV and MS. Also, I recently read some info on CEBV (Chronic Epstein-Barr Virus). The symptoms sound a lot like MS.
* I've also read that AD meds can treat MS. If I remember right (I haven't checked to be sure), I read that in Brain Longevity: The Breakthrough Medical Program that Improves Your Mind and Memory by Dharma Singh Khalsa, M.D. with Cameron Stauth.
* The book I just mentioned has a lot of great info on memory, including some good tips on recognizing the three types of memory: auditory, visual, and kinesthetic.
* I've also read that steroids can actually increase the possibility of exacerbations, especially ON.
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