In Pursuit of ABX - May I have coffee with my milkshake?

A forum for the discussion of antibiotics as a potential therapy for MS

Postby notasperfectasyou » Mon Feb 02, 2009 9:25 am

Pulse 12

I was home New Year’s Day, whereas I’m not normally home when Kim starts her pulse. It wasn’t such a bad day. We all went to PetSmart to get Lucy new dog toys, Kim cooked dinner and we started to undecorate from Christmas. We also went to Mass. I guess I’m saying we did a lot and while Kim seemed to be slowed somewhat the second half of the day, she seemed otherwise fine. Day 2 was pretty much the same as Day 1. On Day 3 we went to Costco and Kim did the entire warehouse with a shopping cart. She’s done this before, but this was a different Costco for us to visit. It was way larger and very crowded. Kim handled the whole trip really well, including walking to the non-handicap space I parked in at the end of the trip. Day 4 was a good day too. I think the Ibuprofen is helping keep the die-off inflammation down. We went to Sears and Kim tried an eliptical. She didn’t like it. She thought a treadmill would be better. Days 5 and 6 were uneventful. Kim was a little more tired than normal at the end of the day, but that was about it. I seriously think the Ibuprofen/COX-2 inhibitor is helping negate the inflammatory effects of the Flagyl. Day 7 was catch up day; Kim got way more tired.

Then on day 1 of post-pulse Kim was cold and shivery and more tired and had poopers. She did not take Ibuprofen beyond day 7 and in hindsight I didn’t think die-off would be an issue once she stopped taking the Flagyl. Wrong! So on day 2 post-pulse I suggested that Kim take some Ibuprofen. She was feeling very tired and her voice was cracky and she sounded like she might have several pulses ago. I imagine that the die off is still there and she needs to keep taking it until the die-off subsides. Over the post-pulse week Kim’s been feeling a little better, but still seems to be experiencing die-off.


25-Foot Walk Update


Walk Date ______ Seconds

02/17/08 ________ 10.53
02/25/08 _________ 9.63
03/03/08 ________ 10.91
03/09/08 ________ 16.75
03/16/08 _________ 9.46
03/22/08 _________ 8.59
03/30/08 _________ 8.06
04/06/08 _________ 9.34
04/11/08 _________ 7.81
04/20/08 ________ 10.81
04/27/08 ________ 12.28
05/04/08 _________ 8.97
05/11/08 _________ 7.81
05/19/08 _________ 6.60
05/31/08 _________ 6.50
06/08/08 _________ 5.78
06/15/08 _________ 6.03
06/22/08 _________ 6.16
06/30/08 _________ 6.06
07/13/08 _________ 7.72
07/19/08 _________ 5.19
07/26/08 _________ 5.53
08/03/08 _________ 4.72
08/10/08 _________ 5.35
08/17/08 _________ 5.50
08/24/08 _________ 4.91
08/31/08 _________ 4.84
09/07/08 _________ 4.62
09/14/08 _________ 5.06
09/28/08 _________ 4.78
10/07/08 _________ 6.03
10/12/08 _________ 4.88
10/22/08 _________ 5.13
10/26/08 _________ 5.10
11/02/08 _________ 5.16
11/09/08 _________ 5.08
11/16/08 _________ 5.25
11/23/08 _________ 5.40
12/07/08 _________ 5.03
12/22/08 _________ 5.09
12/29/08 _________ 4.97
01/04/09 _________ 4.50
01/11/09 _________ 5.00
01/19/09 _________ 5.53

You can tell from the last 3 times that post pulse week (11th) was harder than pulse week and then 2-days before Kim’s appointment we got mystery illness. We’re not sure what it was; food poisoning, extreme anxiety, flu ?????? It clearly affected Kim and the walk time is really much better than she felt. Her stomach still hurt, even after our return home.


Appointment In Vanderbilt #3

Our plan was to leave for Nashville in the late morning and arrive in time for bedtime. Kim was sick the night before, and we went to an urgent care center rather than leaving. She had something like the flu, but we don’t know for sure. She didn’t want to eat or drink, but she was insistent on making the trip and not cancelling her appointment. She got a shot of Phenergan and we left very late and Kim slept nearly the whole trip.

Kim’s MRI was scheduled in the morning and she was expecting an open MRI and she got a closed one. She knew the gadolinium was coming, but she really does not like the closed MRI. Maybe it helped that she felt like a wet noodle to begin with. The medical center in Nashville has the MRI on a network and Dr. Sriram had it before we got to Kim’s appointment an hour later. Kim did not walk well, but still walked in 5.53 seconds. This was pretty good when you consider that a year ago she did the walk in 20.24 seconds and she was doing this on about a quarter of a waffle that she was able to keep down that morning. For the record, Kim was not having an exaserbation last year, the 20.24 second walk was on par with how she felt at the time.

We could not get the 2005 MRI disc to work in the computer that was in the exam room. But, we had the hardcopy films so the doctors kept going back and forth between the exam room computer that had the new MRI and the light boards in the hallway. A team of 3 neurologists looked at the MRI’s and opined that there was no new activity and the gadolinium did not show any active sites. We were very happy, albeit hoping for more.

Kim will stay on her current protocol without any changes. In Kim’s last appointment she was found to have very high levels of chlamydial antibodies and blood was taken to measure this again. Dr. Sriram also took a sample to test her vitamin D levels.

Kim has a much more descriptive version of the experience at her blog – Happy 1st AZITHROVERSARY to me!


How Deep Does Kim Smile?

I can’t help but wonder ………. Kim’s 2005 MRI and 2009 MRI are just points in time. They are apparently level with each other, but does that mean that her disability was constant/flat or could it be that the more appropriate connection between the points would be a down then up/curve like a smile? I speculate on this because the 2005 MRI was before the time Kim started Novantrone. We were told that she had changed from RRMS to SPMS. Kim started on ABX only a year ago, January 2008 and has anecdotal improvement. Is the proper line between 2005 and 2009’s MRI’s a straight line or a curved one? I think it’s curved from a down swing in 2005 to an upswing in 2009. Supporting evidence?

When we made the first appointment at Vanderbilt we needed to get a copy of Kim’s neurology records for Dr. Sriram’s office. The records were sent to us and I made a copy. Here is a bit of chronology:

03/2001: RRMS, Ataxic wide based gait, uses cane, cannot perform Romberg Test, Avonex, Provigil.
02/2005: Condition changed to SPMS, Requires cane to walk more than a few steps, first report of bladder dysfunction, Avonex, Provigil
10/2005: MRI
04/2006: Spastic wide based gait, ambulation difficulty, letter of medical necessity for motorized scooter, Initiate Copaxone, Provigil, Discontinues Avonex.
09/2006: Novantrone Infusion 1
10/2006: Improved to normal gait some spasticity, Copaxone, Novantrone, Provigil
12/2006: Novantrone Infusion 2
03/2007: Novantrone Infusion 3
04/2007: Increasingly difficult wide based spastic gait, Copaxone, Novantrone, Provigil
05/2007: Worsened wide based spastic gait, Initiate IVIG, Copaxone, Novantrone, Provigil
06/2007: Novantrone Infusion 4
07/2007: Improved wide based spastic gait, Copaxone, Novantrone, Provigil
09/2007: Novantrone Infusion 5, discontinued chemotherapy due to failure of continued effect. First report of sexual dysfunction.
01/2008: 25-foot walk time 20 seconds. Improved sexual function. Initiated Combined Antibiotic Protocol, Copaxone, Provigil
05/2008: 25-foot walk time 8 seconds. Kim uses the cane a lot less. Noted improved bladder function and body heat. Combined ABX Protocol, Copaxone, Provigil
06/2008: 25-foot walk time 6 seconds. Combined ABX Protocol, Provigil, Discontinues Copaxone
10/2008: 25-foot walk time 5 seconds. Initiated Aqua Aerobics class. Combined Antibiotic Protocol, Provigil.
01/2009: MRI. Completed first year of Combined Antibiotic Protocol.

As I look at it, it’s not a perfect “U” shaped curve, but more like a “W”. Kim was clearly sliding before the 2005 MRI and her dx was shifted to SPMS before that too. Kim slid further until being put on combined Copaxone/Novantrone therapies. She had improvements, then worsened following an exacerbation. Under Combined Antibiotic Protocol Kim has improved.

Here we Go Steelers, Here we GO! Ken
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Postby Loriyas » Mon Feb 02, 2009 10:19 am

Ken
Thanks for such a thorough post. It is so helpful and I am so glad Kim is doing so well!
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Postby mrhodes40 » Tue Feb 03, 2009 10:06 am

Wonderful observation and documentation, Ken it is really interesting to read. I esp like that you dcumented the post novantrone experience, it is easy to see it did not help a lot though it seemed for a little like it might.

it also describes a person more disabled than I had imagined before, so that makes her sustained improvements all the more compelling. If I remember corretly she surprised you both when she ran a little bit spontaneously a few weeks ago, does she still do that from time to time?

Overall I think your clear, even though anecdotal, data reflects what other people have said was true: some people respond very well to this treatment and have sustained functional recovery to rival anything anyone else is documenting on other forums.

I am glad it is working so well for you!
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Postby notasperfectasyou » Tue Mar 03, 2009 10:44 am

Thanks Marie for sharing your thoughts. Kim has gotten on a bit of a kick the last 2 weeks of February. Yes, infact last week Kim ran about 100 feet back and forth in the kitchen. It seems to us like part of those higher peakes you get everyonce in a while following a pulse - a slightly better top than your last top. As we get into better weather, we'll be looking for more opportunities to test long held boundries.

Pulse 13

Kim’s first pulse of year two was uneventful. As pulses go, it was typical and she had a better than average time with it. I suppose February has been a month that I’ve been slammed, so keeping track of how Kim was doing in minute detail didn’t happen – fox paws.

Vitamin D

Kim got her D results this month, 62. Not bad, but can be better. Last month Kim tried a few days at 9,000 which coincided with die-off, so we backed off to 7,000 again. Just a note, Kim takes 3x - 2,000 Carlson’s/Vitamin Shoppe D3 and the other 1,000 comes from various USANA supplements she takes. I don’t know if it matters, but the USANA stuff is solid. So I recently bought Kim a bottle of Carlson’s 1,000 IU D3 and we’ll start adding one to the daily regime.

Walking

Last weeks 25-foot walk was really good. Kim looked stable and she walked the kitchen in 4.63 seconds. She was disappointed with her time and I didn’t know what to say. I think I said something like, “What are you trying to do? You don’t think 4.63 is good? It’s very good, it’s less than 5!”. There is a spring within Kim to be sprung, I can just feel it. She wanted to know about the 5.5 to 6.5 EDSS that ‘s posted in her CPn Help sig. She wanted to know what she’d have to accomplish in order to lower that. “Hummmmmm……. Looks like walking 200 meters non-stop and unaided is the goal” Kim’s into it, big time. I converted that to basketball court laps since the boys have been playing in the school league for the last 3 months. I told Kim it’s two and a half laps. She walked 3 laps last week at basketball practice.

Tetanus Shot

Kim got one this month when she went to the GP. Wow! It hit her for 3 days like huge die-off. Lack of balance in a big way. Then you read something like this: Tetanus Vaccine and Possible MS Protection. We found that Ibuprofen helped reduce the inflammatory response Kim got. But you kinda got to wonder about what the tetanus shot might have done and could it somehow excite the Cpn?

Meshing CPn and MS: Interleukin-6 (IL-6)

Besides testing the utility of my copy of McAlpine’s as a riser block for Kim’s scooter, I have loads of paper on my desk, journal articles I’ve printed up for years. I was thinking of throwing all of them out. But then, I got a cool idea. I can go back and read them and try to bridge some of the ideas of autoimmune research with the ideas of bacterially caused MS. I’ve sorta started this with my prior posts about MMP-9 and HSP60.

This thread isn’t for everyone and I accept Wallwalker’s observation that much of the detail I write makes it hard to pick out the physical and psychological improvements Kim is experiencing. For me it’s a chronology of impressions and discoveries along the way too – adding color to the events that can bring life to the overall goal of leaving a roadmap to help others. So my new thinking is to try to compare some of the ideas contained in traditional MS research with ideas that relate to CPn and see what happens.

Q: Does the way IL-6 has been implicated in MS correlate with CPn infection?
A: Yes it does. CPn infection is known to upregulate IL-6 and IL-6 is known to be proinflammatory in MS. By reading “Role of Very-late Antigen-4 (VLA-4) in Myelin Basic Protein-primed T Cell Contact-induced Expression of Proinflammatory Cytokines in Microglial Cells” you can see that IL-6 is known to have proinflammatory involvement in MS. I chose this article to link because you don’t have to pay to read the entire article. Here’s another article, IL-6 induces regionally selective spinal cord injury in patients with the neuroinflammatory disorder transverse myelitis, that discusses IL-6 in an MS related illness, Transverse Myelitis. This article provides evidence that IL-6 causes demyelination and axonal injury. Please read “Chlamydia pneumoniae Burden in Carotid Arteries Is Associated With Upregulation of Plaque Interleukin-6 and Elevated C-Reactive Protein in Serum” to see evidence of CPn inducing IL-6 expression.

An Invitation From Pandora

Kim’s now in her second series of aqua aerobics classes. She was recently asked if she wanted to train to become a Class Instructor! Wow was she ever excited! I was so very proud of her. I was very excited. Just think about it, but don’t think too much. It’s a paid position. If you collect social security you can’t have a paid position. While we know Kim has a way to go on the path to being cured, this sort of complexity was unexpected. It’s very rewarding to know that someone else thinks you would be terrific at their job. It’s a heck of a complement. So, as we continue to pursue this new and different path, we now have a whole new thing to ponder, “What might the process of becoming unhandicapped be like?” Think about it ………

Ken
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Postby MacKintosh » Wed Mar 04, 2009 4:15 pm

Okay, what's il6?

And I can't even imagine what mixed feeling 'becoming unhandicapped' elicits! That is WONDERFUL news!
The difference between what we do and what we are capable of doing would suffice to solve most of the world’s problems. Mohandas Gandhi
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Postby mrhodes40 » Wed Mar 04, 2009 4:53 pm

Fabulous news!

Ken, kim can make a limited amount up to I think 860 a month and still be considered for the purposes of SSDI not making "substantial" income. I personally have had the oppportunity to work a little and I find it keeps me very ....in life... I guess is the best to say. If she would like that, you should look into the work rules and learn what is up. I guess you could say they want you to try if you feel you can.

But frankly for me I am so limited it is really hard for me to make something like 860 a month. I am really not able to be reliably "there" for a set time. What if I feel bad? On a pulse? etc. that gets in the way. Full time work or really a real job is realy not plausible for us, that's how wen end up on SSDI to begin with. so I find it is possible really to work at odd obs that come up, for me in the doctor office when they need a week of paperwork catchup that a nurse can do if I can name my own hours and come and go as I feel up to it--I know lucky.

But if she'd like to try it and the payis small, it might give her a real boost to have a small earning. One thing I like to do with my money is buy my darling a present from ME :wink: The other thing is buy something he doesn't think is ncessary, like another new teapot. It makes me feel grownup and self determining in a way a totally dependant person like me misses.
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Postby notasperfectasyou » Wed Mar 04, 2009 8:21 pm

MacKintosh wrote:Okay, what's il6?

And I can't even imagine what mixed feeling 'becoming unhandicapped' elicits! That is WONDERFUL news!


IL-6??? Exactly.

Mac, Great to hear from you and know that you still visit me here. I feel special today. There is a bridge that I think needs to be built. If you read my My old but good post Understanding MS 102: My Doctor is Expressing Cytokines you'll see that there is an entire language of cellular and sub-cellular stuff that science has been discussing in regard to MS for DECADES.

Observation: Just because we have found the answer that we are confident in, we also have found that others have difficulty getting to understand us when we tell them we have licked MS.

Reason: I believe we have traveled so far and we are so distant from the understanding of others, we have an unrealistic expectation that others will get it. We need to back up, all the way back over the great distance we have traveled much like Columbus returning to Spain.

Message: I feel that I have to find a message that speaks the language of the work everyone understands. We can't entirely negate decades of MS research. If what we have is the entire answer, then it needs to be shown to be compatible with the research that has preceded it. Meaning, telling folks they are wrong for thinking MS involves Macrophages expressing IL-6 isn't productive communication. But showing people how CPn can cause Macrophages to express IL-6 can demonstrate our theory by showing that it's actually building on existing theory. No one said the new testament negates the old one

Did I make sense? I feel very strongly about this, I think it's critically important to be able to communicate with the folks who are still looking, but needs to find consistency with much of what they already know to be fact. Ken
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Postby MacKintosh » Wed Mar 04, 2009 9:00 pm

I agree, in theory, Ken. It will be a monumental task, but you've already accumulated a lot of material to begin the cross-referencing.

I'd suggest, before you dive into it, you start a new topic on relating the 'new' antibacterial theory to the 'old' MS research. It will get lost on this post.

Four years ago, it was actually a much simpler decision for me. All sorts of things were going wrong all at once and I found the theory of 'suddenly acquiring an autoimmune disease' not to be sound. It made FAR more sense to me that I'd caught something that people maybe didn't recognize yet as a disease. When I learned it could be cured, well, the decision was easy.

It's becoming a case of 'too much information' these days. We're throwing so many medical words at the explanations, we're alienating the lay folks. (At least, what you're proposing will be invaluable in convincing the medical people.)
The difference between what we do and what we are capable of doing would suffice to solve most of the world’s problems. Mohandas Gandhi
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Postby Loriyas » Thu Mar 05, 2009 6:42 am

Ken
So happy for Kim! Tell her I said congratulations!
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Postby notasperfectasyou » Thu Mar 05, 2009 7:57 am

mrhodes40 wrote:Fabulous news!


Isn't it!

Thanks Marie for the info about Social Security. I'll pass it along to Kim after her pulse and see what she wants to do. Sounds like she would have to coordinate with Social Security and LTD policy through her former employer. How does one approch the wicked LTD carrier with this and not set off red flags? Every year they send her a form to fill out and have her doctor sign to say that she's still disabled. The relationship with the LTD carrier seems adversarial to me. So this is what I mean with my Pandora referrence. Not that it's a huge obstacle, but it's a new one and redtape is always soooooooooo much fun, right?

Ken
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Postby notasperfectasyou » Thu Mar 05, 2009 9:25 pm

MacKintosh wrote:I agree, in theory, Ken. It will be a monumental task, but you've already accumulated a lot of material to begin the cross-referencing.

I'd suggest, before you dive into it, you start a new topic on relating the 'new' antibacterial theory to the 'old' MS research. It will get lost on this post.

Four years ago, it was actually a much simpler decision for me. All sorts of things were going wrong all at once and I found the theory of 'suddenly acquiring an autoimmune disease' not to be sound. It made FAR more sense to me that I'd caught something that people maybe didn't recognize yet as a disease. When I learned it could be cured, well, the decision was easy.

It's becoming a case of 'too much information' these days. We're throwing so many medical words at the explanations, we're alienating the lay folks. (At least, what you're proposing will be invaluable in convincing the medical people.)


I know, I don't want to be too scattered though. I'm working up a post of journal supported Q&A about CPn and MS. When I get to a good size I'll share it with everyone. I also wonder if Jim K would be interested in using it. Sometimes I wonder if I should spend more time at Cpn. But, then I really feel that I need to be helping non-Cpn'ers to learn about it.

What's totally amazing is when you find an article like ........

Dr. Gieffers, et al. 2001 Chlamydia pneumoniae Infection in Circulating Human Monocytes Is Refractory to Antibiotic Treatment

I've read this article 5 times and I don't understand why it's not posted prominently at CPn Help. I will take care of that later. Ken
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Pulse 14 - February 2009

Postby notasperfectasyou » Tue Mar 31, 2009 10:20 am

Pulse 14

Day one we had a big snow storm – that is, big for Northern Virginia. I took the boys sledding and we had a snowball fight. Kim was slowed somewhat on the first day of Flagyl. On day two Kim had some emotional outbursts but mostly a good day. On day 3 Kim was pretty tired at the end of the day. She told me that she wanted to unzip her skin so she could be herself; as if it was a tarp that she was clinging to her body. On day 5, Kim got a very upset, “On Fire” says Kim, stomach. Kim ate some sushi nori, six Tums and a 1gm Chlorella tablet which calmed her stomach by evening. She didn't fog up, but was very tired in the evening and went to bed early. Seemed like a lot of die-off. Days 6 and 7 were low key for Kim. She was feeling swollen all over and cold much of the time (despite it getting up to 80 on Sunday – exactly a week ago it snowed!).

Meshing CPn and MS: Interferon Gama (IFN-y)

Q: Does the way IFN-y {gamma} has been implicated in MS correlate with CPn infection?

A: Yes it does. IFN-y has been associated with exacerbations and oligodenrocyte death. It has been shown that IFN-y expression plays a central role in the bodys effort to control Clamydia Pneumoniae infection. Dr. Panitch, et al. 1987 Treatment of multiple sclerosis with gamma interferon; Dr. Mana, et al. 2006 Deleterious Role of IFN in a Toxic Model of Central Nervous System Demyelination; Dr. Rottenberg, et al. 2000 Regulation and Role of IFN-y in the Innate Resistance to Infection with Chlamydia pneumoniae

But isn’t Pneumonia a Lung Disease?

A: Yes. It has been shown that infected Alveolar Macrophages can transmigrate through the mucosal barrier, thus giving Chlamydia Pneumoniae access to the lymphatic and systemic circulatory systems. It is also notable that Neutrophil Granulocytes (one of the first immune system cells to encounter CPn in the lungs) can host and incubate Chlamydia Pnuemoniae. Dr. Gieffers et al. 2004 Phagocytes transmit Chlamydia pneumoniae from the lungs to the vasculature; Dr. Blasi et al. 2004 Chlamydia pneumoniae: crossing the barriers?; Van Zandbergen, Ger et al. 2004 Chlamydia pneumoniae Multiply in Neutrophil Granulocytes and Delay Their Spontaneous Apoptosis; Rodriguez, Nuria et al. 2005 Polymorphonuclear Neutrophils Improve Replication of Chlamydia pneumoniae In Vivo upon MyD88-Dependent Attraction

But what about the cells of the immune system

Q: Monocytes have been implicated in MS. How does this relate to CPn infection?

A: Monocytes have been found to migrate across the blood brain barrier and contribute to inflammation. Some benefits associated with MS therapies have been linked to their targeting monocytes. Monocytes are easily infected with CPn and can disseminate CPN within systemic circulation. Dr. Bar-Or et al. 2003 Analyses of all matrix metalloproteinase members in leukocytes emphasize monocytes as major inflammatory mediators in multiple sclerosis; Dr. Kopadze et al. 2006 Inhibition by Mitoxantrone of In Vitro Migration of Immunocompetent Cells: A Possible Mechanism for Therapeutic Efficacy in the Treatment of Multiple Sclerosis; Dr. Minagar et al. 2008 Combination Therapy With Interferon Beta-1a and Doxycycline in Multiple Sclerosis: An Open-Label Trial; Dr. Burger et al. 2009 Glatiramer acetate increases IL-1 receptor antagonist but decreases T cell-induced IL-1β in human monocytes and multiple sclerosis; Dr. Hakki et al. 2007 Chlamydia pneumoniae infection modulates cytokine production by human T lymphocytes and monocytes; Dr. Gieffers et al. 2001 Chlamydia pneumoniae Infection in Circulating Human Monocytes Is Refractory to Antibiotic Treatment

Helping the ABX?

Has anyone else looked into this? This idea zinged me recently. MS’ers take some supplements to shoreup the blood brain barrier. I think we need to know which ones they are. I’m wondering if we shouldn’t be taking them. Isn’t the idea to get the ABX into the CNS as much as possible? Don’t we, those on ABX, want to have a more permeable BBB? Has anyone here thought about this before? Ken
Last edited by notasperfectasyou on Tue Apr 14, 2009 12:22 pm, edited 2 times in total.
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Postby SarahLonglands » Tue Mar 31, 2009 12:00 pm

The supplements and antioxidants page on David's website starts thus:

Easing mitochondrial stress in chronic Chlamydia pneumoniae infections: the use of dietary supplements

David Wheldon

Introduction


In health a balanced diet provides all the vitamins and antioxidants necessary to maintain vigour, and supplementation cannot reasonably be recommended.

In disease states, however, the situation is different. Chronic persistent infections with Chlamydia pneumoniae are characterized by high levels of oxidative stress as a result of complex inflammatory processes. Multiple Sclerosis is no exception. The concentrations of reactive oxygen and nitrogen species - superoxide, nitric oxide and peroxynitrite, a toxic metabolite of nitric oxide - increase dramatically in MS not only because of bacterial activity but because of the pro-inflammatory immune response to this activity.


http://www.davidwheldon.co.uk/supplement_rationale.html

There is a lot more to this than merely shoring up the blood brain barrier and most things have more than one use, but if you look up here:

http://www.msrc.co.uk/index.cfm?fuseaction=show&pageid=772
they reckon that the two things the best for shoring up the bbb are bilberry extract and grape seed extract, neither of which has ever figured highly on any supplement list I have used. However, both are useful for people with atherosclerosis, high blood pressure and poor circulation, three things that affect many people with a chronic Cpn infection.

Sarah
An Itinerary in Light and Shadow Completed Dr Charles Stratton / Dr David Wheldon abx regime for aggressive secondary progressive MS in June 2007, after four years. Still improving with no relapses since starting. Can't run but can paint all day.
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Postby notasperfectasyou » Mon Apr 27, 2009 3:16 pm

Pulse 15

The beginning of the pulse hit Kim pretty hard and she was washed out for most of the first 2-3 days. In the middle she felt pretty good and then the last 2 days were hard again. Kim had a few days of stomach burn, a nap or two; but on day 5 she had a two really nice walks – the first walk was 5.03 and the second walk was 4.65! Kim’s feeling up to wanting to walk this spring and I bought a measuring wheel on Ebay. A measuring wheel is the thing you see folks rolling on the end of a stick when they pace off distances. It has a little clicker on it that tells you how many feet you walked. The goal is 200m (328 feet) unaided without stopping. If you are thinking this is a cool idea, it is, but don’t buy the cheapest one. The one I bought was about $15 on Ebay and I don’t like it so much. I think I’ll get a nicer one.


Kim’s Perspective

Kim posted about her 15th pulse too. Her most recent entry is titled, ”S.O.S. - Such Overwhelming Swelling”.


Your Immune System Used Like a Trojan Horse

Q: Besides monocytes, do other immune system cells have behavior that correlates between MS and CPn infection?

A: Lymphocytes are also a major group of immune system cells that exhibit potentially corroborating behavior in MS and CPn infection. T-Lymphocyte and B-Lymphocyte migration through the brain endothelium/blood brain barrier has been associated with Multiple Sclerosis. Chlamydia Pneumoniae has been shown to infect and multiply in Lymphocytes. CPn infected Lymphocytes have been shown to be resistant to some antibiotic therapies. Dr. Alter et al. 2003 Determinants of Human B Cell Migration Across Brain Endothelial Cells; Dr. Prat et al. 2002 Migration of Multiple Sclerosis Lymphocytes Through Brain Endothelium; Dr. Haranaga et al. 2001 Chlamydia pneumoniae Infects and Multiplies in Lymphocytes In Vitro; Yamaguchi et al. 2003 Chlamydia pneumoniae Resists Antibiotics in Lymphocytes

Q: Isn’t apoptosis supposed to protect my body from bacterial infection?

A: Yes, but it doesn’t always work. Your cells are pre-programmed to self-destruct when they become infected through a process called apoptosis. When infected by Chlamydia Pneumoniae, many human cells, including immune system cells, become hosts for the bacteria instead of working to destroy the bacteria. To be absolutely clear, CPn bacteria cell living within your body's cell. It has even been shown that CPn infected host cells can proliferate via mitosis, creating more infected host cells. Lancellotti, Marcelo et al. 2006 Bacteria-induced apoptosis: an approach to bacterial pathogenesis; Geng, Yuemei et al. 2000 Chlamydia pneumoniae Inhibits Apoptosis in Human Peripheral Blood Mononuclear Cells Through Induction of IL-10; Rajalingam, Krishnaraj et al. 2001 Epithelial Cells Infected with Chlamydophila pneumoniae (Chlamydia pneumoniae) Are Resistant to Apoptosis; Fischer, Silke et al. 2004 Protection against CD95-Induced Apoptosis by Chlamydial Infection at a Mitochondrial Step; Fischer, Silke et al. 2004 Chlamydia Inhibit Host Cell Apoptosis by Degradation of Proapoptotic BH3-only Proteins; Green, Whitney et al. 2004 Chlamydia-Infected Cells Continue To Undergo Mitosis and Resist Induction of Apoptosis; Sasu, Sebastian et al. 2001 Chlamydia pneumoniae and Chlamydial Heat Shock Protein 60 Stimulate Proliferation of Human Vascular Smooth Muscle Cells via Toll-Like Receptor 4 and p44/p42 Mitogen-Activated Protein Kinase Activation

Q: Do my cells function differently after they become hosts for Chlamydia Pneumoniae?

A: Yes. Cellular expression can be dramatically altered. Genes related to apoptosis, the cell cycle and host metabolism are permanently differentially regulated by Chlamydia Pneumoniae. Infected human host cells have been found to significantly increase the release of interleukin (IL) 1b, IL-6, IL-8, IL-12, tumor necrosis factor alpha (TNF-a), intercellular cell adhesion molecule 1(ICAM-1/CD54) and gamma interferon (IFN-y). These cytokines stimulate the immune system. In addition CPn activates nuclear factor kappa B (NF-kB) and down regulates major histocompatibility complex class I molecules (MHC-1).
Eickhoff, Meike et al. 2007 Host Cell Responses to Chlamydia pneumoniae in Gamma Interferon-Induced Persistence Overlap Those of Productive Infection and Are Linked to Genes Involved in Apoptosis, Cell Cycle, and Metabolism; Krull, Matthias et al. 2004 Differences in Cell Activation by Chlamydophila pneumoniae and Chlamydia trachomatis Infection in Human Endothelial Cells; Gencay, Mikael et al. 2003 Chlamydia pneumoniae Activates Epithelial Cell Proliferation via NF-κB and the Glucocorticoid Receptor; Yang, Jun et al. 2003 Induction of Proinflammatory Cytokines in Human Lung Epithelial Cells during Chlamydia pneumoniae Infection; Yamaguchi, Hiroyuki et al. 2002 Chlamydia pneumoniae Infection Induces Differentiation of Monocytes into Macrophages; Rodel, Jurgen et al. 2000 Production of Basic Fibroblast Growth Factor and Interleukin 6 by Human Smooth Muscle Cells following Infection with Chlamydia pneumoniae; Gaydos, Charlotte 2000 Growth in Vascular Cells and Cytokine Production by Chlamydia pneumoniae

Q: Can the actual cells of my brain, the ones that are damaged as a result of MS, be infected by and host Chlamydia Pneumoniae?

A: Yes. Appelt, Denah et al. 2008 Inhibition of apoptosis in neuronal cells infected with Chlamydophila (Chlamydia) pneumoniae

Isn’t that interesting? Ken
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Postby notasperfectasyou » Mon Jun 01, 2009 2:59 pm

Pulse 16

No day by day report on the pulse. It was a good pulse and Kim fared pretty well. Nothing new to report about it. Kim capped the pulse with a 4 day Ibuprofen “Top Off”. The idea here was to stop the inflammation and get Kim feeling more like herself faster.

It worked. Kim will try this again next pulse.

A week and a half post pulse Kim had the fastest 25-foot walk yet! 4.28 seconds! Kim did this at 11:30 at night. If you’re not impressed, grab a stop watch and time yourself walking 25 feet. We use decorative kitchen mats to mark the start and finish. I tried to see what 4.28 seconds would “feel” like and I have to say as the non-MS’er, it felt pretty brisk to me. I’d never walk that fast. If I needed to move that fast, I’d jog.

Kim was Pumped! Kim’s had more to say about her pulse at Kimscupoftea’s Blog.

The Blood Brain Barrier: A Sticky Situation

Q: Does the way ICAM-1 has been implicated in MS correlate with CPn infection?

A: Yes. ICAM-1 is barely detectable in the normal brain. However, increased expression of ICAM-1 has been shown on endothelial cells, microglia and astrocytes in active MS. More specifically, ICAM-1 has been shown to be crucial for leukocyte infiltration into the brain, and the process of migration across the brain endothelial layer can accelerate the breakdown of the blood brain barrier. Several lines of evidence indicate that ICAM-1 acts as a docking molecule for lymphocytes before migration. ICAM-1 further facilitates transmigration through the CNS endothelium by rearrangement of the endothelial actin cytoskeleton, meaning ICAM-1 stimulates the altering of the impermeable tight junctions of the blood brain barrier. Chlamydia Pneumoniae can infect human endothelial cells where it induces the expression of ICAM-1, which has also been linked to monocyte migration.

Etienne-Manneville, Sandrine et al. 2000 ICAM-1-Coupled Cytoskeletal Rearrangements and Transendothelial Lymphocyte Migration Involve Intracellular Calcium Signaling in Brain Endothelial Cell Lines; Bullard, Daniel et al. 2007 Intercellular Adhesion Molecule-1 Expression Is Required on Multiple Cell Types for the Development of Experimental Autoimmune Encephalomyelitis; Dai, Jianfeng et al. 2008 ICAM-1 Participates in the Entry of West Nile Virus into the Central Nervous System; Adamson, Peter et al. 1999 Lymphocyte Migration Through Brain Endothelial Cell Monolayers Involves Signaling Through Endothelial ICAM-1 Via a Rho-Dependent Pathway; Buul, Jaap et al. 2004 Signaling in Leukocyte Transendothelial Migration; Lawson, Charlotte et al. 2009 ICAM-1 signaling in endothelial cells; Kol, Amir et al. 1999 Chlamydial and human heat shock protein 60s activate human vascular endothelium, smooth muscle cells, and macrophages; Vielma, Silvana et al. 2003 Chlamydophila pneumoniae Induces ICAM-1 Expression in Human Aortic Endothelial Cells via Protein Kinase C–Dependent Activation of Nuclear Factor- B

My Own CPn Adventure

Its one thing to read about how nasty CPn can be and it’s a whole ‘nother thing to think about it personally. After finding articles that link CPn with other fun illnesses like Alzheimers, I thought ……. I have health insurance, why not get tested?

I have a doctor who runs his office in a somewhat informal way, kinda makes me thing of an old country doctor. I called the office 3 times and got no return call. I popped over at lunch and the nurse told me to stand by his door. So I stood there, in his hallway for about 15 minutes. He walked by a few times, but was busy. Then when he hit a pause, he asked me what I wanted and I told him I wanted to be tested for Chlamydia Pneumoniae because it’s implicated in Arthrosclerosis. I picked Ath because I know his specialty is blood. He said that he has never heard about it before, the insurance might not cover it, but we could learn about it together! I got my permission slip.

It was a Labcorp permission slip. I wanted Quest. The Quest test is way better, though still not perfect. I called my insurance and found that Quest is part of my plan so I popped by the office. They would accept the LabCorp form! So I spent a couple weeks taking NAC to help reduce the likelihood of a false negative. I got the results about a week later – “Antibody Not Detected”. That’s it. No wordy paragraph.

Why Not …. Aspirin?!?!

I have a confluence of thoughts. I think – “I can share that thought in 3 articles” – here goes …..

Duffy, Paula and Zurier, Robert 1979 Lymphocyte Adherence in Multiple Sclerosis: EFFECT OF ASPIRIN. Lymphocytes don’t adhere to the vessel walls as well when you take aspirin. Lymphocytes can be infected with Chlamydia Pneumoniae and assist in its migration.

Casserly, Ivan and Topol, Eric 2004 Convergence of atherosclerosis and Alzheimer's disease: Inflammation, cholesterol, and misfolded proteins. Inflammation is common to both and both respond to aspirin and other nonsteroidal anti-inflammatory drugs (NSAIDs). Chlamydia Pneumoniae has been implicated in both illnesses.

Yoneda, Hiroshi et al. 2003 Aspirin inhibits Chlamydia pneumoniae-induced NF-kB activation, cyclo-oxygenase-2 expression and prostaglandin E2 synthesis and attenuates chlamydial growth. Sorta makes you stop and think, don’t it?

Here are 3 threads that I think should be referenced here:

Stopping inflammation while raising vitamin D levels
Ibuprofen / Inflammation / Flagyl Pulse
Naprosyn / Aleve / Naproxen / Anti-Inflammatory

Kim swapped out Ibuprofen for Aspirin one day. Yes it was only a day, but Kim felt like Aspirin did nothing. It’s tough to argue with her, I mean, she said Ibuprofen is better. I got the enteric kind so if her stomach starts hurting on Ibuprofen, we’ll try the Aspirin again. Ken
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