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Old 10-06-2008, 12:32 PM #21
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Thank you, Jack. That's all helpful and really informative info. Much appreciated!
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Old 10-07-2008, 05:46 PM #22
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Originally Posted by Desinie View Post
Thank you, Jack. That's all helpful and really informative info. Much appreciated!
Thank You for your thank you.

I am going to post the other MMP-9 reducing abstracts later. I have more good info on MMPs in general.

It will cover the following +

QUERCETIN..........................REDUCES MMP-9s

GREEN TEA EXTRACT(EGCGs)... REDUCES MMP-9s

ALPHA LIPOIC ACID (R-lipoic/ R-Dihdro-LipoicAcid) ... REDUCES MMP-9s

NAC N-Acetyl-L-Cysteine .......REDUCES MMP-9s

STATIN DRUGS (i.e Zocor) .....REDUCES MMP-9s

Minocycline/Doxycycline.........REDUCES MMP-9s

Pycnogenol (Pine bark extract)..REDUCES MMP-9s

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Old 10-08-2008, 09:14 AM #23
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[QUOTE=greta;383371]I follow the Swank diet for MS - I consider that similar to supplement because I'm using food in it's natural state to treat.

Hi, which one is the SWANK diet? I have so many.....
Mary
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Old 10-09-2008, 09:30 PM #24
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[QUOTE=mbabic;384533]
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Originally Posted by greta View Post
I follow the Swank diet for MS - I consider that similar to supplement because I'm using food in it's natural state to treat.

Hi, which one is the SWANK diet? I have so many.....
Mary
If you google swank diet, there is a website about it and a book also. It's a study by Dr. Roy Swank done many years ago that has been successful for lots of folks. I think it's similar to a lot of the newer diets also though. The website is swankmsdiet.org.

I think it's great, I see a big difference by following it.

Greta, do you still take rebif also??
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Old 10-26-2008, 11:55 PM #25
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Default Diet - Supplements

Any diet LOW in saturated fat is VERY good at avoiding potentially harmful increases in GAMMA INTERFERON that would occur after consuming high saturated fat foods. Some high bacteria foods also may cause this increase in GAMMA INTERFERON. Some dairy products could do this. So a diet LOW in saturated fat and dairy products would be a VERY GOOD way to NOT AGGRAVATE the MS condition.

THIS IS NOT A TREATMENT!!!! JUST A GOOD WAY NOT TO AGGRAVATE THE MS CONDITION.

Taking foods and supplements that lower MMP-9s would be more like a treatment. You would also need to lower TNF-a, IL-12 and some other "things" to have an effective program. I doubt that food alone would have any great effect. It takes 10 cups of Green Tea day to get a therapeutic effect. I have two large mugs of a mixture of Green and White tea each day. Plus two Green Tea Extracts caps which equates to about 10-12 cups of Green Tea per day.

Lowering excess Glutamate is also something that diet can control. Some food additives can raise Glutamate levels and should be avoided. Some supplements will also lower glutamate levels.

The second stage of MS is neurodegeneration and excess glutamate does considerable neuron damage.

jackD

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Old 10-27-2008, 01:35 AM #26
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Green Tea's EGCGs reduces levels of MMP-9s.

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Quote:
Biochim Biophys Acta. 2000 Mar 16;1478(1):51-60.

Matrix metalloproteinase inhibition by green tea catechins.

Demeule M, Brossard M, Page M, Gingras D, Beliveau R.

Laboratoire de Medecine Moleculaire, Hopital Sainte-Justine - UQAM, C.P. 8888,
Succursale centre-ville, Montreal, QC, Canada.

We have investigated the effects of different biologically active components
from natural products, including green tea polyphenols (GTP), resveratrol,
genistein and organosulfur compounds from garlic, on matrix metalloproteinase
(MMP)-2, MMP-9 and MMP-12 activities. GTP caused the strongest inhibition of the
three enzymes, as measured by fluorescence assays using gelatin or elastin as
substrates. The inhibition of MMP-2 and MMP-9 caused by GTP was confirmed by
gelatin zymography and was observed for MMPs associated with both various rat
tissues and human brain tumors (glioblastoma and pituitary tumors).
The
activities of MMPs were also measured in the presence of various catechins
isolated from green tea including (-)-epigallocatechin gallate (EGCG),
(-)-epicatechin gallate(ECG), (-)-epigallocatechin (EGC), (-)-epicatechin (EC)
and (+)-catechin (C). The most potent inhibitors of these activities, as
measured by fluorescence and by gelatin or casein zymography, were EGCG and ECG.
GTP and the different catechins had no effect on pancreatic elastase, suggesting
that the effects of these molecules on MMP activities are specific.

Furthermore,
in vitro activation of proMMP-2 secreted from the glioblastomas cell line U-87
by the lectin concanavalin A was completely inhibited by GTP and specifically by
EGCG. These results indicate that catechins from green tea inhibit MMP
activities and proMMP-2 activation.

PMID: 10719174 [PubMed - indexed for MEDLINE]
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Old 10-27-2008, 01:39 AM #27
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Green Tea's EGCGs reduces levels of MMP-9s.

jackD
How Green Tea's EGCG helps the MS situation has recently been published. It is in my web storage area shown below.

For some strange reason these CENSORED idiots do not mention in the abstract that what they are writing about is the EGCG in Green Tea and STATINS!!!

They just call it "novel therapeutic targets". Why in HELL they did not want to identify what they had discovered is just ... really stupid!@!!

It appears that the two "novel therapeutic targets" {EGCG in Green Tea and STATINS} work together to protect the brain from demyelination.

I therefore take my second decaffeinated MEGA GREEN TEA EXTRACT (326 mg EGCG) cap at night with my SIMVASTATIN (ZOCOR) statin medication.


jackD


http://home.ix.netcom.com/~jdalton/egcg-neorond-ms.pdf (FULL STUDY)

Below is the DUMB abatract...


Quote:
1: J Neuroimmunol. 2007 Mar;184(1-2):17-26. Epub 2007 Jan 10.

Neurodegeneration in autoimmune demyelination: recent mechanistic insights reveal novel therapeutic targets.

Aktas O, Waiczies S, Zipp F.

Institute for Neuroimmunology, Neuroscience Research Center, Charité -- Universitätsmedizin Berlin, Germany.

Multiple sclerosis (MS) is the most common chronic demyelinating disease of the central nervous system (CNS) and the major cause of neurological disability in young adults in Western countries. In spite of intensive research efforts, treatment options established to date do not sufficiently prevent the accumulation of tissue damage and clinical disability in patients with MS.

We here describe recently identified molecules responsible for the inflammatory and the neurodegenerative processes in MS and its animal model, experimental autoimmune encephalomyelitis (EAE), and review new treatment options targeting both aspects of this disease.

PMID: 17222462 [PubMed - indexed for MEDLINE]

Last edited by jackD; 10-27-2008 at 02:02 AM.
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Old 10-27-2008, 02:19 AM #28
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Default flavonoids

Some flavonoids are of incredible benefit to myelin and those little neurons.

Quote:
1: Biochem Pharmacol 2003 Mar 1;65(5):877-85

Flavonoids inhibit myelin phagocytosis by macrophages; a structure-activity relationship study.

Hendriks JJ, de Vries HE, van der Pol SM, van den Berg TK, van Tol EA, Dijkstra
CD.

Department of Molecular Cell Biology, VU Medical Centre, Van der Boechorststraat
7, 1081 BT, Amsterdam, The Netherlands.

Demyelination is a characteristic hallmark of the neuro-inflammatory disease multiple sclerosis. During demyelination, macrophages phagocytose myelin and secrete inflammatory mediators that worsen the disease.

Here, we investigated whether flavonoids, naturally occurring immunomodulating compounds, are able to influence myelin phagocytosis by macrophages in vitro. The flavonoids luteolin, quercetin and fisetin most significantly decreased the amount of myelin phagocytosed by a macrophage cell line without affecting its viability. IC(50) values for these compounds ranged from 20 to 80 microM. The flavonoid structure appeared to be essential for observed effects as flavonoids containing hydroxyl groups at the B-3 and B-4 positions in combination with a C-2,3 double bond were most effective.

The capacity of the various flavonoids to inhibit phagocytosis correlated well with their potency as antioxidant, which is in line with the requirement of reactive oxygen species for the phagocytosis of myelin by macrophages.

Our results implicate that flavonoids may be able to limit the demyelination process during multiple sclerosis.

PMID: 12628496 [PubMed - in process
]

(FULL STUDY OF ABOVE ABSTRACT)

http://home.ix.netcom.com/~jdalton/Flavonoids%20MS.pdf

OTHER INTERESTING STUDIES ARE BELOW

http://home.ix.netcom.com/~jdalton/L...hageJPET01.pdf

http://home.ix.netcom.com/~jdalton/OxStress-01.pdf

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Old 10-27-2008, 02:27 AM #29
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There are some recent human clinical studies that show it has a favorable result on the course of MS when taken in very high doses. I DO NOT RECOMMEND this high 1800 mg approach. I feel that taking a modest effective dose of a variety of things that lower MMP-9s is better. I can elaborate if asked.

jackD


Quote:
1: J Neuroimmunol 2002 Oct;131(1-2):104-14

Alpha lipoic acid inhibits T cell migration into the spinal cord and
suppresses and treats experimental autoimmune encephalomyelitis.

Marracci GH, Jones RE, McKeon GP, Bourdette DN.
Department of Neurology, Oregon Health and Science University, Portland, OR
97201, USA.

Oxidative injury may be important to the pathogenesis of multiple sclerosis
(MS). We tested the antioxidant alpha lipoic acid (ALA) in an experimental
murine model of MS, experimental autoimmune encephalomyelitis (EAE). ALA was
administered to SJL mice 7 days after immunization with proteolipid protein
(PLP) 139-151 peptide. Mice that received 5-100 mg/kg/day of ALA had
dose-dependent reductions in their 10-Day Cumulative Disease Scores (10-Day
CDS) by 23-100%. Minimal inflammation, demyelination and axonal loss
occurred in the spinal cords (SC) of ALA-suppressed mice, and there was a
marked reduction in CD3+ T cells and CD11b+ monocyte/macrophage cells within
the SC. Mice treated with ALA (100 mg/kg/day) commencing on the first day of
clinical EAE had a significant reduction in 10-Day CDS. SC of ALA-treated
mice had reduced demyelination and axonal loss and a rapid reduction in CD3+
T cells. In vitro, ALA and its reduced form, dihydrolipoic acid, inhibited
the activity of matrix metalloproteinase-9 (MMP-9) in a dose-dependent
fashion.
ALA is highly effective at suppressing and treating EAE and does so
by inhibiting T cell trafficking into the SC, perhaps by acting as a matrix
metalloproteinase inhibitor.

PMID: 12458042 [PubMed - indexed for MEDLINE]
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Old 10-27-2008, 02:35 AM #30
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Default Pine Bark Extract - Pycnogenol

wanted to add that Pycnogenol (Pine Bark Extract) lowers MMP-9 quite well. I take it to help with my swollen right foot. I have some nasty Venous Insufficiency because of numerous unecessary surgeries to my leg.

It is well known that Pine Bark extract (Pycnogenol) can "FIX" this problem. The fact it prevents the condition from killing folks like me is GOOD ENOUGH FOR ME!!!!!!!!!!!@

I no longer have severe PAIN nor INFECTIONS(Cellulites), INFECTED BLACK TOES ETC ETC.

jackD


1: Free Radic Biol Med. 2004 Mar 15;36(6):811-22.

Antioxidant activity and inhibition of matrix metalloproteinases by metabolites
of maritime pine bark extract (pycnogenol).

Grimm T, Schafer A, Hogger P.

Institut fur Pharmazie und Lebensmittelchemie, Bayerische
Julius-Maximilians-Universitat, Wurzburg, Germany.

The procyanidin-rich maritime pine bark extract Pycnogenol has well-documented
antioxidant and anti-inflammatory activity. After oral administration of
Pycnogenol two major metabolites are formed in vivo,
delta-(3,4-dihydroxyphenyl)-gamma-valerolactone (M1) and
delta-(3-methoxy-4-hydroxyphenyl)-gamma-valerolactone (M2). We elucidated the
effects of these metabolites on matrix metalloproteinases (MMPs) and determined
their antioxidant activity to understand their contribution to the effects of
maritime pine bark extract. We discovered strong inhibitory effects of M1 and M2
toward the activity of MMP-1, MMP-2, and MMP-9
. On a microgram-per-milliliter
basis both metabolites appeared more active than Pycnogenol. The metabolites
were more effective than their metabolic precursor (+)-catechin in MMP
inhibition. On a cellular level, we detected highly potent prevention of MMP-9
release by both metabolites, with concentrations of 0.5 microM resulting in
about 50% inhibition of MMP-9 secretion.
M1 was significantly more effective in
superoxide scavenging than (+)-catechin, ascorbic acid, and trolox, while M2
displayed no scavenging activity. Both metabolites exhibited antioxidant
activities in a redox-linked colorimetric assay, with M1 being significantly
more potent than all other compounds tested.

Thus, our data contribute to thecomprehension of Pycnogenol effects and provide
a rational basis for its use in prophylaxis and therapy of disorders
related to imbalanced or excessive MMP activity.


PMID: 14990359 [PubMed - indexed for MEDLINE]

1: J Inflamm (Lond). 2006 Jan 27;3:1.

Inhibition of NF-kappaB activation and MMP-9 secretion by plasma of human
volunteers after ingestion of maritime pine bark extract (Pycnogenol).

Grimm T, Chovanova Z, Muchova J, Sumegova K, Liptakova A, Durackova Z, Hogger P.

Institut fur Pharmazie und Lebensmittelchemie, Bayerische
Julius-Maximilians-Universitat, Wurzburg, Germany. hogger@pzlc.uni-wuerzburg.de

French maritime pine bark extract (Pycnogenol) displays a variety of
anti-inflammatory effects in vivo. Aim of this study was to determine whether
human plasma after oral intake of Pycnogenol contains sufficient concentrations
of active principles to inhibit key mediators of inflammation. Blood samples
from seven healthy volunteers were obtained before and after five days
administration of 200 mg Pycnogenol per day. Plasma samples statistically
significantly inhibited matrix metalloproteinase 9 (MMP-9) release from human
monocytes and NF-kappaB activation.
Thus, we provide evidence that bioavailable
active principles of Pycnogenol exert anti-inflammatory effects by inhibition of
proinflammatory gene expression which is consistent with documented clinical
observations. We suggest that our ex vivo method is suitable to substantiate
molecular pharmacological mechanisms of complex plant extracts in a more
focussed and rational way compared to in vitro studies by taking into account
the processes of absorption and metabolism.

PMID: 16441890 [PubMed]

1: Clin Appl Thromb Hemost. 2004 Oct;10(4):373-7.

Prevention of venous thrombosis and thrombophlebitis in long-haul flights with
pycnogenol.

Belcaro G, Cesarone MR, Rohdewald P, Ricci A, Ippolito E, Dugall M, Griffin M,
Ruffini I, Acerbi G, Vinciguerra MG, Bavera P, Di Renzo A, Errichi BM,
Cerritelli F.

Department of Biomedical Sciences, Irvine2 Vascular Lab, G D'Annunzio University
and San Valentino Vascular Screening Project (Pe), Faculty of Motory Sciences,
L'Aquila University, Italy. cardres@pe.abol.it

The aim of this study was to evaluate the occurrence of deep venous thrombosis
(DVT) and superficial vein thrombosis (SVT) and its prophylaxis with an oral
anti-edema and antithrombotic agent (Pycnogenol, Horphag, Research Management
SA, Geneva, Switzerland) in long-haul flights, in subjects at moderate to
high-risk of DVT and SVT. The study pre-included 244 pre-selected subjects; 211
were included (33 were excluded for several reasons due to logistic problems)
and 198 completed the study; 13 subjects were lost for follow-up at the end of
the flight, all for non-medical problems (i.e., for difficult connections). All
subjects were scanned within 90 minutes before the flight and within 2 hours
after disembarking. Subjects were supplemented with 100 mg Pycnogenol per
capsule. Treatment subjects received two capsules between 2 and 3 hours before
flights with 250 mL of water; two capsules were taken 6 hours later with 250 mL
of water and one capsule the next day. The control group received comparable
placebo at the same intervals. The flight duration was on average 8 hours and 15
minutes (SD 55 min) (range, 7.45-12.33). In the control group there were five
thrombotic events (one DVT and four superficial thromboses) while only
nonthrombotic, localized phlebitis was observed in the Pycnogenol group (5.15%
vs. no events; p<0.025). The ITT (intention to treat) analysis detects 13
failures in the control group (eight lost to follow up + five thrombotic events)
of 105 subjects (12.4%) vs. five failures (4.7%; all lost, no thrombotic events)
in the treatment group (p<0.025). No unwanted effects were observed.

In conclusion, this study indicates that Pycnogenol treatment was effective in
decreasing the number of thrombotic events (DVT and SVT) in moderate-to-high
risk subjects, during long-haul flights.

PMID: 15497024 [PubMed - indexed for MEDLINE]

1: Angiology. 2006 Oct-Nov;57(5):569-76.

Rapid relief of signs/symptoms in chronic venous microangiopathy with
pycnogenol: a prospective, controlled study.

Cesarone MR, Belcaro G, Rohdewald P, Pellegrini L, Ledda A, Vinciguerra G, Ricci
A, Gizzi G, Ippolito E, Fano F, Dugall M, Acerbi G, Cacchio M, Di Renzo A, Hosoi
M, Stuard S, Corsi M.

Irvine2 Vascular Lab and Physiology, Department of Biomedical Sciences, G
'Annunzio, Chieti-Pescara University, San Valentino Vascular Screening Project,
Faculty of Motory Sciences, L'Aquila University, Italy.

The aim of this study was to investigate the clinical efficacy of oral
Pycnogenol (Horphag Research Ltd, UK) in patients with severe chronic venous
insufficiency. Patients with severe venous hypertension (chronic venous
insufficiency, ankle swelling) and history of venous ulcerations were treated
with Pycnogenol. Patients received oral Pycnogenol (50 mg capsules, 3 times
daily for a total of 150 mg daily) for 8 weeks. A group of 21 patients was
included in the treatment group and 18 equivalent patients were observed as
controls (no treatment during the observation period). All 21 patients (age 53
years; range, 42-60 years; M:F=11:10) in the treatment group completed the
8-week study. Also the 18 controls completed the follow-up period. There were no
drop-outs. The average ambulatory venous pressure was 59.3 (SD 7.2; range 50-68)
with a refilling time shorter than 10 seconds (average 7.6; SD 3). There were no
differences in ambulatory venous pressure or refilling time between the
treatment and control patients. The duration of the disease-from the first
signs/symptoms-was on average 5.7 years (SD 2.1). At 4 and 8 weeks, in all
Pycnogenol-treated subjects, microcirculatory and clinical evaluations indicated
a progressive decrease in skin flux, indicating an improvement in the level of
microangiopathy; a significant decrease in capillary filtration; a significant
improvement in the symptomatic score; and a reduction in edema. There were no
visible effects in controls.

In conclusion, this study confirms the fast
clinical efficacy of Pycnogenol in patients with chronic venous insufficiency
and venous microangiopathy. The study indicates the significant clinical role of
Pycnogenol in the management, treatment and control of this common clinical
problem. The treatment may be also useful to prevent ulcerations by controlling
the level of venous microangiopathy.


PMID: 17067979 [PubMed - indexed for MEDLINE]

Last edited by jackD; 10-27-2008 at 02:50 PM.
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