herbals

[cheerleader]

WW...sorry it's been so rough. Jimmy's right about echinacea. We stay clear of that. How about boosting the supplements we know won't hurt your MS?
zinc, vitamin D, vitamin C, omega 3- take a bit more than your normal dosage just for a week or so.
Jeff uses a zinc nasal and throat spray (Throat Rescue) at the first sign of a cough or stuffy nose. It gets the zinc right to the source, to kill any infection. He's also become an OCD hand washer, too!
Being a new Mom is exhausting, even without MS. Make sure you're getting enough rest. And take care of yourself, too. Have a wonderful Christmas with your new son!
AC

[Wonderfulworld]

Thanks Loobie, Jimmy and Cheer.
Know what you mean about not feeling good as a baseline...makes it all the more annoying when you're laid low with too many normal bugs....having MS means we spend more than normal trying to get better anyway.

Jimmy I get 15mg of zinc in the multivit. Never had zinc levels tested. Perhaps with the Vit D/cal/mag at a separate time I need to also increase zinc a bit. I will ask my doc to add it to the tests in January. I do eat red meat about 2-3 times a week.

Cheer that's good advice about boosting the supplements I know I can safely use. Will try that. The zinc spray sounds good, I'm sure I can get something similar here in Ireland. Oh, stop about the OCD handwashing!!! - I have ended up with exzema on my hands from that after my son was born!! No more ocd handwashing! - but I think that each time son goes to his playgroup he picks up a new bug and then with sloppy toddler kisses I'm bound to catch it too!:D I'm glad my hubbie is off work from Wed so I plan some more rest than usual.

Happy Christmas to all of you. You have all been such a help and support this year. Really feel we are getting somewhere with our regimes and the endothelial/venous research....hopefully 2009 will prove a good year for MS'ers.
x

[Miss_Feisty]

Wonderfulworld:
Sorry to hear you feel sick and tired of being sick and tired.

Nothing beats an absurd amount of rest and sleep to heal. It seems to be completely under-rated. Have someone help with kids and spend a day or two in bed.

I run from echinachea even at the store, when it's sitting innocently on the shelf. haha.

Take care, hope you feel better soon.

[NHE]

When I get a cold, I try to double up on my fruit consumption and that seems to help get me feeling better in a few days.

NHE

[DIM]

My wife used to take echinacea and ginseng when sic with no adverse effects at least for short periods.
But as mentioned above you can boost other supplements that we all know help naturally in cold and flu seasons, say:
Vitamin C (200-250mg doses every 2-3 hours), vitamin D (4000IU/day), zinc (at least 50mg dose/day when sic), omega-3 (at least 3gr/day, they increase the anti-inflammatory prostaglandins 1 & 3), pycnogenol, E-tocotrienol (anti-epstein barr form of vitamin E), lauricidin (monolaurinic acid from coconut oil that kills most viruses and bacterials), inosine (anti viral properties), DHEA, NAC (anti-chlamydia penuomiae), polygala (herb extract, anti-chlamydia penuomiae) and many others I can't remember now.
My wife takes only supplements and although she has had last year two colds they lasted less than two days when before she used to stay in bed for more than 4-5 days.
By the way does you old symptoms re-appeared with colds anf flus?

[RuSmolikova]

The best precaution for me is amantadin.
http://www.mult-sclerosis.org/Amantadine.html
I have been using it in a winter. And haven´t had cold/viruses...

[Jaded]

Hi ww

I am not adding much bit just wanted to say what works for me!

I boost my vit c intake when I feel lousy. I take 1000g at a time, and a few of those in a day plus some zinc seems to help. I have fought off colds although have felt pretty tired for a few days at a time!!!!!

I hope you feel better soon.

J

[jimmylegs]

hey there hope the zinc test clears that question up for you!

i agree with DIM 50mg would be the therapeutic dose if the result comes back suboptimal. esp in light of the frequent illness that sounds so annoying.

Jimmy I get 15mg of zinc in the multivit. Never had zinc levels tested. Perhaps with the Vit D/cal/mag at a separate time I need to also increase zinc a bit. I will ask my doc to add it to the tests in January. I do eat red meat about 2-3 times a week.

[DIM]

Jimmy my wife took the first half of last year 25mg Zinc daily and the other half 50mg and all of her tests came exactly at the middle of normal levels!

[jimmylegs]

that's good dim, you want to be at the top of that pesky bell curve if that's where the healthy controls are!

i think i had too many days where i chucked in 100mg zinc and that's why i came back high on my second zn test.

[Sandrine]

When I get a cold, I eat ginger (e.g. soup with carrots and ginger) or that pickled ginger (japanese food store).

Get will soon!

Sandrine

[gibbledygook]

I've been taking quite a lot of these sprouts tablets recently and I wonder if that's why I'm feeling quite a bit better...?

1: J Neurosci. 2007 Sep 19;27(38):10240-8. Links
Enhancing expression of Nrf2-driven genes protects the blood brain barrier after brain injury.Zhao J, Moore AN, Redell JB, Dash PK.
The Vivian L. Smith Center for Neurologic Research and Department of Neurobiology and Anatomy, The University of Texas Medical School, Houston, Texas 77225, USA.

The integrity of the blood-brain barrier (BBB) is critical for normal brain function, and its compromise contributes to the pathophysiology of a number of CNS diseases and injuries. Using a rodent model of brain injury, the present study examines the pathophysiology of BBB disruption. Western blot and immunohistochemical analyses indicate that brain injury causes a loss of capillary endothelial cells and tight junction proteins, two critical components of the BBB. Activation of the transcription factor NF-E2-related factor-2 (Nrf2) by sulforaphane, a naturally occurring compound present in high levels in cruciferous vegetables, significantly increased the expression of endogenous cytoprotective genes in brain tissue and microvessels as indicated by real-time PCR analysis. Postinjury administration of sulforaphane reduced the loss of endothelial cell markers and tight junction proteins and preserved BBB function. These protective effects were dependent on the activity of Nrf2. Injured rats pretreated with decoy oligonucleotides containing the binding site of Nrf2, and mice lacking the nrf2 gene, did not benefit from sulforaphane administration. These findings indicate a potential therapeutic usefulness for Nrf2-activating molecules to improve the function of the neurovascular unit after injury.

PMID: 17881530 [PubMed - indexed for MEDLINE]

link

1: Mol Nutr Food Res. 2008 Jun;52(6):692-700. Links
The diet-derived sulforaphane inhibits matrix metalloproteinase-9-activated human brain microvascular endothelial cell migration and tubulogenesis.Annabi B, Rojas-Sutterlin S, Laroche M, Lachambre MP, Moumdjian R, Béliveau R.
Laboratoire d'Oncologie Moléculaire, Département de Chimie, Centre BIOMED, Université du Québec à Montréal, Quebec, Canada.

Human brain microvascular endothelial cells (HBMECs) play an essential role as structural and functional components of the blood-brain barrier (BBB). While disruption of the BBB by the brain tumor-secreted matrix metalloproteinase-9 (MMP-9) favors tumor invasion, the role and regulation of MMP-9 secretion by HBMEC themselves in response to carcinogens or brain tumor-derived growth factors has received little attention. Our study delineates a unique brain endothelial phenotype in that MMP-9 secretion is increased upon phorbol 12-myristate 13-acetate (PMA) treatment of HBMEC. Sulforaphane (SFN), an isothiocyanate present in broccoli which exhibits chemopreventive properties, selectively inhibited the secretion of MMP-9 but not that of MMP-2. The decrease in MMP-9 gene expression correlated with a decrease in the expression of the mRNA stabilizing factor HuR protein triggered by SFN. PMA-induced HBMEC migration was also antagonized by SFN. Silencing of the MMP-9 gene inhibited PMA-induced MMP-9 secretion, cell migration, and in vitro tubulogenesis on Matrigel. While SFN inhibited the chemoattractive abilities of brain tumor-derived growth factors, it failed to inhibit PMA-induced tubulogenesis. Our data are indicative of a selective role for SFN to inhibit MMP-9-activated, but not basal, HBMEC migration, and tubulogenesis whose actions could add to SFN's antitumor properties.

PMID: 18435488 [PubMed - indexed for MEDLINE]

link

sulforaphane is a histone deacetylase inhibitor which is good as it looks like they inhibit osteoporosis:

1: J Bone Miner Res. 2005 Dec;20(12):2254-63. Epub 2005 Aug 8. Links
Histone deacetylase inhibitors promote osteoblast maturation.Schroeder TM, Westendorf JJ.
Graduate Program in Biochemistry, Molecular Biology and Biophysics, University of Minnesota, Minneapolis, USA.

HDIs are potential therapeutic agents for cancer and neurological diseases because of their abilities to alter gene expression, induce growth arrest or apoptosis of tumors cells, and stimulate differentiation. In this report, we show that several HDIs promote osteoblast maturation in vitro and in calvarial organ cultures. INTRODUCTION: Histone deacetylase inhibitors (HDIs) are currently in phase I and II clinical trials as anticancer agents. Some HDIs are also commonly prescribed treatments for epilepsy and bipolar disorders. Although administered systemically, the effects of HDIs on osteoblasts and bone formation have not been extensively examined. In this study, we investigated the effect of histone deacetylase inhibition on osteoblast proliferation and differentiation. MATERIALS AND METHODS: MC3T3-E1 cells, calvarial-derived primary osteoblasts, and calvarial organ cultures were treated with various commercially available HDIs (trichostatin A [TSA], sodium butyrate [NaB], valproic acid [VPA], or MS-275). The effects of these inhibitors on cell proliferation, viability, cell cycle progression, Runx2 transcriptional activity, alkaline phosphatase production, and matrix mineralization were determined. Expression levels of osteoblast maturation genes, type I collagen, osteopontin, bone sialoprotein, and osteocalcin in response to TSA were measured by quantitative PCR. RESULTS: Concentrations of HDIs that caused hyperacetylation of histone H3 induced transient increases in osteoblast proliferation and viability but did not alter cell cycle profiles. These concentrations of HDIs also increased the transcriptional activity of Runx2. TSA accelerated alkaline phosphatase production in MC3T3-E1 cells and calvarial organ cultures. In addition, TSA accelerated matrix mineralization and the expression of osteoblast genes, type I collagen, osteopontin, bone sialoprotein, and osteocalcin in MC3T3-E1 cells. CONCLUSIONS: These studies show that histone deacetylase activity regulates osteoblast differentiation and bone formation at least in part by enhancing Runx2-dependent transcriptional activation. Therefore, HDIs are a potentially new class of bone anabolic agents that may be useful in the treatment of diseases that are associated with bone loss such as osteoporosis and cancer.

PMID: 16294278 [PubMed - indexed for

link

[gibbledygook]

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

Erratum in:
Angiology. 2008 Jun-Jul;59(3):385.
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]

link

[cheerleader]

Maritime Pine Bark!!!
Pretty cool stuff, huh Alex?
Dmitris has been mentioning this on many threads...so I finally added it to the cocktail last month. Will have to add it to the endothelial paper, too.
Thanks for the research.
AC

[DIM]

Pycnogenol is also iron chelator and stimulates BBB although it works as vasolidator!