herbals

[gibbledygook]

I have been taking salvia miltiorrhiza since August 2008. I initially started with monster high doses which seemed fantastic on the legs. Now, some 5 months later I find that even the smallest doses have a very pronounced effect.

I think that the blood vessels with their stenoses and distensions are now as dilated as they ought to be and only the tiniest amounts of salvia/ginkgo are required.

I shall therefore only have my salvia and ginkgo containing chinese tea in the morning and evening.

[gibbledygook]

Now this aquaporin4 is mentioned in relation to rhubarb and maybe important in MS since Asian populations with neuromyelitis optica with the anti-aquaporin 4 antibody have worse disease than those without:

1: J Neurosci Res. 2005 Nov 15;82(4):499-506. Links
Sulforaphane enhances aquaporin-4 expression and decreases cerebral edema following traumatic brain injury.Zhao J, Moore AN, Clifton GL, Dash PK.
The Vivian L. Smith Center for Neurologic Research and Department of Neurobiology and Anatomy, The University of Texas Medical School, Houston, 77225, USA.

Brain edema, the infiltration and accumulation of excess fluid causing an increase in brain tissue volume, often leads to a rise in intracranial pressure and is a key contributor to the morbidity and mortality associated with traumatic brain injury (TBI). The cellular and molecular mechanisms contributing to the development/resolution of TBI-associated brain edema are poorly understood. Aquaporin-4 (AQP4) water channel is expressed at high levels in brain astrocytes, and the bidirectional transport of water through these channels is critical for the maintenance of brain water homeostasis. By using a rodent injury model, we show that TBI decreased AQP4 level in the injury core and modestly increased it in the penumbra region surrounding the core. Postinjury administration of sulforaphane (SUL), an isothiocyanate present in abundance in cruciferous vegetables such as broccoli, attenuated AQP4 loss in the injury core and further increased AQP4 levels in the penumbra region compared with injured animals receiving vehicle. These increases in AQP4 levels were accompanied by a significant reduction in brain edema (assessed by percentage water content) at 3 days postinjury. These findings suggest that the reduction of brain edema in response to SUL administration could be due, in part, to water clearance by AQP4 from the injured brain. Copyright 2005 Wiley-Liss, Inc.

PMID: 16211562 [PubMed - indexed for MEDLINE]

link

1: Ann N Y Acad Sci. 2008 Oct;1142:58-71. Links
Neuromyelitis optica and asian phenotype of multiple sclerosis.Kira J.
Department of Neurology, Neurological Institute, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan. kira@neuro.med.kyushu-u.ac.jp

Multiple sclerosis (MS) is a demyelinating disease of the central nervous system (CNS), whereas neuromyelitis optica (NMO) is an inflammatory disease of the CNS selectively affecting the optic nerves and spinal cord. The pathological hallmark in MS is sharply demarcated demyelinating plaque with axons relatively preserved, whereas in NMO both axons and myelin are involved, resulting in necrotic cavitation. The nosological position of NMO has long been a matter of debate. In Asians, MS is rare; however, when it appears, the selective but severe involvement of the optic nerves and spinal cord is characteristic. This form, termed opticospinal MS (OSMS), has similar features to those of the relapsing form of NMO in Western populations. Recent discovery of a specific immunoglobulin G (IgG) against NMO, designated NMO-IgG, suggests that NMO is a distinct disease entity with a fundamentally different etiology from that of MS. Because NMO-IgG has been reported to be present in about 50%-60% of OSMS patients with longitudinally extensive spinal cord lesions (LESCLs), OSMS in Asians has been suggested to be the same entity as NMO. About half of the patients with the anti-aquaporin 4 (AQP4) antibody demonstrate brain lesions fulfilling the Barkhof criteria, whereas OSMS patients without the anti-AQP4 antibody show significantly fewer brain lesions. These findings indicate that the mechanism of LESCLs in Asians is heterogeneous, both related and unrelated to anti-AQP4 antibody, and that the disease condition with anti-AQP4 antibody does not completely overlap OSMS in Asians. This review discusses possible mechanisms for OSMS and anti-AQP4 autoimmune syndrome of the CNS.

PMID: 18990121 [PubMed - indexed for MEDLINE]

link

1: Swiss Med Wkly. 2008 Nov 29;138(47-48):692-707. Links
Autoantibodies in inflammatory demyelinating diseases of the central nervous system.Lalive P.
Department of Clinical Neurosciences, Division of Neurology, Geneva University Hospital, Geneva, Switzerland. patrice.lalive@hcuge.ch.

The determination of disease-specific autoantibodies (Abs) is a challenge in any autoimmune disease. The significance of Abs detected in inflammatory demyelinating diseases (IDD) of the central nervous system (CNS), such as multiple sclerosis (MS), is still unclear. Histopathological reports have demonstrated that a humoral (Abs)-mediated pattern of demyelination is detected in >50% of MS patients and is consistently associated with active demyelination. The observation that these patients specifically respond to plasmapheresis reinforces the hypothesis of a specific humoral MS subtype. One of the most intensively studied antigen targets in MS is a glycoprotein of the myelin sheath called the Myelin Oligodendrocyte Glycoprotein (MOG). Recent advances have shown that epitope specificity of MOG is crucial in terms of specificity of the Ab response. Several other auto-Abs, including anti-myelin, oligodendrocyte and neuronal Abs have been studied in MS. These auto-Abs may have pathogenic or protective properties, but could also have no functional role. Recently, the demonstration of a highly specific auto-Ab in an IDD of the CNS called neuromyelitis optica (NMO), directed against the aquaporin-4 (AQP-4) located at the blood brain barrier (BBB), has allowed a refinement of the diagnostic criteria of NMO and classification of this disease as an autoimmune channelopathy. These recent advances have reinforced the interest in tracking the role of the humoral response in the different IDD of the CNS.

PMID: 18951202 [PubMed - in process]

link

[jimmylegs]

read very briefly about sulforaphane enzyme and cancer-fighting in broc sprouts.

broccoli (and sprouts) tons of good stuff for ms-ers. including zinc lol
sprouts, compared to full grown broc, are higher in certain things (like the enzyme above) and lower in others.

about the sprout (not referenced)
"...they are sources of plant estrogens, similar to human estrogen, and so are helpful in cases of PMS, menopause, hot flashes and fibrocystic disease. Nutrient dense, they are rich sources of vitamins A, B, C, E and K, anti-oxidants, the minerals calcium, iron, magnesium, phosphorus, potassium and zinc. Also carotene, chlorophyll, amino acids, trace elements and antioxidants. Broccoli sprouts contain as much as 35% protein."

[gibbledygook]

Wow! That's almost bean-like! I think the sulforaphane is having an anti-inflammatory effect as it is inducing the enzyme Nq01 which is found a lot in the lesions and is useful for mopping up nasty diesel particles.

Also generally good for aging:

1: Nutr Neurosci. 2005 Apr;8(2):101-10. Links
Dietary approach to decrease aging-related CNS inflammation.Noyan-Ashraf MH, Sadeghinejad Z, Juurlink BH.
Department of Anatomy and Cell Biology, College of Medicine, University of Saskatchewan, 107 Wiggins Road, Saskatoon, SK, Canada S7N 5E5.

We demonstrate that the spontaneously hypertensive rat stroke-prone rat (SHRsp) undergoes premature aging of the CNS compared to the related normotensive Wistar Kyoto rat (WKY) as demonstrated by presence of activated microglia/macrophages, increased expression of inducible nitric oxide synthase and increased astrogliosis. We tested the hypothesis that dietary intake of phase 2 protein inducers would decrease these aging-associated degenerative changes. The source of dietary phase 2 protein inducers was dried broccoli sprouts of a cultivar containing high amounts of glucoraphanin that gives rise to phase 2 protein-inducing isothiocyanate sulforaphane. This diet significantly decreased the aging-related degenerative changes in the SHRsp CNS. We conclude that modest changes in diet may have profound effects on the aging CNS.

PMID: 16053242 [PubMed - indexed for MEDLINE]

link

[gibbledygook]

sulforaphane and pro-apoptic gene regulation and MS:

1: Cancer Res. 2005 Mar 1;65(5):2035-43. Links
Bax and Bak are required for apoptosis induction by sulforaphane, a cruciferous vegetable-derived cancer chemopreventive agent.Choi S, Singh SV.
Department of Pharmacology and University of Pittsburgh Cancer Institute, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania 15213, USA.

Sulforaphane, a constituent of many edible cruciferous vegetables, including broccoli, effectively suppresses proliferation of cancer cells in culture and in vivo by causing apoptosis induction, but the sequence of events leading to cell death is poorly defined. Here, we show that multidomain proapoptotic Bcl-2 family members Bax and Bak play a critical role in apoptosis induction by sulforaphane. This conclusion is based on the following observations: (a) sulforaphane treatment caused a dose- and time-dependent increase in the protein levels of both Bax and Bak and conformational change and mitochondrial translocation of Bax in SV40-transformed mouse embryonic fibroblasts (MEF) derived from wild-type mice to trigger cytosolic release of apoptogenic molecules (cytochrome c and Smac/DIABLO), activation of caspase-9 and caspase-3, and ultimately cell death; (b) MEFs derived from Bax or Bak knockout mice resisted cell death by sulforaphane, and (c) MEFs derived from Bax and Bak double knockout mice exhibited even greater protection against sulforaphane-induced cytochrome c release, caspase activation, and apoptosis compared with wild-type or single knockout cells. Interestingly, sulforaphane treatment also caused a dose- and time-dependent increase in the protein level of Apaf-1 in wild-type, Bax-/-, and Bak-/- MEFs but not in double knockout, suggesting that Bax and Bak might regulate sulforaphane-mediated induction of Apaf-1 protein. A marked decline in the protein level of X-linked inhibitor of apoptosis on treatment with sulforaphane was also observed. Thus, it is reasonable to postulate that sulforaphane-induced apoptosis is amplified by a decrease in X-linked inhibitor of apoptosis level, which functions to block cell death by inhibiting activities of caspases. In conclusion, the results of the present study indicate that Bax and Bak proteins play a critical role in initiation of cell death by sulforaphane.

PMID: 15753404 [PubMed - indexed for MEDLINE]

link

1: Ann N Y Acad Sci. 2007 Jun;1107:155-67. Links
Impaired expression of peripheral blood apoptotic-related gene transcripts in acute multiple sclerosis relapse.Achiron A, Feldman A, Mandel M, Gurevich M.
Multiple Sclerosis Center, Sheba Medical Center, Tel-Hashomer, 52621, Israel. achiron@post.tau.ac.il

Differential expression of apoptotic genes may influence the susceptibility of activated lymphocytes to expand and induce acute relapse and persistent inflammation in patients with relapsing-remitting multiple sclerosis (RRMS). The exact relationship between alterations in apoptotic-related gene expression and clinical disease activity has not been broadly evaluated. In this study we studied peripheral blood mononuclear cells (PBMCs) expression of pro- and antiapoptotic genes in RRMS patients during acute relapse in comparison to patients in remission. Using cDNA Affymetrix microarrays platform (U133A2 microarrays) we analyzed the gene expression profile of PBMC derived from 22 RRMS patients in acute relapse (15 females, mean age 34.6 +/- 1.8 years, disease duration 5.6 +/- 0.8 years) in comparison to 20 sex- and age-matched RRMS patients in remission. One thousand five hundred seventy-eight gene transcripts significantly differentiated acute multiple sclerosis (MS) relapse from remission. This characteristic gene expression signature was enriched by an apoptotic-related pathway. The 1578 gene transcripts that significantly differentiated acute relapse from remission were enriched by 55 apoptotic-related genes in that reflected different operating pathways during the acute phase of the disease. These genes mainly involved the caspase-dependent pathway and included overexpression of the negative regulator of FAS-induced apoptosis (TOSO) and the BCL2 antiapoptotic family members (BCL2, BCL2 AA) as well as downexpression of proapoptotic genes like BAX, apoptotic protease-activating factor 1 (APAF1) and caspases 1, 2, 8, 9. and 10. An additional group of antiapoptotic genes related to T cell receptor-mediated apoptosis was also found to be overexpressed in acute relapse and included TCR-binding CD3E antigen, antiapoptotic serine threonin kinase (AKT), and NF kappa B-associated genes like reticuloendotheliosis viral oncogene homolog A (RELA) and human T cell leukemia virus type I-binding protein (Tax1BP) known to inhibit tumor necrosis factor (TNF)-induced apoptosis. Our findings demonstrate impaired apoptotic mechanisms in peripheral lymphocytes from RRMS patients during acute relapse. This suggests that the inflammatory process in active disease is targeted by inhibition of proapoptotic and repression of antiapoptotic genes that allow prolonged abnormal immune responses.

PMID: 17804543 [PubMed - indexed for MEDLINE]

link[/color

1: J Neurol. 2006 Feb;253(2):231-6. Epub 2005 Sep 30. Links
Glatiramer acetate induces pro-apoptotic mechanisms involving Bcl-2, Bax and Cyt-c in peripheral lymphocytes from multiple sclerosis patients.Ruggieri M, Avolio C, Scacco S, Pica C, Lia A, Zimatore GB, Papa S, Livrea P, Trojano M.
Dept. of Neurological and Psychiatric Sciences, University of Bari, Policlinico, Piazza Giulio Cesare, Italy. mruggieri@neurol.uniba.it

Apoptotic deletion of autoreactive T-cells is defective in patients with multiple sclerosis (MS). Glatiramer acetate (GA) treatment seems to restore apoptosis of detrimental T-cells. We analyzed the mitochondria membrane pro- (Bax) and anti-apoptotic (Bcl- 2) and cytosolic pro-apoptotic (Cyt-c, APAF-1) proteins expression in peripheral lymphocytes from relapsing-remitting (RR) MS patients during GA treatment. Blood samples were collected from 8 healthy controls (HCs) and from 8 RR MS patients prior to and every three months during the 9 months of GA treatment. Peripheral blood mononuclear cells (PBMNCs) Bcl-2, Bax, Cyt-c and APAF-1 were quantified by western blot followed by densitometric scanning and Bax/Bcl-2, cytosolic Cyt-c/Bcl-2 and APAF-1/Bcl-2 ratios were calculated. T-cells were in vitro tested for oxygen consumption by a respirometric analysis. Bax/Bcl-2, cytosolic Cyt-c/Bcl-2 and APAF-1/Bcl-2 ratios in untreated MS patients were significantly (p < 0.05) lower than in HCs. Bax/Bcl-2 ratio increased (p = 0.03) and Cyt-c/Bcl-2 ratio showed a trend to increase during the 9 months of GA treatment in MS patients. A reduction of 58% and 59% in oxygen consumption by PBMNCs was evident after GA treatment in vitro or when GA treated patients' cells were compared with those from HCs, respectively. Our findings suggest that GA exerts a regulatory effect on peripheral T lymphocytes through pro-apoptosis mechanisms involving mitochondria and cytosolic proteins.

PMID: 16184340 [PubMed - indexed for MEDLINE]

link

1: J Neuroimmunol. 2003 Jan;134(1-2):158-65. Links
Expression ratios of the Bcl-2 family proteins and disease activity in multiple sclerosis.Sharief MK, Matthews H, Noori MA.
Department of Neuroimmunology, Guy's, King's and St. Thomas' School of Medicine, Guy's Hospital, London SE1 1UL, UK. m.k.sharief@kcl.ac.uk

There is emerging evidence that failure of apoptosis (programmed cell death) of potentially pathogenic T lymphocytes may be involved in the pathogenesis of multiple sclerosis (MS). The commitment of T lymphocytes to die is partly regulated by the Bcl-2 family proteins, which act as a checkpoint upstream of mitochondrial dysfunction. These proteins include the death antagonists Bcl-2 and Bcl-X(L), and death agonists Bax and Bad. Recent studies suggest that altered expression of Bcl-2 family proteins in T lymphocytes is involved in promoting cellular resistance to apoptosis in patients with MS. However, the relationship between these alterations in Bcl-2 proteins expression and clinical disease activity has not yet been evaluated. In this study, we analyzed the expression ratios of pro- to anti-apoptosis Bcl-2 family proteins in patients with clinically active MS and compared results to corresponding ratios in patients with stable MS and relevant control groups. We observed a significant reduction in the expression ratios of pro- to anti-apoptosis Bcl-2 members in peripheral lymphocytes from patients with active MS when compared to corresponding ratios in patients with stable MS or other controls. This imbalance in the expression ratios of pro- and anti-apoptosis proteins was functionally active in reducing cellular susceptibility to apoptosis in active MS. It also correlated with clinical features of disease activity, such as the number of gadolinium-enhancing MRI lesions and clinical relapses. Our findings indicate that dysregulated expression of Bcl-2 family proteins in peripheral lymphocytes is a feature of clinically active multiple sclerosis.

PMID: 12507784 [PubMed - indexed for MEDLINE

link

[gibbledygook]

Maybe this is why I need less of the vasodilating salvia:

1: Proc Natl Acad Sci U S A. 2004 May 4;101(18):7094-9. Epub 2004 Apr 21. Links
Dietary approach to attenuate oxidative stress, hypertension, and inflammation in the cardiovascular system.Wu L, Noyan Ashraf MH, Facci M, Wang R, Paterson PG, Ferrie A, Juurlink BH.
Department of Anatomy and Cell Biology, College of Medicine, University of Saskatchewan, Saskatoon, SK, Canada S7N 5E5.

Imbalance between production and scavenging of superoxide anion results in hypertension by the inactivation of nitric oxide, and the increased oxidative stress from the resultant peroxynitrite that is produced promotes inflammatory processes such as atherosclerosis. Induction of phase 2 proteins promotes oxidant scavenging. We hypothesized that intake of dietary phase 2 protein inducers would ameliorate both hypertension and atherosclerotic changes in the spontaneously hypertensive stroke-prone rat. For 5 days/week for 14 weeks, we fed rats 200 mg/day of dried broccoli sprouts that contained glucoraphanin, which is metabolized into the phase 2 protein-inducer sulforaphane (Group A), sprouts in which most of the glucoraphanin was destroyed (Group B), or no sprouts (Group C). After 14 weeks of treatment, no significant differences were seen between rats in Groups B and C. Rats in Group A had significantly decreased oxidative stress in cardiovascular and kidney tissues, as shown by increased glutathione (GSH) content and decreased oxidized GSH, decreased protein nitrosylation, as well as increased GSH reductase and GSH peroxidase activities. Decreased oxidative stress correlated with better endothelial-dependent relaxation of the aorta and significantly lower (20 mm Hg) blood pressure. Tissues from Groups B and C had considerable numbers of infiltrating activated macrophages, indicative of inflammation, whereas animals in Group A had few detectable infiltrating macrophages. There is interest in dietary phase 2 protein inducers as means of reducing cancer incidence. We conclude that a diet containing phase 2 protein inducers also reduces the risk of developing cardiovascular problems of hypertension and atherosclerosis.

PMID: 15103025 [PubMed - indexed for MEDLINE]
PMCID: PMC406471

link

[gainsbourg]

The lady in my local health food shop persuaded me to purchase an alternative pine bark extract - Enzogenol. The developers of Enzogenol seem to be really hot with researching their product and have carried out dozens of studies. Some of the results are breathtaking and I would say it could turn out to be the best antioxidant on the planet. Unlike Pycnogenol it is extracted using pure water instead of solvents that leave residues.

Plus its cheaper than its rival!

Take a look at the research. They claim it even reverses the DNA damage of oxidative stress:

http://www.mln.ca/en/pdfs/enzo_complete.pdf

http://www.enzogenol.com/Default.aspx?page=1063



gains

[gibbledygook]

broccoli kills off the T cells:

1: Cell Mol Life Sci. 2002 Nov;59(11):2004-12. Links
Cyclin D3 and p53 mediate sulforaphane-induced cell cycle delay and apoptosis in non-transformed human T lymphocytes.Fimognari C, Nüsse M, Berti F, Iori R, Cantelli-Forti G, Hrelia P.
Department of Pharmacology, University of Bologna, Via Irnerio 48, 40126 Bologna, Italy.

Despite experimental evidence that sulforaphane can exert chemopreventive effects, whether these effects are specific for neoplastic cells is not known. Following our previous demonstration that sulforaphane induces cell cycle arrest and apoptosis in human T lymphoblastoid Jurkat leukemia cells and increases p53 and bax protein expression, we tested sulforaphane on non-transformed phytohemagglutinin-stimulated human lymphocytes. Here, we demonstrate that sulforaphane arrested cell cycle progression in G, phase, through a decrease in the protein expression of cyclin D3. Moreover, sulforaphane induced apoptosis (and also necrosis), mediated by an increase in the expression of p53. These findings suggest that sulforaphane is a growth modulator for T cells. Our in vitro evidence that sulforaphane is active and even cytotoxic in normal as well as transformed lymphocytes raises important questions regarding its suitability for cancer chemoprevention.

PMID: 12530531 [PubMed - indexed for MEDLINE]

link

and here's something on p53 which sulforaphane increases. not sure if this is good or bad....

1: Ann Neurol. 2005 Oct;58(4):577-84. Links
Defective ATM-p53-mediated apoptotic pathway in multiple sclerosis.Deng X, Ljunggren-Rose A, Maas K, Sriram S.
Department of Neurology, Vanderbilt University Medical Center, Nashville, TN, USA. xinqing.deng@vanderbilt.edu

Defective elimination of autoreactive cells is thought to play a role in the development of autoimmune diseases including multiple sclerosis (MS). We examined the activation of the ATM-CHK2-p53 pathway in MS patients after subjecting their peripheral blood mononuclear cells to gamma-irradiation. We found that peripheral blood mononuclear cells from a subset of MS patients show resistance to cell death induced by irradiation. This defect is due to impaired constitutive expression and activation of ATM (ataxia telangiectasia mutated), resulting in impaired stabilization of p53. We predict that these fundamental defects likely alter the regulation of the immune population of cells in MS and may contribute to the development or progression of the disease.

PMID: 16178012 [PubMed - indexed for MEDLINE

link

[CureOrBust]

I gave this a go once, i didn't notice any effects.

[DIM]

From what I can see it only contains as extra quercetin and vitamin C, not a big deal!

[gainsbourg]

Hmm, interesting feedback. I decided to phone them and to my surprise they put me straight through to their top scientific guy, Matt Frevell. Obviously he is biased towards Enzogenol but told me that it contains a much broader spectrum of antioxidants and proanthocyanidins due to the fact that they extract everything with a specially developed technique that uses only water. He claims that when they process Pycnogenol significant antioxidants and flavanoids are inevitably lost because they still use chemical solvents.

I doubt there's much difference so I suppose maybe I'll try them both and compare results.

One thing is for sure - the human and animal experiments really impressed me for both products, but the Enzogenol studies used mega (240mg) doses compared to Pycnogenol. If such high doses are needed it would work out much more expensive.

gains

[CureOrBust]

In case I wasn't clear, when I said I have tried it, I meant Pycnogenol, not Enzogenol

[gibbledygook]

capsaicin good for the endothelium:

1: Regul Pept. 2008 Oct 9;150(1-3):66-72. Epub 2008 Jun 3. Links
Transient receptor potential vanilloid 1-mediated expression and secretion of endothelial cell-derived calcitonin gene-related peptide.Luo D, Zhang YW, Peng WJ, Peng J, Chen QQ, Li D, Deng HW, Li YJ.
Department of Pharmacology, School of Pharmaceutical Sciences, Central South University, Changsha, Hunan 410078, China. dan962307@yahoo.com

Calcitonin gene-related peptide (CGRP), the principal transmitter in sensory nerves, could also be expressed in vascular endothelium. Transient receptor potential vanilloid 1(TRPV1), which modulates the synthesis and release of CGRP in sensory nerves, is also present in endothelial cells. The present study tested whether TRPV1 modulates the release and synthesis of CGRP in endothelial cells, and evaluated the protective effect of endothelial cell-derived CGRP. Human umbilical vein endothelial cells (HUVECs) were treated with capsaicin or hyperthermia. The level of CGRP mRNA was detected by RT-PCR, and protein level was measured by radioimmunoassay. Endothelial cell injury was induced by lysophosphatidylcholine, and evaluated by cell viability and lactate dehydrogenase activity. HUVECs expressed CGRP, both alpha- and beta-subtype. Capsaicin increased the level of CGRP in the culture medium, and up-regulated the expression of CGRP in endothelial cells. Hyperthermia also increased the level of CGRP mRNA. These effects were abolished by capsazepine, a competitive antagonist of TRPV1. Capsaicin significantly attenuated the endothelial cell damage induced by LPC, which was prevented and aggravated by capsazepine or CGRP(8-37,) antagonist of CGRP receptor. These results indicate that TRPV1 also regulates the expression and secretion of endothelial cell-derived CGRP, which affords protective effects on endothelial cells.
PMID: 18584893 [PubMed - indexed for MEDLINE]

link

[gibbledygook]

broccoli downregulates the apoptosis inhibitory pathway and upregulates the apoptosis pathway:

bloody great for cancer. Has proved very good for my bladder control but not sure re anything else yet...

1: Biochem Pharmacol. 2002 Mar 15;63(6):1085-97. Links
Bcl-2 family-mediated apoptotic effects of 3,3'-diindolylmethane (DIM) in human breast cancer cells.Hong C, Firestone GL, Bjeldanes LF.
Department of Nutritional Sciences and Toxicology, University of California, Berkeley 94720-3200, USA.

3,3'-Diindolylmethane (DIM) is a major in vivo derivative of the putative anticancer agent indole-3-carbinol (I3C), which is present in vegetables of the Brassica genus. At concentrations above 10 microM, DIM inhibited DNA synthesis and cell proliferation in both estrogen receptor replete (MCF-7) and deficient (MDA-MB-231) human breast cancer cells in a concentration- and time-dependent manner. These antiproliferative effects were accompanied by characteristic indications of programmed cell death in both cell lines, including externalization of phosphatidylserine, chromatin condensation, and DNA fragmentation. Furthermore, Western and Northern blot analyses, as well as coimmunoprecipitation assays, revealed that in both MCF-7 and MDA-MB-231 cells, DIM treatment decreased total transcript and protein levels of the apoptosis inhibitory protein Bcl-2, and the amount of Bcl-2 bound to the pro-apoptotic protein Bax. DIM treatment also caused an increase in Bax protein levels, but did not affect the level of Bax that was bound to Bcl-2. As a functional test of the role of Bcl-2 down-regulation in the DIM-induced apoptotic response, ectopic expression of Bcl-2 in MCF-7 cells was shown to attenuate the apoptotic effect of DIM. These results demonstrate that DIM can induce apoptosis in breast cancer cells independent of estrogen receptor status by a process that is mediated by the modulated expression of the Bax/Bcl-2 family of apoptotic regulatory factors.

PMID: 11931841 [PubMed - indexed for MEDLINE]

link

[radeck]

I've been following this thread with some interest. Is there a strategy for how to move forward purchasing this fungus, and how to prepare it? I'm guessing that there is ample experience in Chinese medicine on what are safe doses. The tea form can't be worse than pill form, as it's fresher.

Most importantly, this would be a great backup in case the Fingolimod doesn't get approval by the FDA. It would also help those who lost health insurance because of their ailment to be able to access the drug without moving to Europe.