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Having pared the dosages of salvia and ginkgo right back I had noticed an increase in night leg pain and also night spasms. Yesterday I continued to take 2x 120mg gingko and 2 x 600mg salvia with 3 x 400mg curcumin and 10mg bioperine before breakfast, lunch, supper and last thing at night but for the night dose I added an extra dose of ginkgo 120mg. Within an hour the spasms and the pain were attenuated and I could feel the herbs coursing through the system!! It's like taking steroids! Woooeeeeeeeee!!!!! I am so pleased to have discovered all of this.

The other weird thing I have noticed. I used to bruise without apparent cause. On Tuesday I got very inebriated with an old friend. I drank one and a half bottles of red. By the time he left I could barely stand and at some point fell down onto the concrete floor in the kitchen badly hurting my knee and hand. Yet today, Saturday, I still have barely any bruising. This is the 2nd time I have fallen hard and have barely bruised. I'm sure that the salvia and ginkgo are the reason for this change.

Yesterday I again took 2 120mg of ginkgo, 2 600mg of salvia and 3 400mg of curcumin with 10mg of bioperine before breakfast, lunch, supper and last thing at night but I take an extra 120mg of ginkgo at breakfast and last thing at night. I had no spasms and barely any pain in bed. At 3am in the morning my right leg felt really amazingly smooth and not stiff. By 7am that had somewhat changed to the worse. So at 7am I take my herbs; 3x 120mg ginkgo, 2x 600mg salvia, 3x 400mg curcumin, 10mg bioperine. At 10am I walk rather briskly 400meters to and from the shop as it is cold. The post walk tingling in my left knee is quite prolonged this am. It's certainly not a series of constant improvements. However generally my walking is better, the stiffness is less, the bladder control and bowel control are significantly better and I haven't noticed any phosphenes in a while.

I have increased my dose of ginkgo to 3x 120mg before breakfast, lunch, supper and last thing at night with 2x 600mg salvia at the same time and 3x 400mg curcumin sometimes with 3x 600mg scutellaria. Yesterday was the first day which I had taken 3x 120mg ginkgo 4 times daily AND in the afternoon I also tried a combination pill called Veinfactors. This contains 1g diosmin, and an unstated 475mg combination of soluble citrus extract, citrus powder from lemon peel, citrus bioflavanoids, horse chestnut leaf, butcher's broom, venocin (contains 20% aescin from horsechestnut), centenillin (from gotu kola) and more butcher's broom. It was quite hard to determine how much to take as the instructions were just "take 3 capsules, preferably with meals". Is that 3 capsules daily or 3 every meal? At any rate, unlike the last 3 nights, I had bad night spasms which I felt was probably from too much veinfactors since I had taken 3 capsules at a late lunch and another 3 at an early supper. I wonder if perhaps diosmin is a bit strong for the MS vein. On the positive side there was NO burning sensation when I got into bed which is very unusual although of late increasingly common. I am a bit uncertain about the varicose vein treatments as the vasodilators, ginkgo and salvia are so great that I wonder if the horsechestnut etc might be too vasoconstrictive. I shall resume a pure ginkgo/salvia nights and then reintroduce horsechestnut and butcher's broom and hesperidin separately.

So last night (3/10/2008) I had barely any pain/burning in my left leg and only a tiny moment of spasms in the right leg after a day of 3x120mg ginkgo, 2x 600mg salvia and 3x400mg curcumin before breakfast, lunch, supper and last thing at night. I took no veinfactors. This morning at about 7am I took my herbal dose and about 40mins later I could feel the drugs coursing through my veins/capillaries and CHANGING the feeling in my legs. This is so exciting!!!! I can't believe I spent 4.5 years without these herbs. I can't believe that when I was first diagnosed 4.75 years ago one of the first things I did was to take herbs, including ginkgo and curcumin but I only took a tiny amount. Doooooooh! What a fool not to experiment then.
So the next part of the experiment will be the GRADUAL introduction of horse chestnut and butcher's broom. I'm getting married on Friday so I might wait till next week.

Will it be a landslide? Politics is almost as exciting as herbal remedies!!!!

1: Acta Pharmacol Sin. 2004 Jul;25(7):869-75.Links
Effects of sodium beta-aescin on expression of adhesion molecules and migration of neutrophils after middle cerebral artery occlusion in rats.Hu XM, Zhang Y, Zeng FD.
Institute of Clinical Pharmacology, Tongji Medical College of Huazhong University of Science and Technology, Wuhan 430030, China.

AIM: To investigate the effects of sodium beta-aescin on neutrophil migration and expression of adhesion molecules (ICAM-1 and E-selectin) after middle cerebral artery occlusion (MCAO) in rats. METHODS: Rats were pretreated with sodium beta-aescin for 7 d and then subjected to cerebral ischemia/reperfusion (I/R) injury induced by an MCAO. After a 2-h ischemia and a 24-h reperfusion, the infarct volume and neurological deficit were determined by the method of TTC staining and the Longa's score. The effect of sodium beta-aescin on the migration of neutrophils was evaluated by measuring the activity of myeloperoxidase (MPO) enzyme. The expressions of adhesion molecules were determined by immunohistochemistry and Western blot. RESULTS: Sodium beta-aescin significantly reduced the cerebral infarct volume and ameliorated the neurological deficit (P<0.05 or P<0.01). The MPO activity and the expressions of ICAM-1 and E-selectin in the vehicle-treated rats were increased significantly (P<0.01) after cerebral I/R. After treatment with sodium beta-aescin, the enzymatic activity of MPO and the expressions of these adhesion molecules were significantly reduced compared with the vehicle-treated group (P<0.05 or P<0.01). CONCLUSION: Sodium beta-aescin can attenuate brain injury, down-regulate the protein expressions of ICAM-1 and E-selectin, and reduce the migration of neutrophils after cerebral I/R.

PMID: 15210059 [PubMed - indexed for MEDLINE]

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1: Neurosci Lett. 2008 Oct 24;444(2):195-8. Epub 2008 Aug 15. Links
Elevated myeloperoxidase activity in white matter in multiple sclerosis.Gray E, Thomas TL, Betmouni S, Scolding N, Love S.
MS Laboratories, Burden Centre, University of Bristol Institute of Clinical Neurosciences, Frenchay Hospital, Bristol BS16 1JB, United Kingdom.

Recent studies have revealed extensive axonal damage in patients with progressive multiple sclerosis (MS). Axonal damage can be caused by a plethora of factors including the release of proteolytic enzymes and cytotoxic oxidants by activated immune cells and glia within the lesion. Macrophages and microglia are known to express myeloperoxidase (MPO) and generate reactive oxygen species during myelin phagocytosis in the white matter. In the present study we have measured MPO levels in post-mortem homogenates of demyelinated and non-demyelinated regions of white matter from nine patients with MS and seven controls, and assessed MPO immunoreactivity within MS brain. In homogenates of MS white matter, demyelination was associated with significantly elevated MPO activity when compared to controls. Immunohistochemistry showed MPO to be expressed mainly by macrophages within and adjacent to plaques. Demyelination in MS is associated with increased activity of MPO, suggesting that this production of reactive oxygen species may contribute to axonal injury within plaques.

PMID: 18723077 [PubMed - in process]

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1: Free Radic Biol Med. 2008 Sep 1;45(5):726-31. Epub 2008 Jun 3. Links
Microglia and myeloperoxidase: a deadly partnership in neurodegenerative disease.Lefkowitz DL, Lefkowitz SS.
School of Biological Sciences, Section of Molecular Genetics and Microbiology, University of Texas at Austin, 1 University Station A5000, Austin, TX 78712-0162, USA. sslefkowitz@yahoo.com

The role of inflammation in Alzheimer's disease, Parkinson's disease, and multiple sclerosis has recently come under increased scrutiny. Associated with these inflammatory responses are tumor necrosis factor-alpha (TNF-alpha) and reactive oxygen species (ROS), both believed to be derived from brain microglia. In addition to the above, the presence of myeloperoxidase (MPO) in these diseased brains has been reported by a number of investigators. However, the possible role of MPO and enzymatically inactive MPO (iMPO) as the "choreographers" of the destruction done by TNF-alpha and ROS is not generally recognized. Previously, our laboratory has reported that MPO/iMPO enhance macrophage generation of ROS and expression of proinflammatory cytokine genes as well as gene products. Recent studies in our laboratory indicate that the same response occurs with microglia. A paradigm is presented for the perpetuation of inflammation associated with neurodegenerative diseases. This model describes the unrecognized consequences of the stimulation of microglia by MPO or iMPO. Both MPO and iMPO and/or its receptor may represent new therapeutic targets for the treatment of these diseases.

PMID: 18554520 [PubMed - indexed for MEDLINE]

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1: Brain. 2008 Apr;131(Pt 4):1123-33. Epub 2008 Jan 29. Links
Myeloperoxidase-targeted imaging of active inflammatory lesions in murine experimental autoimmune encephalomyelitis.Chen JW, Breckwoldt MO, Aikawa E, Chiang G, Weissleder R.
Center for Systems Biology, Massachusetts General Hospital, Harvard Medical School, 5404 Building 149, 13th Street, Charlestown, MA 02129, USA. chenjo@helix.mgh.harvard.edu

Inflammatory demyelinating plaques are the pathologic hallmark of active multiple sclerosis and often precede clinical manifestations. Non-invasive early detection of active plaques would thus be crucial in establishing pre-symptomatic diagnosis and could lead to early preventive treatment strategies. Using murine experimental autoimmune encephalomyelitis as a model of multiple sclerosis, we demonstrate that a prototype paramagnetic myeloperoxidase (MPO) sensor can detect and confirm more, smaller, and earlier active inflammatory lesions in living mice by in vivo MRI. We show that MPO expression corresponded with areas of inflammatory cell infiltration and demyelination, and higher MPO activity as detected by MPO imaging, biochemical assays, and histopathological analyses correlated with increased clinical disease severity. Our findings present a potential new translational approach for specific non-invasive inflammatory plaque imaging. This approach could be used in longitudinal studies to identify active demyelinating plaques as well as to more accurately track disease course following treatment in clinical trials.

PMID: 18234693 [PubMed - indexed for MEDLINE]

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And butcher's broom:

1: Int Angiol. 1999 Dec;18(4):306-12.Links
Effect of Ruscus extract and hesperidin methylchalcone on hypoxia-induced activation of endothelial cells.Bouaziz N, Michiels C, Janssens D, Berna N, Eliaers F, Panconi E, Remacle J.
Laboratoire de Biochimie et Biologie Cellulaire--Facultés Universitaires Notre-Dame de la Paix--Namur, Belgium.

BACKGROUND: Ruscus aculeatus extract and the flavonoid hesperidin methylchalcone (HMC) are drugs used in the treatment of chronic venous insufficiency. METHODS: In the present study, we investigated their effects on the activation of endothelial cells by hypoxia, a condition which mimics venous blood stasis. RESULTS: We observed that Ruscus extract was able to inhibit the activation of endothelial cells by hypoxia: the decrease in ATP content, the activation of phospholipase A2 as well as the subsequent increase in neutrophil adherence with a maximal protection obtained at 50 microg/ml. HMC was also able to inhibit the hypoxia-induced decrease in ATP content. Furthermore, the effects of Ruscus extract and of HMC on this decrease seem to be additive. CONCLUSIONS: The biochemical mechanism evidenced in this work might explain some of the beneficial therapeutic effects of these products in the treatment of chronic venous insufficiency patients.

PMID: 10811519 [PubMed - indexed for MEDLINE]

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1: J Pharmacol Sci. 2008 Oct;108(2):198-205. Links
Possible Mechanism of the Anti-inflammatory Activity of Ruscogenin: Role of Intercellular Adhesion Molecule-1 and Nuclear Factor-kappaB.Huang YL, Kou JP, Ma L, Song JX, Yu BY.
Department of Complex Prescription of TCM, China Pharmaceutical University, China.

Ruscogenin (RUS), first isolated from Ruscus aculeatus, also a major steroidal sapogenin of traditional Chinese herb Radix Ophiopogon japonicus, has been found to exert significant anti-inflammatory and anti-thrombotic activities. Our previous studies suggested that ruscogenin remarkably inhibited adhesion of leukocytes to a human umbilical vein endothelial cell line (ECV304) injured by tumor necrosis factor-alpha (TNF-alpha) in a concentration-dependent manner. Yet the underlying mechanisms remain unclear. In this study, the in vivo effects of ruscogenin on leukocyte migration and celiac prostaglandin E(2) (PGE(2)) level induced by zymosan A were studied in mice. Furthermore, the effects of ruscogenin on TNF-alpha-induced intercellular adhesion molecule-1 (ICAM-1) expression and nuclear factor-kappaB (NF-kappaB) activation were also investigated under consideration of their key roles in leukocyte recruitment. The results showed that ruscogenin significantly suppressed zymosan A-evoked peritoneal total leukocyte migration in mice in a dose-dependent manner, while it had no obvious effect on PGE(2) content in peritoneal exudant. Ruscogenin also inhibited TNF-alpha-induced over expression of ICAM-1 both at the mRNA and protein levels and suppressed NF-kappaB activation considerably by decreasing NF-kappaB p65 translocation and DNA binding activity. These findings provide some new insights that may explain the possible molecular mechanism of ruscogenin and Radix Ophiopogon japonicus for the inhibition of endothelial responses to cytokines during inflammatory and vascular disorders.

PMID: 18946195 [PubMed - in process]

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Curiously myeloperoxidase seems to be upregulated and downregulated in Ms:

1: J Neurol Neurosurg Psychiatry. 2003 Jul;74(7):953-5. Links
Low leucocyte myeloperoxidase activity in patients with multiple sclerosis.Ramsaransing G, Teelken A, Prokopenko VM, Arutjunyan AV, De Keyser J.
Department of Neurology, Academisch Ziekenhuis Groningen, Groningen, Netherlands.

The gene for myeloperoxidase (MPO) has been implicated in multiple sclerosis (MS). By measuring H(2)O(2) dependent oxidation of 3,3'5,5'-tetramethylbenzidine with spectrophotometry the authors investigated MPO activity in peripheral blood leucocytes from 42 patients with MS (12 with secondary progressive MS, 17 with primary progressive MS, and 13 with relapsing remitting benign MS) and 32 healthy controls. Leucocyte MPO activity was significantly lower in patients with benign MS (mean (SEM) 0.086 (0.029) U/mg protein; p<0.01), secondary progressive MS (0.038 (0.009) U/mg protein; p<0.001), and primary progressive MS (0.057 (0.016) U/mg protein; p<0.001) compared with healthy controls (0.322 (0.053) U/mg protein). These data suggest that low MPO, which may be genetically determined, plays a part in MS pathogenesis.

PMID: 12810789 [PubMed - indexed for MEDLINE]

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1: J Neuroimmunol. 2001 Jan 1;112(1-2):97-105. Links
Mice lacking myeloperoxidase are more susceptible to experimental autoimmune encephalomyelitis.Brennan M, Gaur A, Pahuja A, Lusis AJ, Reynolds WF.
Departments of Medicine, Microbiology and Molecular Genetics and Human Genetics, UCLA, 47-123 Center for Health Sciences, Los Angeles, CA 90095, USA.

EAE is a demyelinating disease which serves as an animal model for multiple sclerosis (MS). Myeloperoxidase (MPO) has been implicated in MS through its presence in invading macrophages, and by association of a -463G/A promoter polymorphism with increased risk. Also, MPO at 17q23.1 is within a region identified in genome scans as a MS susceptibility locus. We here examine the incidence of EAE in MPO knockout (KO) mice. MPO is detected in invading macrophages in the CNS of wild-type mice, yet unexpectedly, MPO-KO mice have significantly increased incidence of EAE: Ninety percent of MPO-KO mice developed complete hind limb paralysis as compared to 33% of wildtype (WT) littermates (P<0.0001). This is the first evidence that MPO plays a significant role in EAE, consistent with its postulated role in MS.

PMID: 11108938 [PubMed - indexed for MEDLINE]

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this sounds pretty emphatic:

1: J Neuroimmunol. 1997 Sep;78(1-2):97-107. Links
Immunohistochemical and genetic evidence of myeloperoxidase involvement in multiple sclerosis.Nagra RM, Becher B, Tourtellotte WW, Antel JP, Gold D, Paladino T, Smith RA, Nelson JR, Reynolds WF.
Neurology Research Service, West Los Angeles VA Medical Center and Brain Research Institute, CA 90073, USA.

The myeloperoxidase enzyme (MPO) is expressed specifically in myeloid cells and catalyzes the formation of hypochlorous acid and other cytotoxic oxidants. We previously reported that two alleles of MPO exist which differ in promoter strength due to a base difference in an Alu-encoded hormone response element. The present study shows that the higher expressing MPO genotype is overrepresented in early onset multiple sclerosis in females, implicating MPO in this demyelinating disease. Contrary to the general conception that macrophages lack MPO, immunohistochemical analysis shows that MPO is present in microglia/macrophages in and around MS lesions as shown by colocalization with major histocompatibility antigens HLA-DR and phagocytized myelin. Also, MPO mRNA sequences are detected in cDNA derived from isolated human adult microglia. This is the first evidence that MPO is present in microglia/macrophages at MS lesions, that MPO gene expression occurs in microglia and that MPO plays a role in MS pathogenesis as shown by the allelic disequilibrium in early onset disease.

PMID: 9307233 [PubMed - indexed for MEDLINE]

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I have to say I think the dose of ginkgo I'm currently taking at 3x120mg 4 times daily seems pretty optimal at the moment. Of course I am combining it with 2x600mg of salvia. But my legs are feeling very good and very different. This morning I did 2 minutes on one of those power plate machines. Normally I do just 1 minute. Normally I get loads of quite nice tingling in my bad right leg. Today there was tingling but it stopped quite quickly and wasn't very intense. What is going on?!!!!

gibbledygook, just to let you know, last week I received a delivery from iHerb.

I have since tried 4 x 4 x 60mg (960mg spread over the day) of "GinkoGold" and can not distinctly say I noticed anything by the end of the day.

I have also tried 2 x 4 x 1,020 "Salvia with MSV 60" (ie 1g Chinese Salvia Root with 20mg Chinese Salvia Root Extract, which comes to 8g of Salvia) and again, I can not say I noticed anything distinctive on that day.

However, I have also added, in addition to my usually flurry of supplements and meds:
Activated Quercetn (1g with 300mg bromelain) x 9
EGCG (700mg x 6)
R-Lipoic Acid (100mg x 3)
Increased my Curcumin (665mg x 9, I have noticed in the past this alone affects the tingling)
"Myelin Sheath Support" by "Planetary Herbals"
Pea Protein (to help my muscles strengthen with exercise, as I think I may be allergic to soy & whey proteins)

As I said, I did not notice anything on a single day, but, my feet MAY be tingling a very small amount less. But this has been slowly improving over time anyway.

I just thought you may like to hear the effects of ginko and salvia on another rat.

Cureo, I'm glad you are giving it a go but sad that you haven't experienced any change. I applaud your dosages though which are much more conservative than when I first started. I can't believe how much ginkgo I started with! I currently take somewhat more than you on a daily basis: 1.44g of ginkgo "extract" and 4.8g of salvia. I think that this is a good minimum for me. When I took somewhat less about a week ago the tingling returned with the spasms. I weigh about 57kg to 60kg and am 5foot 7 inches. Maybe weight and height are also factors...

gibbledygook wrote:which are much more conservative than when I first started. I can't believe how much ginkgo I started with! I currently take somewhat more than you on a daily basis

Is that a dare? huh?

gibbledygook wrote: and 4.8g of salvia.

Thats almost nothing

gibbledygook wrote:I weigh about 57kg to 60kg and am 5foot 7 inches. Maybe weight and height are also factors...

I am about 67kg and 5foot 10 (...and a bit...), so that means (using dosage per kg) I would need to take just under 20% more than you.

I actually gave it a rest today, as was too busy to swallow so many capsules. I'll try to give the Ginkgo a big hit tomorrow, and report back.

Not a dare! No way. I think it's much better going slowly (although that is not what I ever seem to do). Actually, looking at your dose of salvia it seems odd that you're not noticing anything. I'll have to look back at my interminable diary to see how much I was taking when first I noticed an effect. I'm sure it was about 10grams of salvia alone with no ginkgo. So to take 8grams of salvia and nearly a gram of ginkgo should be having an effect. But then you are a bit heavier. I'm perplexed. But go slowly!! Don't do what I do and neck a bottle just to see what happens!!!!!

Yes, it was 10grams of salvia alone that was the dosage that had such an impressive effect on me. The combination of salvia and gingko may also have a synergistic effect. good luck, cureo. I really hope it has a good effect for you.

gibbledygook wrote:Not a dare! No way. I think it's much better going slowly (although that is not what I ever seem to do).

Sure, the old "do as I say, not as I do"

gibbledygook wrote:Actually, looking at your dose of salvia it seems odd that you're not noticing anything... Yes, it was 10grams of salvia alone that was the dosage that had such an impressive effect on me....But go slowly!!

I slowly (ie over 3 days for both Salvia and Ginkgo) built to the dosages I mentioned, just in case I had any negative effect.

gibbledygook wrote:But then you are a bit heavier. I'm perplexed.

Thoughts; your MS may be more based around a damaged BBB? the ginkgo I use is supposedly the one they used in one of the trials, and so may have less of the negative chemical in it, and it may be this chemical that you actually reacted badly to, not the ginkgo. I don't know either.

gibbledygook wrote:Don't do what I do and neck a bottle just to see what happens!!!!!

OK, you win!

I do have to find out soon if these have any benefit for me, because, even at these slightly lower doses than you, the bottles (a single on each) are running out pretty damn fast .

I think we all have a damaged BBB and so all of us have a problem in the vasculature but maybe for me ginkgo and salvia are THE drugs. I do have to reiterate that a week or so ago I pared right back on the ginkgo and salvia to get to the right minimal dose and when I did so the night spasms and painful tingling returned. I then gradually increased to my current dose which seems to be the minimum effective amount. When I first started taking the salvia with around 5grams I didn't notice anything at all and it was just luck that I decided to double the amount. That was when I REALLY noticed something. Playing around with the dosages maybe the thing.

Annoyingly I have also noticed that when I reintroduce the horsechestnut in even quite minimal dosages a return of spasms occurs. Yesterday I tried 1.8g horsechestnut and at night before the last dose of ginkgo kicked in I felt quite a few spasms. Half an hour later I had the sensation from the ginkgo and salvia and the spasms calmed down. The return of spasms also happened a few days ago when I tried a herbal extract containing horsechestnut, diosmin and butcher's broom. This suggests that these herbs aren't so good for my vasulature as the research suggests and as my initial trial of high dose horsechestnut initially felt.

I also keep noticing an odd feeling of pressure behind the skull in the forehead/sinus? area. This, I feel sure, is the ginkgo. Perhaps I am still taking too much although at lower dosages the tingling and spasms return. I shall switch my 3rd ginkgo pill at lunch and supper to a quercetin pill and see how that goes.

what is the most curcumin you have tried in a single day?

I have taken very large quantities of curcumin with no ill effects. I think the most I have taken is 18 of the life extension brand which is 400mg of curcumin which they CLAIM is the equivalent of 2,772mg of standard curcumin. I would therefore have taken over a period of several days to weeks about 50grams daily of curcumin! There were no serious side effects that I noticed.

Owing to the continued feeling of compression in the brain, I reduced my lunch time ginkgo to just 2x 120mg and replaced the usual 3rd with 1gram of quercetin. The sensation of compression has reduced. So, now I know what the increased blood flow to the brain feels like from ginkgo. I shall now take my supper doses but again only take 2x120mg ginkgo with 2x600mg salvia and 3x400mg curcumin, 3x600mg scutellaria with this time 2grams quercetin to see if an extra gram can combat the now increased tingling in the left leg. It really does feel like I can control the tingling/spasms with 3 x 120mg of ginkgo and 2x600mg salvia, 4 times daily but that this does go hand in hand with this curious feeling of pressure in the forehead.

I just saw my Chinese doctor who told me that salvia has a distinct red appearance. My salvia from herbalextractsplus is distinctly green. Is it in fact salvia?! I shall switch to the brand available from iherb tomorrow and see what happens then.

He also told me that there is blood stasis MS, stomach MS, inflammatory MS, spleen MS and kidney MS. There were a certain amount of epithets such as dry, damp and so on grouped with each organ. Perhaps this blood thinning herbal medication will only work for certain people...but I just don't buy that. I reckon we all have excessive vasoconstriction which causes blood to leak into the CNS and this provokes an inflammatory cascade. But I suppose if Cureo doesn't see some effect from ginkgo and salvia soon then my hypothesis is wrong.

gibbledygook wrote:I just saw my Chinese doctor who told me that salvia has a distinct red appearance. My salvia from herbalextractsplus is distinctly green. Is it in fact salvia?! I shall switch to the brand available from iherb tomorrow and see what happens then.

This is the Salvia i purchased from iHerb. It is not red either. In real life I think I can see a very slight tinge of dark green.

Wow, thanks for the picture! In fact I have also purchased the very same salvia from Iherb because of the inconsistencies in the salvia which I purchased from herbalextractsplus. The herb which I took at 10grams or so and is labelled salvia from herbalextractsplus is distinctly green and smells very like the herb, sage. And in fact salvia miltiorrhiza is related to salvia officinalis which is the sage used in meat stuffing. I can't help wondering if herbalextractsplus sent me sage instead of salvia miltiorrhiza as the pills, you have shown, both smell and look completely different to the original pills. I'll just have to see if I get the same effect from the iherb salvia pills. At least the iherb company is likely to be more consistent than herbalextractsplus.