480mg/day Polypodium Leucotomos Reduce Infection Rates in High Performance Athletes by 75%! Plus: Extract Protects Against UV Radiation, Cancer, Trauma & Could Be Ergogenic

Don't worry if you have not heard of Polypodium leucotomos before. After all, that's why you're here! To get your daily dose of SuppVersity news and learn, right?

It's starting to get cold and wet outside and aside from my always healthy self, everyone around is getting sick... sounds familiar? Or are you one of those ailing people who always wonder how the others beard the common cold and did not have a single flu in their whole life? I can assure you, it's not just zinc + vitamin C ;-)

That said, I honestly don't believe that the supplement today's news is about will get the job done, if you don't have your diet and workout regimen in check, but if it reduces the incidence of infections in high performance athletes by 75% it can hardly be useless when it comes to protecting yourself from the sniffers and nose blowers all around, can it?

Dear SuppVersity reader, meet Polypodium leucotomos your immune systems best friend!?

Assuming that I've now gotten your attention, let's get right to the facts. The said supplement is an extract from Polypodium leucotomos a fern that is native to the tropical and subtropical regions of the Americas and has a long history as a folk remedy in Honduras, where it is used for a wide variety of ailments. Interestingly, respective extracts have been sold under the label "anapsos" ever since the 1970s. Nevertheless, I am not sure if anybody who does not know the LEF product catalog by heart has ever heard of Polypodim (if you did, probably in relation to skin health) -- specifically not in the context of infectious diseases in high performance athletes, which was what Bartolomé Marí Solivellas and Teo Cabanes Martín were interested in, when they conducted their 3 months study on the effects 480 mg/day Polypodium leucotomos extract (Armaya fuerte; Centrum laboratories, Alicante, Spain / researchers report no conflict of interest) on the onset of infectious processes and relapses during an 8-month follow up from June 2010 to January 2011 (Solivellas. 2011).

The study participants were all athletes who took part in competitive activity, trained or competed for 20 hours per week and had and still were periodically monitored in a sports medicine clinics. Overall, a total of 116 athletes (58 men and 58 women, aged 18-30 years) were included. 63 of them in the Polypodium leucotomos extract-treated group (PL) and 53 in the control group (C), with 58 males and
58 females aged 18–30 years (subjects with autoimmune or chronic disease were excluded; 14 additional athletes were excluded during the trial, either because they left or were non compliant, i.e. didn't take their supps). Most of them were competitive volleyballers, football players, track & field athletes and cyclists.

The protocol: A 2x 240mg/day preload from June to August

The participants in the active arm of the trial had to consume their daily dose of 480mg in two 240 mg servings, one in the morning and one at night, while the the control group did not take Polypodium
leucotomos extract (no question: The fact that the study was not placebo controlled is a bummer!). This means that the acute supplementation did not coincide with the aforementioned period of sniffing and nose blowing, and any effect that would be seen over the whole 8-months follow-up must be due to permanent benefits in response to the supplementation in those first three months (it also reduces the influence of the placebo effect, after all we are quite forgetful and don't really think about the pills we popped in the summer, when we are getting sick in autumn).

The results: 75%! less infections in the treatment group

Table 1: Prevalence of infectious processes in the control group and study group (Solivellas. 2012)

Even at a very cursory glance at the data in table 1 you should notice the two most important figures: "28" and "7", as in 28 infections in the control (=unsupplemented group) and only 7 infections in the treatment (=480mg/day Polypodium leucotomos extract) group - that's a pretty impressive number. Since, both study arms had been of the same size (n = 50), after a couple of athletes had been excluded from the active arm due to non-compliance, this is a 75% reduced risk of catching any type of infection (see table 1 for detailed breakdown). According to the authors, of those, ...

"[...] the cases of pharyngoamygdalitis were the most noteworthy – 12 patients (24%) in the control group compared to three patients (6%) in the Polypodium leucotomos extract"-treated group." (Solivellas. 2011)

The incidence of infections was yet not the only thing that was reduced. What's probably about as important as the number / rate of infections are the facts that

• the "symptomatic improvement was more favorable" (Solivellas. 2011) in patients from the study and 
• the number of relapses, i.e. a 1/7 vs. 12/28 in the active and passive arm of the study, were significantly lower (-66%)

Since the SuppVersity user stats tell me that most of you are living in the Northern Hemisphere and that it stands out of question that all of you work out (right? ;-), these results alone would be reason enough to take a closer look at Polypodium leucotomos, Calaguala, Anapsos, Heliocare, Kalawalla, Polypodiaceae or whatever other funky name the herb may go, where you are currently living.

Anapsos can do more than render athletes 'infectious disease proof', much more!

This would not be the SuppVersity, though, if I would not tell you "the whole story" about what turns out to be quite an outstanding fern species with beneficial health effects that go well beyond giving your immune system a major boost. And though I have to admit that I did not go back into the 1970s, when the first commercially available extract that goes, as I've mentioned before, by the name Anapsos hit the market. Even the research that has been done in the 21st century only did suffice to compile a pretty impressive list of scientifically backed beneficial health effects, of which I have selected only those, I thought you may be interested in:

• Protection against skin cancer  and related pathologies - PL protects the melanocytic nevi in your skin from forming sporadic melanoma in response to UV radioation, dark eyed patients with higher UVR sensibility (lower basal minimal erythematous dose) would benefit most (dosage 1080mg of PL; Aguilera. 2012). Similar results in rodents, where 300mg/kg of PL 5 days before UVR exposure "reduced the number of proliferating cells by 13%, increased the number of p53(+) cells by 63%, enhanced the antioxidant plasma capacity (ORAC) by 30% and reinforced the network of dermal elastic fibres" (Rodríguez-Yanes. 2012). Also helps against photo aging, polymorphic light eruption, idiopathic photodermatosis, UV-B induced immuno-suppression in the skin,
• Prevention of hyperpigmentation (and psoriasis) - Hydroquinone has been a cornerstone for the treatment of hyperpigmentation; however, concerns regarding adverse effects have prompted a search for alternative agents, one that was suggeted only recently is Polypodium leucotomos (Konda. 2012). Ameliorative effects have also been observed in psoriasis patients, although it appears that more research would be necessary to make any recommendations (Middelkamp-Hup. 2004)
• Remission of subacute cutaneous lupus erythematosus (SCLE) - SCLE is an uncommon autoimmune disease that results in substantial photosensitivity of affected patients. Eruptions often are triggered or exacerbated by UV light (UVL) exposure and a recent case in Cutis shows that while the disease was at best "moderately controlled" with hydroxychloroquine sulfate, "near total remission of disease" was achieved after the addition of oral Polypodium leucotomos supplement (Breithaupt. 2012).
• Amelioration of atopic dermatitis, reduction of antihistamine requirements - Scientists have only shown recently in a phase IV randomized, double-blind, placebo-controlled, multicenter trial involving 105 patients aged between 2 and 17 years who were receiving topical corticosteroids to treat moderate atopic dermatitis that PL administered for 6 months led to a statistical significant reduction in oral histamine use of  4.5% (for those interested, patients received Anapsos 120 mg manufactured by Especialidades Farmacéuticas; Ramirez-Bosca. 2012).
• Prevention of the shift in Th1/Th2 (immune characteristics) in response to trauma - In 2007 already researchers from the University of Zaragzoa found that PL blocked the postoperative (day 1) increases in IL-6 and IL-10 in rats undergoing fracture..On postoperative day 7, "rats undergoing fracture showed an increase of IL-6 levels", the latter was not observed in the PL supplemented rats who had increased levels of the "good" inflammatory cytokine IL-12 on postoperative day 7, instead (Navarro-Zorraquino. 2007)

"Hold on, but didn't you say on SHR and in a couple of blogposts that ROS are necessary?" True, ROS (radical oxygen species) are necessary, as they are a signalling molecule and 'toxic junk', both at a time. Whenever your body is however, figuratively speaking, unable to 'read the signals for the signals' -- which happens to be the case for unfortunate majority of the sedentary Western society -- you better cut back on the forest of signs than have them accumulate in the form of toxic metabolic waste and damage (oxidize) your tissue. Always keep in mind: Whenever we are talking about physiological processes it's all about balance and simply about good or bad and black and white.

The list above did already skip a couple of skin related benefits and still: As I mentioned before, there is probably lots more you could find once you start digging deeper and going further back in the archives. What the hitherto elucidated and probably also all future benefits do have in common is that they are in one way or another related to the potent antioxidant effects of certain not exactly specified molecules the (sub-)tropical fern apparently contains.

Whatever antioxidant (I rather suppose it's a synergistic cocktail) Polypodium leucotomos may contain, it must -- contrary to many other antioxidants which fall victim to their own kamikaze tactics (aka "free radical scavenging") often way before they make it to the target tissue-- actually get to where it is needed and can thus exert its potent antioxidant effects right in the skin, the wound, the broken bone,... and maybe the strained muscle!?

If the latter was the case, and the antioxidants in this peculiar American farn had similar effects in muscle tissue as they were observed by Navarro-Zorraqino et. al. in their rodent model -- namely the induction of an increase in IL-12 and a faster decrease in IL-10 expression -- the concerns about 'too much of a good thing' I addressed in the red box to the right, would not just have been unwarranted; in view of the established pro-anabolic effect of IL-10 (cf. Argilé. 2001) they would actually be absurd (just as the common understanding that all cytokines were "bad", by the way).

Bottom line: I guess, you will agree: This stuff is interesting. However, there have been plenty of "interesting" supplements in the past, which did not deliver. So, if you are merely interested in the last mentioned ergogenic effects, which could obviously be present, you better wait for a respective trial and the corresponding SuppVersity news, before you fill your supplement rack with tons of Polypodium leucotomos. If you are supplement fanatic, got some money to spare and are interested in the immune boosting or UV protective effects, you may want to give it a try.

References:

• Aguilera P, Carrera C, Puig-Butille JA, Badenas C, Lecha M, González S, Malvehy J, Puig S. Benefits of oral Polypodium Leucotomos extract in MM high-risk patients. J Eur Acad Dermatol Venereol. 2012 Jul 31.
• Argilés JM, Meijsing SH, Pallarés-Trujillo J, Guirao X, López-Soriano FJ. Cancer cachexia: a therapeutic approach. Med Res Rev. 2001 Jan;21(1):83-101.
• Breithaupt AD, Jacob SE. Subacute cutaneous lupus erythematosus: a case report of Polypodium leucotomos as an adjuvant therapy. Cutis. 2012 Apr;89(4):183-4.
• Konda S, Geria AN, Halder RM. New horizons in treating disorders of hyperpigmentation in skin of color. Semin Cutan Med Surg. 2012 Jun;31(2):133-9.
• Middelkamp-Hup MA, Pathak MA, Parrado C, Garcia-Caballero T, Rius-Díaz F, Fitzpatrick TB, González S. Orally administered Polypodium leucotomos extract decreases psoralen-UVA-induced phototoxicity, pigmentation, and damage of human skin. J Am Acad Dermatol. 2004 Jan;50(1):41-9.
• Navarro-Zorraquino M, García-Alvarez F, Martínez-Fernández AR, Pastor C, Larrad L, Salinas JC, Lozano R. Pharmacological immunomodulation of surgical trauma. J Invest Surg. 2007 Sep-Oct;20(5):283-9. 
• Ramírez-Bosca A, Zapater P, Betlloch I, Albero F, Martínez A, Díaz-Alperi J, Horga JF; Grupo de Anapsos en Dermatitis Atópica y centros de realización del estudio. Polypodium leucotomos extract in atopic dermatitis: a randomized, double-blind, placebo-controlled, multicenter trial. Actas Dermosifiliogr. 2012 Sep;103(7):599-607. Epub 2012 May 3.
• Rodríguez-Yanes E, Juarranz Á, Cuevas J, Gonzalez S, Mallol J. Polypodium leucotomos decreases UV-induced epidermal cell proliferation and enhances p53 expression and plasma antioxidant capacity in hairless mice. Exp Dermatol. 2012 Aug;21(8):638-40.
• Solivellas B, Martin TC. Polypodium leucotomos Extract use to prevent and reduce the risk of infectious diseases in high performance athlete. Infection and Drug Resistance. 2012 Oct 15.

Inflammation Is a True Fat Burner: BSO-Induced Glutathione Depletion Wards off Fat Gains on Hypercaloric Diet

Image 1: This little bugger obviously has too little inflammation going on ;-)

Are you "on fire"? Inflammation has been implicated as the root cause of almost all modern disease: obesity, diabetes, heart disease, cancer, you name it. Soothing the flames via natural and supplemental anti-oxidants has thusly been proposed and marketed as a solution for many of the aforementioned health problems.

Yet, despite tons of vitamins, anti-oxidants and all the other "healthy" stuff we are taking and consuming on a daily basis, the number of morbidly obese people, diabetics and heart attack patients appears to be ever-increasing... how can that be?

A possible answer to that question comes from scientists from the Saha Cardiovascular Research Center at the University of Kentucky College of Medicine in Lexington, Kentucky, US (Findeisen. 2011) - we simply got everything wrong! The observation that insulin resistance and beta-cell dysfunction usually occur in the presence of large amounts so-called reactive oxygen specimen (ROS) lead scientists to propose that there was a causative relationship between these two events, of which the data only shows that they are corollary.

Image 2: Whenever there is a fire, the firefighters are not far away, but does this correlation indicate that all firefighters are firebugs? (img texarkanagazette.com)

Despite the fact that the distinction between correlation and causation should be obvious, correlations have a long history of being mistaken as causative factors in the history of science. The corollary elevation of total cholesterol in heart disease patients, for example, is the reason that millions of well-educated people world-wide still believe that cholesterol would cause heart disease - an erroneous conclusion for which my friend, Carl Lenore, has coined a very fitting analogy (actually the analogy spans all those "corollary causation"): When there is a fire in down-town New York, it won't take long until the place is packed with firefighters, nevertheless, no sane observer would get the idea that the corollary appearance of firefighters on the scene would be the reason for the fire.

Here, at the SuppVersity, you have already learned that a group of researchers from Germany has invested a lot of work into research on the beneficial effects of inflammation (Ristow. 2010). Now, with the data from Hannes M. Findeisen (who unquestionably is a German or has German ancestors, as well ;-) et al., evidence begins to accumulate that the role of reactive oxygen specimen in glucose homeostasis could in fact be a beneficial and not a detrimental one. After all, Findeisen and his colleagues were able to show that the pharmacological depletion of glutathion, our natural broadband fire-extinguisher, made mice resistant to diet-induced obesity, increased energy expenditure and enhanced insulin sensitivity.

If you have listened to all the installments of the Amino Acids for Super Humans Series on Carl Lenore's Super Human Radio, you will already have heard me mention that a methionine/cysteine-free diet has been shown years ago to have profound fat-burning, or I should say, weight-reducing effects on mice - no wonder, with methionine and cysteine being essential substrates for mammalian gluthation production, a lack of these dietary sulfur-amino acids induced a similar glutathion depletion as the addition of 30mmol/l BSO to the drinking water of the mice in the Findeisen study (for more on the glutathion depleting effects of BSO, cf. Skapek. 1998; Mira. 2002; Cattan. 2008)

Even before the works of Ristow et al. and now Findeisen et al., it has been well-established that reactive oxygen specimen, the purported villains of the 21st century, enhance cellular signaling (Veal. 2007). About a year ago, Chang and Chang  reported that H2O2, in particular, is a potent activator of protein signaling pathways, including insulin signaling and can even mimic insulin's effects by the inhibition of oxidation-sensitive protein tyrosinases (Chang. 2010). With glutathion being the primary H2O2 scavenger in mammalian tissue, it is thus not surprising that the BSO treated and thusly glutathion depleted mice in the Findeisen study displayed a more favorable response to a glucose tolerance test after 6 weeks of treatment with BSO and a 45%(high)-fat diet (cf. figure 1).

Figure 1: Glucose levels in mg/dl after oral glucose tolerance test in mice after 6 weeks on a high-fat diet (47% fat) with or without 30mmol/L BSO in their drinking water (data adapted from Findeisen. 2011)

These results are surprising, also because the daily food and water intake of the mice was identical. The latter cannot be said of their calorie-expenditure, daily activity level (cf. figure 2) and the activity of the "fat burning" uncoupling protein UCP2 (+100%), the elevation of which increases thermogenesis and energy expenditure.

Figure 2: Relative changes in energy expenditure and daily activity due to BSO induced glutathion depletion in mice on a high fat diet compared to non-treated control (data calculated based on Findeisen. 2011)

Now, most importantly for you, as a physical culturist, may be that glutathione depleted mice did not simply fail to thrive or shrivel away - they were, as Findeisen points out...

completely protected from diet-induced obesity, despite similar food intake and water consumption. Analysis of body composition in mice fed a HFD diet confirmed significantly decreased fat mass in BSO-treated mice without significant differences in lean body mass, indicating that the difference in body weight was due to reduced fat mass in BSO-treated mice.

If you don't believe the words, I suggest you take a look at the data in figure 3 - while the control mice had a body fat percentage of whopping 32% the mice on BSO with their ~16% body fat were well within the normal range for lab-mice.

Figure 3: Fat and lean mass (in g) of mice from the control group and the glutathion-depleted group after 6 weeks on a hypercaloric high fat diet (data adapted from Findeisen. 2011)

Even the researchers appeared to be surprised by the profound effects glutathion depletion had on the rodent's ability to accumulate body fat. As far as the underlying reasons are concerned, they speculate that it was ...

[...] possible  that  the  observed  increase in the expression of UCP-2 and UCP-3 in BSO-treated mice induced  mitochondrial  uncoupling [...] Alternatively, the enhanced energy expenditure in BSO-treated mice  might  be  the  result  of  increased  locomotor  activity.  In skeletal muscle, ROS are necessary for optimal contractile function, force production, and exercise-induced adaptations. Furthermore, particularly H2O2 is increasingly recognized as
a potent neuromodulator. It is therefore conceivable, that glutathione depletion may lead to activity-stimulating changes in the redox environment of muscle or brain.

Now, it is however questionable in how far any of these three phenomena would occur in human beings, as well. While the lack of large amounts of UCP-sensitive brown adipose tissue would decrease the UCP induced thermogenic response to glutathione depletion, locomotor activity is something that appears to be completely blocked in the modern couch potato, anyways. It would thus warrant further research (and studies into the general safety of this approach) before it would appear warranted that you take a spoon of BSO with every meal to counter the negative effects of your last binge ;-)

Not All Vitamin C is Created Equal: AA-2βG, a Powerful Vitamin C Analogue From Goji Berries Outperforms Its Cousin L-Ascorbic Acid and Teaches Scientists "Nature Still Knows Best!"

Vitamin C, also known as L-ascorbic acid probably is the best known of all anti-oxidants; and the marketing  departments of the food companies know that and how to make use of its popularity with slogans like "Extra rich in vitamin C", "Extra Vitamin C", etc. Back in the days, when food was still exclusively nourishing and nobody expected it to heal the ailments it, or other food was causing, ascorbic acid was mostly added to products to extend their shelf-life (this is still common practice, btw.). Today, however, the highly processed foodstuff the unhealthy majority of the fast food society, we have become, is consuming on a daily basis contains vitamin C to... well, I guess to be more marketable. After all, scientific evidence for the purported beneficial effects of vitamin C in isolation, i.e. outside of the natural nutrient mix of real food (vegetables, fruits, meat, eggs, etc.) is scarce and a recent study (Zhang. 2011) from the College of Life Science at the Ningxia University in Yinchuan, Ningxia, China, suggest that structural and compositional differences between vitamin C as we know it, i.e. l-ascorbic acid, and the naturally occurring mix of ascorbic acids and its structural analogues may be the actual reason for the lack of effect all the added ascorbic acid in our foodstuff has on the health of its consumers.

Image 1: Dried Goji or Wulfberries, a
natural source of powerful VitaminS(!) C.
1 gram of the dried fruit contains about
5mg of the power-antioxidant AA-2βG
(data from Toyoda-Ono. 2004)

The paper (Zhang. 2011), which appeared in the May issue of the Archives of Pharmacological Research, reports the results of in-vitro and in-vivo analyses of the anti-oxidant activities of AA-2βG, a natural vitamin C analogue from Goji berries (Lycium barbarum L.). From a molecular perspective, 2-O-β-D-Glucopyranosyl-L-ascorbic acid (AA-2βG) is nothing but plain ascorbic acid (AA) with an added D-glucose moiety and a β-glucoside linkage at the C2 position of the AA molecule. While the fact that this "extension" should (see below) reduce the count of hydrogen radicals or electrons the molecule can donate to scavenge NO2- molecules from two (AA) to one (AA-2βG), it adds to the stability of the molecule, which in its original form (ascorbic acid) cannot "is poorly stored in the body [which] makes it difficult to sustain high concentrations of AA within the body for therapeutic interventions". So, other than science, nature, in her infinite wisdom ;-), obviously knew about the storage problem with vitamin C all along and hid the solution in a fruit that, despite having being used in traditional Chinese medicine for hundreds of years, appeared on the screen of western medical science (and in a huge amount of commercial supplements) only very recently: Goji berries, lat. Lycium barbarum L., the dry fruit of L. barbarum (cf. image 1).

For the alpha- variety, AA-2αG (also known as AA-2G), which has a D-glucose moiety and an α-glucoside linkage at the C2 position, studies similar to the one performed by Zhang et al. had already found that despite the reduced amount of donable hydrogen radicals or electrons (see above), compared to normal ascorbic acid, the AA-2G radical that formed in the process of a first DPPH  [2,2-diphenyl-1-picrylhydrazyl is a dark-colored crystalline powder composed of stable free-radical molecules used to test the in-vitro anti-oxidant capacities of various chemicals compounds] scavenging was "able to react with another DPPH molecule to form a covalent adduct", this covalent adduct from the second reaction was then capable of "slowly quenching a third DPPH radical molecule to generate an unidentified product", so that one molecule of this vitamin C analogue, despite ostensible structural inferiorities, scavenges one additional DPPH radical compared to plain L-ascorbic acid. And while the 2-O substituted AA derivative does lack the ability to to scavange O2−radicals in vitro,

[...] it was more efficient at scavenging H2O2 and OH- than AA (p < 0.01 and p < 0.05, respectively) (Figs. 2B, 3A). This implied that the AA-2βG and AA [ascorbic acid] antioxidant mechanisms differ such that the antioxidant activities of AA-2βG are efficient at scavenging H2O2 and OH- instead of directly scavenging O2−radicals.

With different mechanisms of action, however, the radical scavenging effects of L-ascorbic acid and its derivative(s) add up. This makes the naturally occuring mix of vitamins C an even more potent weapon in the nutritional, supplemental and pharmacological war against oxidative stress reduction and the prevention of lipid peroxidation and cell damage (e.g. erythrocyte hemolysis; cf. figure 1).

Figure 1: Percentage of hemolytic red blood cells in a solution with 500µM H2O2 at various concentrations of Ascorbic Acid (AA) and AA-2βG cells vs. control (0µM) without added anti-oxidants (data adapted from Zhang. 2011)

If you bear in mind that even in the absence of H2O2 roughly 9% of the erythrocytes are damaged by oxidation, the level (~13%) at which the protective effects of AA-2βG saturate (cf. figure 1) indicates that the vitamin C analogon blocks H2O2 induced hemolysis almost completely.

Figure 2: Liver-protective effect of different doses of AA-2βG(dose in mg/kg) in CCl4-induced mouse injury
model; ALT, AST on primary, MDA on secondary axes (data adapted from Zhang. 2011)

Similarly astonishing are the liver protective effects of AA-2βG, of which Zhang et al. found in experiments with CCl4 intoxicated rodents that, in contrast to untreated animals,

[...] serum ALT and AST levels in animals pretreated with AA-2βG were reduced significantly compared to those in the untreated group (Table III) [and] AA-2βG exhibited dose-dependent protection against liver injury, as serum ALT and AST activities in mice given a high AA-2βG dose (300 mg/kg) decreased dramatically to levels similar to those in untreated animals.

So, after all, this seems to be another instance, where nature knew best. Even with all the bioflavonoids, esters, minerals or whatever else supplement producers keep adding to plain L-ascorbic acid to justify the exorbitant prices of their products, the natural vitamin C mix in a bunch of fresh Goji or Wulfberries still outperforms the fanciest supplement.

Taurine Decreases Oxidative Stress After Eccentric Exercise in Rats: Human Equivalent Dose ca. 3.5g-4g

Regular readers of the SuppVersity will certainly be familiar with the sulfur-amino-acid taurine and its various benefits on exercise performance, insulin sensitivity and weight management. So, it may not come as a surprise that a recent study conducted by young scientists from the Postgraduate Program in Health Sciences at the Universidade do Extremo Sul Catarinense in Brazil found that 14-days "preloading" with 300mg/kg taurine per day reduced the exercise induced increase in oxidative stress in rats.

Taurine supplementation was found to decrease superoxide radical production, CK [creatine kinase], lipoperoxidation and carbonylation levels and increased total thiol content in skeletal muscle, but it did not affect antioxidant enzyme activity after EE [excentric exercise].

It is rather speculative, whether standard dose equivalent calculations apply to one situation or another - IF they did, you could probably get away with as little as 3.5-4.0g of taurine per day to achieve similar results. It would however warrant further investigations to find out, how, for example, the consumption of beta-alanine (cf. News on the Taurine vs. Beta Alanine Antagonism) would increase the need for supplemental taurine.

Additional advice: Do not buy your taurine in caps. Rather go for some bulk powder. It is cheap as hell and, at the suggested dose of 4.0g, a 500g pot will last you 125 days. And just another thing: Better take your taurine in divided doses. I've heard of people getting severe diarrhea from doses greater than 2g.