Astragalus membranaceus: Purported Telomerase Activator Increases Exercise Capacity by +56%, Fights Cancer and May Be a Healthy Adjunct to Chemotherapy and Vaccines

Image 1: Astragalus membranaceus, one of the 50 fundamental herbs in traditional Chinese medicine (TCM). A purported telomerase activator that contains potent antioxidants.

There is hardly one month passing without some media reports about a group of scientists who supposedly found the royal route to health and longevity. With all those potentially life-extending drugs, herbals and nutritional supplements that have thus surfaced in the course of the last decades, it is actually almost surprising that we still die like flies, isn't it? Well, one possibility would obviously be that the scientifically-backed wonder-potions you can buy in the snake-oil shops all over the Internet do not work at all - impossible? I don't think so. Consequently, I was and still am very skeptical about the dubious claims about the "life-extending" effects of a patented Astragalus membranaceus (also Astragalus propinquus) extract - and that despite or, I should say, because of its "scientifically proven" effect on telomerase length in 114 older (63 +/-12 years) subjects. After all, the respective study was not only by the owner of the company which holds the patent for T-65(R), a (I quote) ">95% pure single chemical entity isolated from a proprietary extract of the dried root of Astragalus membranaceus" (Harley. 2011), but the authors (guess what all somehow involved in the sale of the product) also use several more or less clever tricks to polish their results. While they have to admit that

Two independent measures of median or mean telomere length (by FlowFISH and qPCR) showed no consistent change with time on PattonProtocol-1 (data not shown).

they cleverly handpicked 7 out of 13 tested subjects in which the percentage of nuclei with short telomeres had declined at 12-18 months compared to baseline. Now, while this decline may be statistically significant (p<0.05, according to the scientists), I wonder what happened to the other 6 subjects... and even if you were among those lucky 7, this does by no means indicate that that will actually prolong your life.

Who wants to live forever, anyway...

That I did nevertheless dig a little deeper into the research on astragalus had two reasons. One was that I wanted to find any other data on its potential effects on telomerase length - and more importantly its practical outcome in rodents or even my "favorite" subject of medical research, the roundworm Caenorhabditis elegans, or "C. elegans" (do I have to say that there are no such studies?). The other reason was that astragalus membranaceus has been used in Traditional Chinese Medicine for centuries. So, even if it would not make you live forever there obviously had to be some benefits to this flowering plant from the family of Fabaceae. And as it turned out, Chinese researchers have been performing numerous studies into its antioxidant, anti-diabetic, anti-hypertensive, and immunomodulatory activity within the last decades, of which a very recent one could be of particular interest for fitness enthusiasts and even professional athletes.

... isn't performance the only thing that counts?

Image 2: While this is not the exact model that has been used in the study, this is what "exercise" looks like if you are one of those poor lab rats... well, not so much different from what a whole host of trainers still suggest their clients should do to lose weight... but I am digressing, here ;-)

If you look at the sales-ranks of various dietary supplements, it is quite obvious that (potential) long-term effects on health and longevity usually stand second to immediate benefits like increased energy, well being, weight loss or exercise performance. "If you don't feel it, it doesn't work!" is the mantra of many fitness enthusiasts; a montra on which the manufacturers of purported fat-burners and pre-workouts, 99% of which are only caffeine, geranamine and yohimbine loaden stimulants, monetize big time. And as long as those cheap stims keep the sales of their products up, the producers obviously would be stupid if they changed their formulas and included more expensive "adaptogens" - chances are the customers would not be willing to pay the price, anyway. Accordingly, you won't find references to studies like the one Deng and Hu recently published in the Academic Journals on any of the labels of the currently available mainstream supplements (Deng. 2011).

In what they themselves claim is one of the few studies (to my mind the first to be published in an international journal) investigating the effects of Astragalus membranaceus polysaccharides (AMP) on exercise performance, the scientists from the Kunming University in China orally administered 50, 100 or 200mg/kg of previously extracted pure astragalus polysaccharides to 6-8 week old male Sprague-Dawley rats for 30 successive days. In the course of the last week of the experimental period the rats, who had been fed ad-libitum for the whole study period, were accustomed to running on a treadmill for 15-20min at 15-30 m/min (=0.9-1.8km/h), so that they would be able to perform an exercise test that consisted of running on a 10° incline (30m/min, ~75%VO2Max) until exhaustion on day 30.

Figure 1: Running time to exhaustion (in s, left) in rats who received either saline control or astragalus membranaceus polysaccharides at a dosage of 50, 100 or 200mg /kg per day and the extrapolated dose-response relationship (data calculated based on Deng. 2011)

As the data in figure 1 shows, the supplemental regimen, which had no effects on the body weight of the then 12-week old rats, significantly improved the running endurance of the laboratory animals. Interestingly, the extrapolation of the dose-dependency suggests that dosages above 300mg/kg (human equivalent ~50mg/kg) will probably not yield much better results than the 200mg/kg maximal dose that was used in the study (human equivalent ~35mg/kg).

Figure 2: Effects of astragalus supplementation on anti-oxidant enzymes after exhaustive endurance training in rats; values expressed relative to unsupplemented control (data calculated based on Deng. 2011)

The post-exercise glutathione peroxidase (GSH-Px) activity exhibits a similarly logarithmic dose-response relation (cf. figure 2). The decreases in malondyaldehyde (MDA), as well as the increase in superoxide dismutase (SOD), on the other hand appear to be almost linear. And, lastly, the lower increase in catalase (CAT) in the high dose astragalus group could be a consequence of the fact that, with GPH-Px and CAT both being responsible for the catalyzation of hydrogen peroxide to water, there simply was no need for additional cat activity, when the GPH-Px activity already increased by >100%.

If (the big if ;-) those results could be confirmed in human trials, the +56% increase in exercise endurance in the 200mg/kg (i.e. 35mg/kg for humans) of astragalus could in fact be the "next big thing" in terms of natural ergogenics. For the time being, it is yet only another item on the list of purported benefits, I am now going to conclude on another anon more health related note.

Beyond exercise performance: Cancer protection and immuno-modulation

While I initially voiced some doubts with regard to the purported longevity effects of astragalus, its relatively well-established anti-carcinogenic effects could well help many of us to substantially prolong our lives. After all, numerous studies have established the anti-cancerous activity of various natural constitutents of astragalus. Among the cancer cell lines that were tested were  

• colon cancer cells (Tin. 2007, Auyeung. 2010),  
• breast cancer cells (Zhou. 2009; Gülcemal. 2011),  
• cervical cancer cells (Yalcin. 2011), 
• human gastric adenocarcinoma cells (Auyeung. 2011),  
• human hepatocellular carcinoma (HCC) cells  (Hu. 2009; Auyeung. 2009)

If you look a the publication dates and authors, you will notice that despite its longstanding tradition within TCM scientists have only lately begun to realize that we could have overlooked a vital contribution in the ongoing battle against cancer - and what's more, the studies are mostly done by TCM practitioners at the School of Chinese Medicine, who certainly ain't under suspicion to be interested in monetizing on a new drug. After all, natural medicine is not patentable.

From the petri dish to the bedside: APS improved quality of life in cancer patients.

Image 3: Astragalus has already proven its usefulness as an adjunct to the toxic cocktail cancer patients receive as part of their chemotherapy

In a first trial (Guo. 2011), the intravenous administration of astragalus polysaccharides (APS) at 250mg/day in connection with chemotherapy for 7 days lead to statistically significant improvements in the overall quality of life of advanced non-small-cell lung cancer patients. Personally, I find it most remarkable that it reduced the chemotherapy induced fatigue by >50% (as measured by a standardized Quality Of Life questionnaire). The objective response rate to chemotherapy was higher, as well: 42.64% (29/68) in the APS supplemented patients vs. 36.76% (25/68) in the control arm of the study, but these effects did not reach statistical significance (P = 0.483, indicating that chances are about 43% that this was just "conincidence").

In view of the immune-weakening effects of chemotherapy, it may also be important that astragalus has established anti-viral effects. It has been tested as an adjunct to interferon alpha-2b in anti-herpes therapy (Zhang. 1998) and against (chronic) hepatitis B infections (Wu. 2001; Dang. 2009) - the effects are yet rather mediocre and may be mediated by the same general immune-stimulatory effects of the herb (Block. 2003; Jiang. 2010). In this context, it is particularly noteworthy that a paper on herbal medicinces for viral myocarditis published in the reputable Cocraine Database of Systematic Reviews that ...

[..a]stragalus membranaceus (either as an injection or granules) showed significant positive effects in symptom improvement, normalisation of electrocardiogram results, CPK levels, and cardiac function.

And with the current vaccination-hysteria, we may soon see the practical realization of a proposal that has been made by Lin et al. in a recent paper on the effects of Astragalus polysaccharides (APS) on foot-and-mouth disease in swine (Lin. 2010), i.e. the addition of APS as an immuno-modulator for various vaccines (I guess it would certainly be better than mercury, don't you think ;-).

Conclusion: A promising herb... without a future?

Image 4: If all the info got you interested, Carl Lanore from Super Human Radio has recently sourced a bulk powdered version of astragalus. The bulk source is probably the only way not to run out of money before you notice any effects ;-)

Despite the accumulating evidence for the many health benefits that could be derived from the administration of crude extracts or isolated fractions of astragalus, chances that it will make it from Carl Lenore's Super Human Radio shop to the mass market are low ... or I should say non-existent, as long as the latter is still controlled by BigPharma and their right-hand men and women in the bureaucracy. After all, Astragalus membranaceus is not only non-patentable, it also does not appear to have any side-effects, the pharma companies could monetize on ;-) So regardless of whether future studies will validate or maybe falsify the hopes many naturopaths and TCM practitioners are pinning on this herb, MDs who follow the official guidelines, which state that the...

evidence for using astragalus for any health condition is limited. High-quality clinical trials (studies in people) are generally lacking (NCCAM. 2010),

will probably never prescribe it to their patients... unless, well unless some genius of a molecular biologist in one of the pharma-companies applies a few minor melcular tweaks to some of the active ingredients of astragalus, so that his company can file a patent application that goes beyond the extraction technique that has been patented for Harley's (questionable) T-65(R).

CoQ10 for Ultra-Endurance Athletes: 150mg of Ubiquinone Reduce Stress & Inflammation and Stabilize Cell Membranes in 52.4 Mile Torture from 640m to 3,393m!

Image 1: Susan Kokesh, blogger and the Crazy Running Mum at the Sierra Nevada ultra-endurance run a 52.4 miles "double marathon"
  in September 2010; I probably would not even have survived this torture - respect!

As a health conscious physcial culturist, you are probably aware that the vitaminesque nutrient CoQ10, which, due to its ubiquitous presence in all living beings, is also known as ubiqinone, plays a fundamental role in cellular bioenergetics. It is a necessary cofactor in the mitochondrial electron transport chain (i.e. your cell's way of "breathing", its respiratory chain) and is therefore essential for the production of ATP, the fundamental energy unit your cells are operating on. In that, CoQ10 works as a mobile redox agent that shuttles electrons and, interestingly, also protons (those little blue and red balls from Bohr's atom model ;-) in the electron transport chain. Within the health and fitness community, it is however better known for its antioxidant value, as in its reduced form, ubiquinol, it is a potent lipophilic (which means that it does not combine with fats) antioxidant, which is able to recycle and regenerate other antioxidants, such as vitamin E and vitamin C (Ernster. 1995). Moreover, CoQ10 participates in cell signaling and gene expression and has been used as a dietary supplement (among others) for the treatment of neurodegenerative diseases and statin-induced myopathies.

In view of its pluripotent influence on mammalian metabolism (on a side note: the "-10" in CoQ10 indicates the length of the isoprenoid sidechain that is attached to the common benzoquinone ring structure; the latter is unique and can be found in humans and a few other mammals only), it should thus not surprise you that Chavier Díaz-Castro and his collegues from the University of Granada report that the intake of 150mg of the natural version of CoQ10 (2,3-dimethoxy-5-methyl-6-decaprenyl-1,4-benzoquinone; natural = has trans configuration), profoundly modulated "the undesirable effects of the evoked oxidative stress and inflammation signaling during high-intensity" (Díaz-Castro. 2011).

Illustration 1: Supplementational protocol used in the study; CoQ10 was administered as 2,3-dimethoxy-5-methyl-6-decaprenyl-1,4-benzoquinone in powder form in 30mg capsules.

As you can see in illustration 1, the 20 highly trained male amateur athletes (all had run The Sierra Nevada ultra-endurance race in the previous 2 years), who participated in the study were not given the whole dose of 150mg of CoQ10 at once, but followed what I would like to call a "loading protocol" in the two days before the event. The placebo group received an identically looking product containing beer yeast, cellulose,
acacia, silica stearic acid, magnesium stearate, cellulose gum, and maltodextrin.

The total distance of The Sierra Nevada run is >50km. It is considered one of the hardest trials worldwide, mainly because the run, in the course of which the participants "climb" from 640m to a final altitude of  3,393m is almost on a continuous incline! A 5.5 hour torture, for which the CoQ10 supplemented athletes needed on average ~25min less than the subjects in the placebo group. In this study, the exercise performance was yet of negligible importance. What the scientists were really interested were the markers of oxidative damage and inflammation and as the following data shows, those were markedly influenced by the ingestion of this rather "mediocre" (compared to what you see some "health-gurus" advocate) amount of CoQ10.

Figure 1: Effects of CoQ10 supplementation of total bilirubin, triglycerides and urinary creatinine in 20 ultra-endurance runners (data calculated based on Díaz-Castro. 2011)

As you can see in figure 1, CoQ10 induced a significant reduction in urinary creatinine even before the race started (figure 1, left column). Moreover, there were significant differences in the bilirubin (indicates heme catabolism), triglycerides and (again) creatinine (indicates net protein catabolism):

Intense physical exercise resulted in an increase in net protein catabolism and an increase in
creatinine excretion in the PG after the physical test (p < 0.001); however, the urinary levels of creatinine were lower (p < 0.05 before and p < 0.001 after the physical test) in the CoQ10 treated group. Other interesting result was that although there was an increase in urinary creatinine in the CG, it was lower than in PG (38.77 ± 10.20 vs. 88.23 ± 11.21, p < 0.05). We also observed a decrease in the bilirubin concentrations in the CG after the run (p < 0.001) with lower values compared to PG group.

There were also significant differences in the inflammatory response, with (statistically significant, p<0.05) lower values of interleukin 6 (IL-6; -32%) and TNF-alpha (-23%) before the start of the race, and -22% lower TNF-alpha values after the "torture". Moreover, the basal hydroper-oxide content in the erythrocyte membranes, the scientists measured as an indicator of the degree of oxidative stress were lower before and after the exercise test, as the scientists call it.

Taken together, these results suggest that the addition of a small dose of CoQ10 to your supplemental regimen could induce unexpectedly profound cell-stabilizing benefits, of which it would yet be interesting to see how those translate into performance benefits, health and longevity, in the long run.

Endurance Athletes Bath in Cortisol: Dose-Dependent Elevations in Hair Cortisol of Triathletes and Runners.

Image 1: There are two types of endurance exercise - the one that is healthy for obese diabetics and the one that chronically stresses and, in the worst case, eventually kills healthy but overambitious hobby athletes; the photo shows a collapsed runner at the 2007 London Marathon, where 22 of his comrades died
(source thisislondon.co.uk)

In view of the fact, that the series of blogposts on High Intensity Interval Training (HIIT) I made in the course of the last weeks were pretty popular, I thought it may also be of interest that there are interesting new results on the effects of resistance training which goes beyond the common "we took 12 obese sedentary post-menopausal women and had them ride a stationary bike for 45min three times a week" approaches, as well. One of these studies happens to come from a group of German scientists from the Universities of Dresden, Marburg and Hamburg (Kirschbaum. 2011); and the results underline my previous comments on the difference between endurance exercise as it is understood by the medical orthodoxy (and as I described it in the previous sentence) and endurance exercise as many hobby athletes and fitness enthusiasts define it. While the former is unquestionably beneficial for obese diabetics or anyone else who would otherwise sit on the couch watch TV and stuff himself with potato chips and ice-cream, 3x45 min of riding a bike probably won't improve the physical condition of a reasonable conditioned hobby athlete. Now, the Kirschbaum study shows quite convincingly that the opposite extreme, i.e. jogging / running and training loads way beyond 40km per week, comes with another certainly more annoying sting in the tail: chronic stress.

In their study, Clemens Kirschbaum et al. analyzed the hair samples of 304 amateur endurance athletes (long-distance runners, triathletes and cyclists; 190 females, 114 males,  mean age ~38 years) and 70  active control subjects (all recruited at local sport events or from friends and family of the authors ;-) and found on average +42% higher hair cortisol concentrations in the endurance athletes.

Figure 1: Relative increase in hair cortisol levels in endurance athletes compared to controls (Kirschbaum. 2011)

As figure 1 goes to show the increase and, more specifically, it's statistical significance largely depended on the type and the duration of exercise. While both cycling and 10k runs increased cortisol levels by about +36%, in this group there were too many "outlayers", i.e. persons with either much higher or much lower cortisol levels, for this increase to reach statistical significance (as defined by a p-value of p<0.05, meaning that chances that this observation happens to be mere coincidence are <5%). In the study participants who stated that they were running half-marathons, triathlons and marathons, on the other hand, the increases in cortisol (+36%, +48% and +66%) were statistically significant, and in case of the marathon runners even dead (consider this a "forerunner" of what may befall marathon junkies) certain.

Figure 2: Relative increase in hair cortisol levels of endurance runners in relation to average weekly training load in kilometers (calculation based on a regression with r=0.32, indicating a below average precision; Kirschbaum. 2011))

If we disregard any reservations concerning the general validity of hair analysis as long-term marker of cortisol levels (recent studies like Manenschijn. 2011 a.o. would suggest that they are valid), Kirschbaum et al. are thusly right to conclude that their data suggests ...

that repeated physical stress of intensive training and competitive races among endurance athletes is associated with elevated cortisol exposure over prolonged periods of time.

Even more important is their advice that, due to the possibly important implications of these findings, it would be necessary to study potentially detrimental effects on the somatic and mental health of the athletes in the future! Well, I probably don't have to tell you that the SuppVersity is going to be the place, where you will read about those studies first ;-)

Growth-Retarding Effect of "Cardio"-Training is not Prevented by BCAA Supplementation. Endurance-Trained Rats Still -3% Smaller than Age-Mates.

Image 1: Haile Gebrselassie,
probably the greatest distance
runner in history, set 27 world
records; is his sort stature a
result of too much "cardio"
(image by Alexxx86)

Did you ever wonder if Haile Gebrselassie (image 1) is such a great long distance runner, because he is only 5'5" (1.65m, imdb)? Well, after all it could turn out that is is just the other way around - Haile could be only 5'5", because he is a great runner! Rumors have it Gebrselassie ran to school every day as a boy... what? You do not see a relation here, well then you should have a look at the data of a recent rodent study from the Faculty of Pharmaceutical Sciences at the University of Sao Paulo in Brazil (Campos-Ferraz. 2011).

For 5 weeks, Patricia Lopez de Campos-Ferraz and her colleagues, put 32 male Wistar rats (21 days old) on one of four experimental protocols:

1. 45mg/kg BCAA  + swimming - Sup/Ex
2. Standard chow + swimming - Ctrl/Ex
3. 45mg/kg BCAA + sedentary - Sup/Sed
4. Standard chow + sedentary - Ctrl/Sed

The endurance of the swimming protocol increased by 10 minutes per week - from 20min in the first week to 50 minutes in the fourth and fifth week of the experiment.

Figure 1: Effect of treatment (BCAA + "cardio" or "cardio" only) on cartilage weight, skull-to-tale length and tibia length in adolescent rats (data adapted from Campos-Ferraz. 2011)

As the data in figure 1 goes to show, the "cardio"-induced reduction (-95%, Sup/Ex; -97% Ctrl/Ex) in proteoglycan synthesis is so profound that the +30% higher synthesis rate in the BCAA group could not prevent the statistically significant growth retardations in the sixteen rats of the exercise groups (Sup/Ex + Ctrl/Ex).

Image 2: If the Hulk loves HIIT,
he probably has a healthier
heart than many marathon
runners (image from
cdn.healthhabits.ca)

Note: I am deliberately using the expression "cardio" here, because ardeous endurance exercises like these, are what the general public thinks heart-healthy exercise should look like. Only a few days ago, Hafstad et al. published a study in the Journal of Applied Physiology (Hafstad. 2011) showing (once again!) that high intensity interval training and not moderate endurance training provides the greatest benefit in terms of increasing aerobic exercise capacity, and cardiac efficiency! While this study was conducted with a rodent model, it corroberates results from human studies such as Ziemann et al. who found that high-intensity interval training performed at a work-to-rest ratio of 1:2 "provided sufficient stimulus to significantly improve markers of anaerobic and aerobic performance in recreationally active college-aged men" (Ziemann. 2011). As long as you do not have existing heart problems, HIIT should be your choice when it comes to training your heart, which is what "cardio"(-vascular training) should be all about, no?

Isn't it ironic, how those poor little critters experienced exactly what the huge group of people who are against strength training for adolescents usually suggest would happen, when kids start to lift weight? I guess, if it was not for the BCAA-induced increases in proteoglycan synthesis and the slight amelioration (-0.5%) of the retarding effect of endurance training on skull-to-tale length, the "anti-strength"-crowd would probably try to blame the effect on the "steroids" (this is how this folks usually refer to all supplements, BCAAs included), the rats received - fortunately, the study design does not allow misinterpretations like that.

Figure 2: Liver and muscle glycogen content in the four groups (data adapted from Campos-Ferraz. 2011)

Before this turns into an "anti-'cardio'-post" I want to mention a few interesting side-findings of the study: While there were no significant differences in muscle weight between the groups, there was a significant effect of BCAA supplementation on food intake in the sedentary group. The rats (all fed ad libitum) who receiving the chow with additional branch-chain-amino acids consumed roughly 7% less food. What I found more surprising, however, was the effect the amino acid supplement had on liver glycogen levels in the trained rats: The small dose [45mg/kg in rats equals ~7.3mg/kg in humans, i.e. ~584mg/day for an 80kg human being] of supplemental BCAAs raised liver glycogen levels by 12.4% (Sup/Sed) and 16.2% (Sup/Ex). The latter finding stands in line with similar elevations in liver glycogen stores after alanine or glutamine, histidine and proline supplementation in Tipton and Wulf (Tipton. 1998) and Aoyama et al. (Aoyama. 1993), respectively and corroborate previous findings by Araujo et al. (Araujo. 2006), who found a 226% increase in liver glycogen in exercised rats supplemented with a significantly higher amount (~1g/day) of BCAAs.

Figure 3: Muscle protein and RNA content in the four groups (data adapted from Campos-Ferraz. 2011)

Finally, while the small dose of branched chain amino acids did suffice to modulate liver (and to a certain degree muscle, cf figure 2) glycogen stores and storage capacity, it failed to result in a higher protein concentration in the trained rats. A finding of which the researchers state that

[t]his is in accordance with another study, in which oral administration of 270mg leucine to rats enhanced phosphorylation of the eu-karyotic initiation factor (eIF) (4F-BP1), but no differences in protein synthesis were found in the liver, which led them to conclude that the translation of mRNA is disjointed from the rates of total protein synthesis but is related to the degree of SK61 phosphorylation (Anthony et al., 2001).

While this may be the case, Campos-Ferraz et al. simply ignore that their "exercise" (I am inclined to say "torture") program was devoid of the most important stimulus of muscle growth, which is muscular overload - what is really surprising is thus not that the rats did not turn into hulk-like muscle-monsters, but rather that the supplemented rats (Sup/Ex) had a statistically non-significant, yet slightly reduced increase in muscle protein content (+3.92mg% vs. +5.52mg%) compared to their exercised peers (Ctrl/Ex) - despite a +23% greater increase in muscle RNA.

Interestingly, we see diametrically opposed effects in the sedentary group, where muscle RNA content is identical, and the BCAA group (Sup/Sed) has a slightly higher muscle protein content (cf. figure 3). So that, after all, we have come full circle to the detrimental effects of arduous "cardio"-training on adolescents ;-)

On Short Notice: Worst Transfat Offenders Cookies & Co + Cinnamophilin For Joints + Tomato Powder Battles Cancer Like Aspirin + Creatine Protects Cell Walls + Carboholism Starts in the Womb, Intermittent Fasting Helps... + More!

Image 1 (lecker.de): They may look cute and harmless, but they are just one of the many incarnations of the worst transfatty acids offenders in the diets of the "average American" cake, cookie and pastry lovers. Believe it or not: Some of them manage to eat almost 100g of the proatherogenic fats per day (!)

Saturday and therefore time for a handful of "On Short Notice" news. We've got some ground to cover, today, so let's get started right away: We will start out by taking a look at the joint-healing / -protective effects of cinnamophilin, a compound from the roots of the cinnamomum trees. We will reconsider the importance of adiponectin for the non-obese physical culturist, switch from aspirin to tomato powder as our cancer prevention "drug" of choice and re-appreciate the newly discovered cell-protective value of a supplement 90% of you are probably already taking: creatine! Once we are done with that we revisit the potential connection between chronically low blood glucose, chronic catecholamine over-expression and the chronic fatigue syndrome. We will then take a look at how high carb diets and intermittent fasting of pregnant rats program the orexin A expression in the brains of their offspring and how that can predispose them to become obese.

During a brief water-break we will discard the idea of hyperhydration as idiotic and decide against carrying another kg of water weight around for the rest of this installment of "On Short Notice". Eventually we will reject pulses as a new staple diet food due to their potential to damage our gut mucosa and their strange gender-specific effects on insulin release and shake our heads over the average and not so average American's daily trans-fatty acid intake, which borders - in some cases - the 100g (!) ceiling of unhealthy absurdity.

• 

  Image 2: I must admit that I am not 100% sure if you would see similar benefits from regular cinnamon, not just because it is probably not from Cinnamomum philippinense, but also because the active ingredieant cinnamophilin has originally been extracted from the roots of the tree, not it's bark, which is what regular cinnamon is made from - it is obviously likely that some, yet probably lower amounts, would also be contained in the bark and a teaspoon of regular cinnamon probably won't hurt, anyway (cf. Wu. 1994 and Lu. 2012)

  Do your joints a favor and dig up some cinnamomum roots. While I am honestly not sure if cinnamophilin content of regular cinnamon (-bark) vs. Cinnamomum philippinense (nor whether this stuff is even in the bark, which is the raw material for "regular" cinnamon - a paper by Wu would suggest that it is extracted from the roots; cf. Wu. 1994), as it was used in a recently published study from College of Medicine, Taipei Medical University, will be sufficient, it is relatively certain that the anti-inflammatory effects of this highly lipophilic antioxidant and free radical-scavenging agent, which has also been shown to inhibit thromboxane synthase and the thromboxane A2 receptor (means it will reduce unwanted blood clots; Yu. 1994), to block Na+ and Ca2+ inward currents in rat cardiac cells (means it helps to protect the contractile function of your heart; Su. 1999), and to reduce brain infarction and protect against transient focal cerebral ischemia (rodent studies by Lee. 2005 & 2009), would silence any ongoing joint inflammation.
  And while Ju et al. can only speculate about the exact mechanism it appears to involve the modulation of NF-κB or ERK/p38 MAPK downregulation and/or suppresion of p-c-Jun pathways. Since both are involved in the etiology of other inflammatory, degenerative diseases, as well, it appears almost certain that there will soon be more exciting applications for yet another medicinal component from your kitchen cupboard.
• Adipokines are not necessarily your friend - not even adpinonectin: Despite being the latest and (supposedly) greatest of the powerful cytokines that are released from your body fat, may keep you healthy when you are fat, it's negative correlation Pisto et al. observed in an epidemiological cross-sectional study involving 54 normotensive, non-smoking men with normal OGTT, clearly suggests that increasing adiponectin expression probably ain't the best way to get big and buffed (Pisto. 2012). Rather than that, you better diet and work out till you are big and buffed and wait for adiponectin (and leptin, which was by the way not significantly correlated with muscle size after adjustment for total adiposity) to fall in place.

• 

  Image 3: Tomato(powder)'s aspirin-like anti-cancer effects could be another reason for the health benefits of the so-called Mediterranean Diet

  Tomato powder mimics aspirins cancer protective effects At least in the gastrointestinal tract the COX-2 inhibition of tomato powder appears to exert similar protective effects against colorectal cancer (Tuzcu. 2012); and in view of the fact that the rodents in the Turkish study were fed a 5% enriched chow you would however not even have to consume tons of it - 90g or 1.14g/kg body weight would suffice ;-) If that's still more than you want or can stomach, just eat more tomatoes and/or (even better) tomato paste, which is quasi the water-containing version of the dry extract.
  And if you can't do tons of either, don't forget: Just like all the bad junk that may not be a problem if you ingested just junk A and maybe junk B, from time to time, becomes really nasty once C, D, E, etc. join the assault, it may be the pound of tomatoes you ate over the course of the last 2 weeks that helped you to avoid that the literal last straw that would otherwise not have broken the camel's but your back.

• 

  Figure 1 : Lipid vesicle permabilization after exposure to melittin + (1) NaCl , (2) 100 mM DMBG), (3) Creatine, or (4) PCr (Tokarska-Schlattne. 2012).

  (Phospho-)Creatine protects lipids in cell walls! In their latest paper a group of French and Swiss researchers report that they demonstrated for the first time that phosphocreatine (PCr), the explosive power, short-term energy substrate you are trying to increase, when you are taking creatine (monohydrate or whatever else), is more than just an energy source (Tokarska-Schlattne. 2012). As the data in the figure 1 shows, it has direct protective effects on the lipid fraction of your cells as well. And while this observation does not make creatine a bit more effective, it does provide another piece to the puzzle that explains why it is also useful in so many sports-unrelated areas such myopathies and a plethora of neurodegenerative diseases.
• Constant subphysiological glycemia (= hypoglycemia without symptoms) could be the reason that you centrally fatigue, after all the constant elevation of epinephrine and glucagon, Ana María Arbeláez and her colleagues observed in a cleverly conducted study, where they limited the glucose levels in 8 healthy human volunteers to 65 mg/dL (3.6 mmol/L) for two hours showed a constant elevation of epinephrine and glucagon (Arbeláez. 2012). That the latter will only work for so long hardly suffice to keep you functioning normal (by no means optimal) should be clear... So how do you prevent that? Don't overtrain, don't undereat, don't eat only protein and don't be f***ing scared of eating as much carbs and fats, as you need to fuel an active lifestyle (Arbeláez. 2012).

• 

  Figure 2: Orexin A expression in the PvNP in the offstring of rat dams on different pregnancy diets

  You have the choice: Obese or normal kids? It all depends on the way you eat during pregnancy, at least that is the result of a soon-to-be-published study in Brain Research (, which found that compared to the normal pregnancy diet, a diet with an extra load of carbohydrates lead to a lower body weight at birth, but increased orexin A expression in the parvocellular part of the paraventricular nucleus (PvNP) which predisposed the rat pubs of the high carb dams to gain weight at a faster rate and catch-up and overtake the rodents from the control group after no more than 9 weeks.
  Another 10 weeks later, the rodents born to rats in the high carb group were already the heaviest of the four experimental groups and still as hungry as before.
  Now that alone would not necessarily make a SuppVersity news, if the scientists had not, without even noticing made a (imho) very relevant discovery. In addition to the group with free access to normal chow, they had another group which mimicked the time-restricted feeding pattern in the high fat and high carb groups, who received their chow only within a fixed 6h window, which would essentially equate to intermittent fasting; and while I doubt that the results reach statistical significance, it is still quite telling that the pubs born to the intermittently fastest (IF) rats on the regular diets, were normal weight at birth, had the lowest orexin A (hunger signal expressed in the brain) expression in the PvNP and were subsequently the lightest at the 19 week weight in...
  I still wouldn't suggest you start to fast intermittently, just because you notice you are pregnant, after all we don't know whether or how this translates to humans and if the pubs of the IF-dams were not simply undermuscled and therefore exhibited a lower body weight.

• 

  Image 4: As long as you got a couple of tables with water, sugary electrolyte bevarages, or even better salted coconut water along the roadside, you don't need to carry another 2lbs of water weight with you on your 1/2 marathon races.

  If you want to carry another kilo of useless weight around in the heat, go on and practice hyperhydration, otherwise you better stick to a bottle of water with some salt and sugar in it on your next 18km TT run in the heat (and cold). This is the actually not very surprising take home message of a recently conducted randomized cross-over trial from the University of Sherbrooke, in Canada, in the course of which Pierre-Yves Gigou and his colleagues investigated the effects of hyperhydration (=water loading) with 26 mL/kg bodyweight of a 130 mmol/L sodium solution before four successive 4.5 km blocks alternating between 2.5 km at 1% and 2 km at 6% gradient on a treadmill (Gigou. 2012).
  For the well-trained triathletes in the study, it did not make a difference whatsoever, as long as they could guzzle away their 500ml of gatorade during the 80-90min of running they were fine.
• Are pulses superfoods, for women only or simply not suitable for daily consumption? It appears that similar to their nasty brethren, the soybeans, yellow peas, chickpeas, navy beans and lentils have the potential to become e hip diet food that could do more harm than good, especially to its male consumers. In a recently conducted study, a group of researchers from the University of Toronto found that pulses can help both men and women lose weight without prescribed caloric restriction (Mollar. 2012).

  

  Image 5: Pulsing of protein is something you are familiar with, but what about eating pulses.. yeah, we are talking about yellow peas, chickpeas, navy beans and lentils; that stuff your grandma maybe told your patents to eat from time to time. Are they the good twin of the evil soy bean?

  Contrary to the subjects in the calorically restricted "control" arm (-500kcal/day) of the study, the overweight or obese (mean BMI 32.8 kg/m²) adults in the pulse group, who were provided with a whopping dose of five cups of pulses per week (on average 896 g/week), had reduced their energy intake ad-libitum to about the same level as their peers "involuntarily" and accordingly seen similar reductions in body weight, waist circumference, systolic and diastolic blood pressure (statistical significance for intergroup differences were non-significant, i.e.  p >> 0.05, for all). At the end of the 8 week period there were however a couple of unwanted side-effects: While the minimal increase in HDL form the pulses would certainly count as a plus, increasing  C-peptide levels already suggest that there appears to be a problem with the glucose management in the pulse-eaters.
  And in fact, while the average female participants insulin AUC (the area under the insulin curve is a measure for the total amount of insulin the pancreas spills out in response to an oral glucose tolerance test, as it was performed in the study at hand) did go down by 13.9%, there was a profound increase (27.3 % in males) in the male pulse eaters.

  

  Figure 3 (radiancenutrition.com): Daily consumption of pulses appears appears to entail the risk of developing leaky gut.

  And even the women would have been better off (at least from a glucose tolerance perspective) without their yellow peas, chickpeas, navy beans and lentils - on the classic diet, they lost the same amount of weight and improved their insulin response by 24.2% and thus still 19.4% more than the men (the men had a reduction of -4.8 % in insulin AUC) and 10.3% more than with the pulse diet. I am therefore not convinced whether the scientists' euphoric conclusion that the "frequent consumption of pulses in an ad libitum diet reduced risk factors of the MetSyn [metabolic syndrome] and these effects were equivalent, and in some instances stronger, than counselling for dietary energy reduction" is not a little too optimistic - and that despite the fact that the HOMA-IR Mollar et al. reference as their indicator of improved insulin sensitivity suggests that they may be right...
  And before I forget it, the significant, but still meager improvements in LDL scientists from the University Saskatchevan report in another pulse diet study from the same supplement to the British Journal of Nutrition involving only elderly subjects would not convince me to eat 2x150g of beans, chickpeas, peas or lentils every day, either (Abeysekara. 2012) - why? Contrary to Whitlock et al. who are apparently not very concerned about the "abrasive" effect of pulses on the thickness of the mucosa in the gut (-25% in rodent experts; cf. Whitlock. 2012), I am not going to open up my "internal doors" to foreigners for a minuscule reduction in LDL, alleged improvements in glucose metabolism (see above) and some weightloss that comes about because you are so bloated that you become anorexic by twice let alone thrice daily pulse consumption.

• 

  Figure 5: Fat, TFA intake across age groups and sources (Kris-Etherton. 2012)

  Transfats (TFA): Cakes, cookies, pies and pastries are the worst offenders That's the unsurprising finding of the latest analysis of data from the National Health and Nutrition Examination Survey (NHANES; data from 1999-2002; Kris-Etherton. 2012). Among the 16,669 individuals (age ≥3 years) the median TFA intake was 2.3 % of calories (5 g/day) with 0.9–4.5 % of energy (1.5–13.1 g/day) over different quintiles of intake. The mean (that's the arithmetic mean vs. just the value right in the middle, which is the median) TFA intake was 2.5 % of energy (6.1 g/day).
  The overall range of TFA intakes in the highest quintile was almost crazily broad and ranged from already health compromising 8.8 up to 92.4 g/day. In view of the fact that the lions-share of this shit (sorry, but I just can't find a better name for it) came from cakes, cookies, pies, and pastries, the easiest solution to the problem and a major relief to the future public health insurance system in the US would be to ban this junk from the supermarkets or at least require the use of TFA-free and heat-stable fats in their production... but I think we all know that this is not going to happen, anytime soon.

"What? That's it, already?" If that's what you are just thinking I suggest you take a detour to the SuppVersity Facebook Wall and check out how Citrulline may protect your brain from aging, how your heart might protect itself by becoming insulin resistant and many other recent news from the realms of exercise, nutrition and health science!

References

• Arbeláez AM, Rutlin JR, Hershey T, Powers WJ, Videen TO, Cryer PE. Thalamic Activation During Slightly Subphysiological Glycemia in Humans. Diabetes Care. 2012 Aug 13.
• Abeysekara S, Chilibeck PD, Vatanparast H, Zello GA. A pulse-based diet is effective for reducing total and LDL-cholesterol in older adults. British Journal of Nutrition. 2012; 108:S103-S110.
• Beck B, Richy S, Archer ZA, Mercer JB. Early and persistent up-regulation of hypothalamic orexigenic peptides in rat offspring born to dams fed a high-carbohydrate supplement during gestation. Brain Research. 17 August 2012.
• Gigou PY, Dion T, Asselin A, Berrigan F, Goulet EDB. Pre-Exercise Hyperhydration-Induced Bodyweight Gain Does Not Alter Prolonged Treadmill Running Time-Trial Performance in Warm Ambient Conditions. Nutrients. 2012; 4(8):949-966.
• Kris-Etherton PM, Lefevre M, Mensink RP, Petersen B, Fleming J, Flickinger BD. Trans Fatty Acid Intakes and Food Sources in the U.S. Population: NHANES 1999-2002. Lipids. 2012 Aug 18.
• Lu YC, Hsiao G, Lin KH, Hsieh MS, Jayakumar T, Wu TS, Sheu JR. Cinnamophilin Isolated from Cinnamomum philippinense Protects against Collagen Degradation in Human Chondrocytes. Phytother Res. 2012 Aug 18.
• Lee EJ, Chen HY, Lee MY, et al. Cinnamophilin reduces oxidative damage and protects against transient focal cerebral ischemia in mice. Free Radic Biol Med. 2005; 39: 495–510.
• Lee EJ, Chen HY, Hung YC, et al. Therapeutic window for cinnamophilin following oxygen-glucose deprivation and transient focal cerebral ischemia. Exp Neurol. 2009; 217: 74–83.
• Mollard RC, Luhovyy BL, Panahi S, Nunez M, Hanley A, Anderson GH. Regular consumption of pulses for 8 weeks reduces metabolic syndrome risk factors in overweight and obese adults. British Journal of Nutrition. 2012;108:S111-S122.
• Pisto P, Santaniemi M, Turpeinen JP, Ukkola O, Kesäniemi YA. Adiponectin concentration in plasma is associated with muscle fiber size in healthy middle-aged men. Scand J Clin Lab Invest. 2012 Sep;72(5):395-402.
• Su MJ, Chen WP, Lo TY, Wu TS. Ionic mechanisms for the antiarrhythmic action of cinnamophilin in rat heart. J Biomed Sci. 1999;6: 376–386.
• Tokarska-Schlattner M, Epand RF, Meiler F, Zandomeneghi G, Neumann D, Widmer HR, Meier BH, Epand RM, Saks V, Wallimann T, Schlattner U. Phosphocreatine interacts with phospholipids, affects membrane properties and exerts membrane-protective effects. PLoS One. 2012;7(8):e43178. 
• Tuzcu M, Aslan A, Tuzcu Z, Yabas M, Bahcecioglu IH, Ozercan IH, Kucuk O, Sahin K. Tomato powder impedes the development of azoxymethane-induced colorectal cancer in rats through suppression of COX-2 expression via NF-κB and regulating Nrf2/HO-1 pathway. Mol Nutr Food Res. 2012 Aug 1.
• Whitlock KA, Kozicky L, Yee AJH, Ha C, Morris J, Field CJ, Bell RC, Ozga JA, Chan CB. Assessment of the mechanisms exerting glucose-lowering effects of dried peas in glucose-intolerant rats. British Journal of Nutrition. 2012;108:S91-S102. 
• Wu TS, Leu YL, Chan YY, Yua SM, Tenga CM, Sua JD. Lignans and an aromatic acid from Cinnamomum philippinense. Phytochemistry. June 1994;36(3):785–788
• Yu SM, Ko FN, Wu TS, Lee JY, Teng CM. Cinnamophilin, a novel thromboxane A2 receptor antagonist, isolated from Cinnamomum philippinense. Eur J Pharmacol. 1994; 256: 85–91.

The Ergogenic Effect of Nonalcoholic Beer Front- & Back Loading + 15 Beerish Health Facts Everyone Should Know

Image 1: Erdinger Weißbräu Alkoholfrei your first choice for peri workout isotonic carbohydrate supplementation!?

Where else, if not from Germany, "The Land of Beer and Weißwurst" as it is falsely perceived by the average foreign Oktoberfest visitor, could the data for a study on the ergogenic effects of nonalcoholic beer originate from? In their recently published paper Johannes Scherr and his colleageas from the Department of Prevention and Sports Medicine at the Klinikum rechts der Isar of the Univerisity of Munich report that a 'forntload + post-supplementation' strategy (3 weeks before, 2 weeks after) with 1-1.5l/day of Erdinger Weißbräu Alkoholfrei led to statistically significant reductions in post-race total blood leukocyte counts (-9%) and interleukin-6 (-24%) and 66% lower incidence of upper-respiratory tract infections in the 58 beer-drinking subjects (age: 36-51y), when compared to their 63 peers(age:35-49y) who received an isocaloric control beverage, which differed from the beer only in terms of its polyphenol content (Scherr. 2012).

It's not all about Erdinger Alkoholfrei  - 15 Beerish Health Facts You Should Know

In fact, the ergogenic effects Scherr et al. observed in their most recent study are probably nothing but one of the manifold downstream effects of the nutrient dense non-alcoholic fraction of 'amber nectar', which consists of a whole host of bioactive ingredients with at least as many, mostly beneficial health effects (the following is in part based on Sohrabvandi. 2010; where other references were used, additional references are provided):

How exactly is nonalcoholic beer produced?

• Fermentation-free brewing and dilution procedures won't produce results European or US costumers will be happy with, therefore it is mostly used in Islamic countries
• Alcohol removal by vacuum destillation, adsorptive alcohol removal, dialysis, reverse osmosis, or osmotic distillation
• Restricted alcohol fermentation uses yeast that can only partially ferment the wort or represses or interrupts fermentation by applying different compositional and/or process procedures (interrupted fermentation technique)
• Fermenting with GMO bacteria which lack the alcohol dehydrogenase (ADH) enzyme and produce no or minimal amonts of alcohol.
• Reducing fermentable fractions / glucose content in wort by adjusting the concentration of sugar in the primary formulation so that no considerable sugar residue remains after the restricted fermentation period.
• Heating or pressurizing the wort to inactivate yeast cells and inhibit the subsequent alcoholic fermentation, as soon as the desired flavor profile of the wort was achieved

Note: The beer in the study at hand was brewed under tightly controlled temperature (the exact method is apparently a company secret, though).

• has potentially blood pressure lowering effect due to high potassium to sodium ratio (typically 4:1) 
• is relatively rich in magnesium and to less extent in phosphorous
• contains glutathione precursors and co-factors zinc, copper, selenium and amino acids
• features physiologically active immuno-modulatory peptides and proteins
• has 35+ phenolic compounds (about 80–90% from malt and 10–20% from hops)
• may prevent and improve obesity and type-2 diabetes, improve lipid metabolism, and suppress atherosclerosis due to beneficial health effects of the bitter substances in hops (Kondo. 2004)
• has been shown to improve sleep and lactation in women; probably due to bioactive molecules from hops (Koletzko. 2000; Franco. 2012)
• contains folate and glycine betaine which exert antimutagenic effects and reduce homocysteine
• has up to 6.2g fiber per liter
• its β-pseudouridine content may protect against radiation damage (Monobe. 2003)
• contains silicic acid which increases renal excretion of aluminum (Aluminum has been associated with age related diseases and neurodegeneration; cf. Krewski. 2007)
• is associated with higher hip mineral density in older men who drink 2 regular beers/day; probably due to its silicon content (Tucker. 2009)
• provides more antioxidants per day than wine to the U.S. diet (Vinson. 2003)
• exerts anti-oxidative effects on lipoproteins (=cholesterol) which are superior to that of its vitamin & antioxidants, alone (Vinson. 2003)
• unfortunately, allegedly gluten-free barley based beers contain significant amounts of hordein (=gluten) and are not suitabe for patients with celiac disease (Colgrave. 2012)

Now compare that to your average energy drink, which - as you should by now be aware of - may deliver zero fat calories and will still add 18g /day of body fat right to your frame, when consumed on a daily basis (cf. "Fat Content Per Energy Drink 0g, Body Fat Gain Per Energy Drink 18g!")

Image 2 (FOX): Homer always knew what Schütze et al. confirmed in 2009: "Beer consumption leads to [waist circumference] gain [...] closely related to overall weight gain. This study does not support the common belief of a site-specific effect of beer on the abdomen."

Implications: In view of the fact that carbohydrate supplementation is still common practice among endurance athletes, I don't see why a refreshing nonalcoholic beer (1.5l of Erdinger Weißbreu Alkoholfrei contain 375kcal and ~75g of carbohydrates)  that has been brewed according to the German purity law should not be at least as good as one of those sugar-laden electrolyte drinks or gels with artificial colorings and what not.

Moreover, the relatively high phenolic content of the beer (~400 mg of gallic acid equivalents per day), of which Scherr et al. speculate that it was the underyling reason for the observed benefits, could render the use of other polyphenolic supplements obsolete, save you money and keep you healthy and sane, as only few people are like me don't like the taste of beer and can thus sit in the Biergarten with nothing but plain water, while their friends hoist brew after brew... although, when I come to think about it: Maybe I should order some Erdinger later today? *rofl*

---

Note: The study was financed from a fund that was established by the Erdinger Weissbraeu, Werner Brombach GmbH. Contrary to some other researchers Scherr et al. do yet openly disclose the funding and state that "the funders had nodirect role in the study’s design, conduct, analysis, interpretation of data, and reporting" - and before you start lamenting, now, think about who finances and conducts the studies on pharmaceuticals...

References:

• Colgrave ML, Goswami H, Howitt CA, Tanner GJ. What is in a beer? Proteomic characterization and relative quantification of hordein (gluten) in beer. J Proteome Res. 2012 Jan 1;11(1):386-96.
• Franco L, Sánchez C, Bravo R, Rodríguez AB, Barriga C, Romero E, Cubero J. The sedative effect of non-alcoholic beer in healthy female nurses. PLoS One. 2012;7(7):e37290. Epub 2012 Jul 18.
• Koletzko B, Lehner F. Beer and breastfeeding. Adv Exp Med Biol. 2000;478:23-8. Review.
• Kondo K. Beer and health: preventive effects of beer components on lifestyle-related diseases. Biofactors. 2004;22(1-4):303-10.
• Krewski D, Yokel RA, Nieboer E, Borchelt D, Cohen J, Harry J, Kacew S, Lindsay J, Mahfouz AM, Rondeau V. Human health risk assessment for aluminium, aluminium oxide, and aluminium hydroxide. J Toxicol Environ Health B Crit Rev. 2007;10 Suppl 1:1-269.
• Monobe M, Arimoto-Kobayashi S, Ando K. Beta-pseudouridine, a beer component, reduces radiation-induced chromosome aberrations in human lymphocytes. Mutat Res. 2003 Jul 8;538(1-2):93-9.
• Scherr J, Nieman DC, Schuster T, Habermann J, Rank M, Braun S, Pressler A, Wolfarth B, Halle M. Nonalcoholic beer reduces inflammation and incidence of respiratory tract illness. Med Sci Sports Exerc. 2012 Jan;44(1):18-26.
• Schütze M, Schulz M, Steffen A, Bergmann MM, Kroke A, Lissner L, Boeing H. Beer consumption and the 'beer belly': scientific basis or common belief? Eur J Clin Nutr. 2009 Sep;63(9):1143-9. Epub 2009 Jun 24.
• Sohrabvandi S, Mousavi SM, Razavi SH, Mortazavian AM, Rezaei K. Alcohol-free Beer: Methods of Production, Sensorial Defects, and Healthful Effects, Food Reviews International. 2010;26:4, 335-352
• Tucker KL, Jugdaohsingh R, Powell JJ, Qiao N, Hannan MT, Sripanyakorn S, Cupples LA, Kiel DP. Effects of beer, wine, and liquor intakes on bone mineral density in older men and women. Am J Clin Nutr. 2009 Apr;89(4):1188-96.
• Vinson JA, Mandarano M, Hirst M, Trevithick JR, Bose P. Phenol antioxidant quantity and quality in foods: beers and the effect of two types of beer on an animal model of atherosclerosis. J Agric Food Chem. 2003 Aug 27;51(18):5528-33.

Rodent Study Suggests: Selenium, Nature's Neuronal Corrosion Inhibitor Could Protect the Brains of Hard Training Athletes from Oxidative Damage.

Image 1: Selenium is a naturally occurring mineral
involved in a host of metabolic processes.

Are you a hard training athlete? A weekend warrior? Marathon runner? Or just an an average fitness-enthusiast? Yes? Did you ever think about what an exhausting workout, let alone arduous marathon running may do to your brain? No? Then it may come as a surprise to you that other than regular moderate physical exercise, which has repeatedly been shown to exert beneficial effects on mental and physical development, intense exercise precipitates oxidative stress not only in the working muscle groups, but within your whole body - including your brain, where the exercise-induced increase in free-radicals may dramatically increase lipid oxidation (Goldfarb.1996; Kanter. 1998).

Based on observations with other antioxidants and the well-established involvement of selenium in the activation of the master-antioxidant glutathion, researchers from the Selcuk University in Konya, Turkey, hypothesized that supplementation with yet to be determined amounts of selenium might ameliorate the detrimental effects of arduous exercise (Akil. 2011). To verify their hypothesis, the Akil et al. subjected a group of 4-6 month old Sprague-Dawley rats to one out of four treatments for 4 weeks:

• group 1: unsupplemented sedentary control
• group 2: selenium supplemented, sedentary control
• group 3: swimming control (30 minutes in a closed glass-swimming pool; 50x50cm)
• group 4: selenium supplemented + swimming (same as group 3)

Both, the animals in group 2 and group 4 were supplemented with additional  0.6mg/kg of selenium selenite per day. For an 80kg adult human being the human equivalent dose of 0.098mg or 90mcg per kilogram of body weight would amount to 7.8mg of additional selenium per day, a dose, of which textbook knowledge tells us that it is way beyond the upper-limit of 0.8mg/day. Yet, for the rats, this supposedly toxic amount of selenium turned out to be quite beneficial.

For more on the beneficial effects high doses of selenium may have and a short discussion of toxicity issues, see my previous post on "NAC + Zinc + Selen = Silver Bullett Against Mercury Poisoning"

As the data in figure 1 shows, the non-supplemented arduously exercising rats (group 3) had by far the highest malondialdehyde (MDA is an accepted marker of unwanted oxidation) levels. On the other hand, the MDA levels of the supplemented group were reduced by 11%. Compared to the sedentary controls, which had identical (i.e. within the statistical margin) MDA levels, the malondialdehyde content of their brains was still elevated by 57%. While selenium supplementation may thus have ameliorated the increase in brain MDA levels, it was not able to completely protect the rat-brains from free-radical induced oxidation processes.

Figure 1: Malondealdehyde (MDA) and glutathione levels in rat brains after 30 minutes of exhaustive swimming exercise (data adapted from Akil. 2011)

Interestingly, in both, the supplemented, as well as the non-supplemented exercise groups brain glutathion levels (GSH) increased by 124% and 71%, respectively - probably to protect the brain from extensive oxidation. Under this assumption the selenium induced increase in glutathione levels, which lead to a 53% greater GSH increase in the brains of the rats in the selenium supplemented swimming group, would adequately explain the lower MDA levels of the high selenium group.

While it would have been nice to see a comparison of the effects of different doses and exercise protocols, the study at hand is just another hint a the importance of a mineral, that was believed to be toxic up to the late 1950. Consequently, this is neither the first, nor will it be the last time you read about this extraordinary mineral on the SuppVersity - stay tuned for more!

The Ugly Side of Recovery

So, the big events for the year are over.  Most of my blogging is about the weeks leading up to a race, but this post is all about race day to race day + 30, and the things many of us go through after a race, most of which aren't as fun as racing, or training to race.

The Post Race Blues

After both my big events for the year I was a little down.  It’s very normal to feel this way, most athletes go through it.  It’s not about not meeting goals.  In my case I did what I set out to do.  It’s more about realigning yourself.  For months, you train for this huge event.  You balance your life to train for the event, eat so you’re faster, sleep to recovery from that training, and then…it’s over.  It feels a bit like the 10 minutes after Christmas morning as a child. 

One of the best things you can do to fight the post race blues is to have a plan.  Where are you going from here?  What’s next?  The time after a race is a great time to plan your next block of training, and your next goal. 

Also, be sure to celebrate your success.  Talking about your race with friends, writing race reports, or even blogging (like I am right now), are all good ways to keep these anticlimactic feelings in check.

Supersized Weight Gains

After a race that requires me to put it all out there, I gain a TON of weight.  This didn’t really happen to me until this year, which I attribute to this being the first year I possessed the strength to really push my body to its fitness limits.  I normally weigh anywhere from about 177-182 at racing weight.  Immediately after the 70.3 and the mary my weight jumped up to the 190-200 range.  My body fat numbers based on the caliper also jumped up.  The week after the 70.3 I was measured by the Bod Pod at ISU and it was crazy high as well.  Those numbers stayed very elevated for a week, and then after one night of many many bathroom trips, all was back to normal. 

The first time it happened, after the 70.3, I freaked out a bit and started eating at a caloric deficit.  Not only did this not help the scale number but it took over a month for me to be able to push on the bike at the level I was pre-race.  I saw the big numbers, reacted with my gut instead of my head, and the result was that I screwed up my recovery.  IMPORTANT:  The week or weeks after your big event are NOT the times to be running a caloric deficit. 

Constant Hunger

I do believe that fiber, fat and protein consumption all play a role in abating hunger, however another key contributor to hunger is the volume of food you’re eating.  If you are used to eating 4000 calories of healthy food a day in the build up to a big event, and then suddenly you no longer have those energy needs and you’re back to 2000 calories a day, you’re going to be hungry. 

Here are some ways I cope with this:

1.   Meet Your Energy Needs – Even if you have some weight to lose, the weeks after a big event aren’t the weeks to lose it.  Recovery comes first, and you can’t rebuild your body nearly as quickly when running a caloric deficit.

2.   Know Recovery Requires Energy – You might want to estimate your energy needs a little on the high side when recovering from a big event.

3.   Follow Your Cravings – Within reason, indulge your cravings and consider what they are telling you.  After my 70.3 I wanted red meat, which is very unusual for me because that’s a food I eat very rarely.  So, I ate some steak, and burgers once or twice.   This was likely a signal to eat fat, protein, or perhaps increase my iron.  After the Marathon I was craving leafy green vegetables and pecans.  Again, this may have been a signal to increase my fat and iron.  Either way, making sure my diet is high in protein, healthy fat, and lots of micronutrients like iron is a great way to speed recovery and fight that hungry feeling. 

4.   Volume - Focus on high volume, nutrient dense, low caloric density foods (plants).

5.   Get A Little Fatter – This is one of those do as I say things.  My history causes me to struggle with this one.   There is a body of research that shows it’s healthy for athletes to gain a little weight in the off season, and work back down to your racing weight.  I’m clearly not good at this, but I figured I’d put it out there anyway, for the sake of completeness.

Getting Back On Your Feet

That first ride or run after a big race might be a little rough, if not on your body, on your mind.  After racing at a fully tapered race pace, that first easy run might seem not so easy.  For a few weeks though, anything more than very easy, is probably going to hurt more than help. 

1.   The Day After - After a big event, I like to take at least one day completely off.  I will spend my time walking around, which helps keep loose and increases blood flow, hopefully minimizing soreness.  The day after my 70.3, Lana and I picked blueberries at a local farm.  The day after the marathon we walked the grounds of an art museum I ran through as part of the marathon course.  Seeing the sights at a destination race is probably the most fun way to keep active post race. 

2.   Start In The Water - I always start with swimming when I’m ready to train again.  Swimming is pretty easy on the body.  It’s the shortest of the three events in a triathlon, and I’m not a strong enough swimmer to really push that hard anyway, so it tends to be a pretty safe bet that an easy swim is a good first step back to training. 

3.  Run Last – I’ll add in some high cadence low effort cycling when I’m ready.  Running comes last.

4.   No Schedules – For the 2-3 weeks following a big event, I make all my training unscheduled.  I just do as much or as little as I feel like, when I feel like doing it, as long as it’s all easy.  This is as much for the mental break as the physical rest. 

5.   Avoid Threshold Work – It’s worth saying again, the goal here is to burn some calories, flush out all the garbage in your legs and arms, and get in some active recovery.  Work at, or near, threshold breaks things down more than it speeds recovery.  It’s best to avoid training at any real intensity during a recovery period.

6.   Clear those Nagging Injuries – So, it’s been a few weeks, I’m feeling fresh and my muscles don’t hurt or feel sluggish…but is that knee still bothering me?   You know all those nagging overuse problems you developed in a big build that you’ve been ignoring? This is the time to clear them out. 

Believe me, I don't have it all figured out.  I learned alot about recovery this season though, and this is some of the stuff that has really helped me.  Hopefully it might help you too.