3g Taurine Improve Post-Workout Glycogen Resynthesis, Protect the Testes of Doping Sinners & Battles Alzheimer's

Taurine - A useful supplement for chemical, natural athletes and even sedentary slobs who are afraid of diabetes.

Taurine, or 2-aminoethanesulfonic acid, as Wikipedia says, is an organic acid widely distributed in animal tissues. It is a major constituent of bile and can be found in the large intestine, and accounts for up to 0.1% of total human body weight. That does not sound like much, but taurine has many fundamental biological roles, such as conjugation of bile acids, antioxidation, osmoregulation, membrane stabilization, and modulation of calcium signaling. It is essential for cardiovascular function, and development and function of skeletal muscle, the retina, and the central nervous system and you were thus probably not too surprised, when you've recently read on the SuppVersity Facebook Page that taurine may help with Alzheimer's disease.

You can learn more about taurine & other amino acids at the SuppVersity

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In the corresponding paper that was published only recently in the ScientificReports on Nature.com Kim et al. report that orally administered taurine via drinking water rescued the cognitive deficits in a standard rodent model of Alzheimer's (APP/PS1 mice) and brought them back up to age-matching wild-type mice.

Figure 1: Improvement in spatial and hippocampal learning behaviours in taurine-treated transgenic mice. 7-month old wild-type (Wt) and agematched APP/PS1 transgenic (Tg) male mice were orally administered water or taurine (1,000 mg/kg/day) for 6 weeks (n 5 8–10 per group). After 6 weeks, behavioural tests were administered to the 8.5-month old mice. (Left) Y-maze. Average alternation (%) of each group of mice was calculated. (Right) Passive avoidance. Average latency time in seconds for each group of mice was measured (Kim. 2014).

That's unquestionably impressive, but what's more impressive is that this is by far not the first study to report that taurine exhibits a plethora of physiological functions in the central nervous system.

But taurine gives me diarrhea! If it does try taking it with a meal that will greatly reduce the risk of having to rush to the toilette and should not reduce the physiological benefits significantly. At least for the muscular effects its unlikely that it will matter at all. For the beneficial effects on the brain, it may be necessary to achieve higher serum peak levels. In view of the fact that the rodents in the aforementioned study by Menzie et al. received the taurine in the drinking water, even this is yet unlikely. If the taurine "goes right through", though, it's certainly not going to help you ;-)

In a recent review in the scientific journal Amino Acids review, Janet Menzie et al. describe the mode of action of taurine and its clinical application in the neurological diseases: Alzheimer’s disease, Parkinson’s disease and Huntington’s disease and conclude that taurine...

"[...] functions through multiple neuroprotective mechanisms: regulation of cellular osmolarity , anti-oxidant, neuromodulator of GABAergic transmission, maintenance of calcium homeostasis, inhibition of glutamate excitotoxicity, attenuation of endoplasmic reticulum stress, modulation of mitochondrial pore permeability, downregulation of a range of proapoptotic proteins while upregulating anti-apoptotic proteins and downregulation of inflammatory mediators." (Menzie. 2014)

Moroever, Menzie et al. believe that there is "strong evidence" of the existence of a specific taurine receptor, which is activated exclusively by taurine, but not by structurally similar amino acids such as glutamate, GABA and glycine and could be responsible for many of the beneficial effects taurine exerts in the context of central nervous system disorders. More specifically existing evidence clearly suggests protective effects in Alzheimer’s, Parkinson and Huntington diseases. Three pathologies that share a number of broad mechanisms: Oxidative stress, mitochondrial dysfunction, excitotoxicity, calcium imbalance, inflammatory changes apoptosis - and *tadaa* a reduced level of (Arai. 1985; Alom. 1991; Molina. 1997).

Enough of the health stuff, what about the post-workout goodness?

I know, as long as we are healthy we don't really care about debilitating central nervous system disorders... well, ok. I will spare you my moral pointing finger and get straight to the similarly unsurprising results of a recent study from the University of Tokyo. A study which clearly indicates that the provision of taurine after workouts can lead to a significant enhancement of the already elevated glycogen synthesis after your workouts.

Figure 2: Muscle and liver glycogen and serum free fatty acids (FFA) before and after the workout (Takahashi. 2014).

In two rodent studies, the Japanese researchers tested whether the oral administered of taurine  at a dosage of 0.5 g/kg body weight (for human beings that's 0.04g/kg or approximately 3g total | the SuppVersity suggested dose from previous articles, by the way) immediately after treadmill running at 25 m/ min for 90 min would alter the metabolic response and glycogen synthesis after workouts when it was (A) administered alone or (B) as part of a glucose solution containing taurine and glucose at a ratio of 1:2 - in this case 0.5g/kg taurine and 1.0g/kg glucose.

Figure 3: AUC for glucose after for 60min and 120min after the ingestion of the taurine + glucose solution. As the data indicates taurine helped to "clear" the sugar from the blood stream (Takahashi. 2014).

As the scientists point out, their "results show that post-exercise taurine administration enhances glycogen repletion in skeletal muscle" (Takahashi. 2014). The underling cause, however, is still speculative. Takahashi et al. believe that it is triggered by

1. 

   Figure 4: Changes in general oxidative damage (TBARs), protein damage and exercise performance in response to taurine vs. placebo vs. bet alanine supplementation; expressed relative to untrained control (Dawson. 2002).

   an acceleration of glucose uptake, and
2. an increase in fat oxidation

of which the latter will have a carbohydrate sparing effect and will thus leave a higher amount of carbs for glycogen repletion. In conjunction with previously established benefits of taurine, such as

• the attenuation of exercise-induced DNA damage during workouts (young men | Zhang. 2004),
• the amelioration of cytotoxic (cell damaging) effects of exercise (rodents | Dawson. 2002),
• an increase in exercise performance (specifically endurance ex. | Dawson. 2002; Miyazaki. 2004),
• additional effects on the benefits of BCAA intake for the delayed-onset muscle soreness and muscle damage induced by high-intensity eccentric exercise (Ra. 2013),
• an improvement in osmoregulation (water balance) of the muscle (Cuisinier. 2002), and
• decreases in oxidative stress during eccentric exercises (Silva. 2011)

The optimal dosing for performance increments, by the way, is between 1.2-6.0g for 2 weeks (other timing has not been tested, so it's possible that one week will suffice, too). That's at least what the only hitherto published study that investigated the effects of different doses of taurine as a means to improve the endurance performance (Miyazaki. 2004). If you want the nutrient partitioning effects, though, you would have to consume CHO + taurine after the workout - 3g of taurine should suffice. Judged by the hitherto published studies this should automatically help you to increase your workout performance after 2 weeks (the beneficial effects will, just as it is the case for creatine, accumulate until the levels are saturated).

And there are more benefits - health benefits, for juicers and non-juicers

The former, i.e. the juicers will probably be happy to hear that taurine does not just have liver protective effects (Miyazaki. 2005), but will also reverse the nandrolone decanoate induced perturbations in sperm characteristics, normalize the serum testosterone level, and restore the activities of the key steroidogenic enzymes in rodents that are treated with nandrolone and taurine (at a dosage equivalent to only 1.3g/day | Ahmed. 2014).

In spite of the fact that the administration of taurine did also prevent the nandrolone decanoate-induced testicular toxicity and DNA damage by virtue of its antioxidant, anti-inflammatory, and anti-apoptotic effects, I would like to point out that this article is not intended as an incentive for nandrolone doping.

While taurine is not made from the sperm of Belgian Blues it may still boost your testosterone levels - whether that's going to be by 140% as in this study is questionable, though.

From performance to health doping: If you are not into "natural performance enhances" and don't care about the direct performance increases, reduced oxidative damage and increases in glycogen repletion during workouts. I would recommend you reread the previous SuppVersity article about the testosterone boosting effects of taurine, it's ability to improve your strength and recovery during and after resistance training sessions, as well as it's ability to improve your glucose metabolism (Franconi. 2006; Carneiro. 2009), to increase your glucose sensitivity (Han. 2004; Nakaya. 2000), to prevent insulin resistance in hyperglycemic states (Haber. 2003), to prevent the development of hypertension as a result of fructose overfeeding (Rahman. 2011), to prevent the cardiac damage due to iron overload (Oudit. 2004), to protect you from the kidney damaging assault of chemotherapy (Saad. 2010), and god knows which benefits I have simply forgotten in the aforementioned list | Comment of Facebook!

References:

• Ahmed, Maha AE. "Amelioration of Nandrolone Decanoate-Induced Testicular and Sperm Toxicity in Rats by Taurine: Effects on Steroidogenesis, Redox and Inflammatory Cascades, and Intrinsic Apoptotic Pathway." Toxicology and Applied Pharmacology (2014).
• Alom, J., et al. "Cerebrospinal fluid taurine in Alzheimer's disease." Annals of neurology 30.5 (1991): 735-735.
• Arai, Heii, et al. "A preliminary study of free amino acids in the postmorten temporal cortex from Alzheimer-type dementia patients." Neurobiology of aging 5.4 (1985): 319-321. 
• Carneiro, Everardo M., et al. "Taurine supplementation modulates glucose homeostasis and islet function." The Journal of nutritional biochemistry 20.7 (2009): 503-511.
• Cuisinier, Claire, et al. "Role of taurine in osmoregulation during endurance exercise." European journal of applied physiology 87.6 (2002): 489-495.
• Dawson Jr, R., et al. "The cytoprotective role of taurine in exercise-induced muscle injury." Amino acids 22.4 (2002): 309-324. 
• Franconi, Flavia, et al. "Taurine supplementation and diabetes mellitus." Current Opinion in Clinical Nutrition & Metabolic Care 9.1 (2006): 32-36.
• Haber, C. Andrew, et al. "N-acetylcysteine and taurine prevent hyperglycemia-induced insulin resistance in vivo: possible role of oxidative stress." American Journal of Physiology-Endocrinology and Metabolism 285.4 (2003): E744-E753.
• Han, Jin, et al. "Taurine increases glucose sensitivity of UCP2-overexpressing β-cells by ameliorating mitochondrial metabolism." American Journal of Physiology-Endocrinology and Metabolism 287.5 (2004): E1008-E1018. 
• Kim, Hye Yun, et al. "Taurine in drinking water recovers learning and memory in the adult APP/PS1 mouse model of Alzheimer's disease." Scientific Reports 4 (2014).
• Menzie, Janet, et al. "Taurine and central nervous system disorders." Amino acids 46.1 (2014): 31-46.
• Miyazaki, T., et al. "Optimal and effective oral dose of taurine to prolong exercise performance in rat." Amino Acids 27.3-4 (2004): 291-298.
• Miyazaki, Teruo, et al. "Taurine inhibits oxidative damage and prevents fibrosis in carbon tetrachloride-induced hepatic fibrosis." Journal of hepatology 43.1 (2005): 117-125.
• Molina, José A., et al. "Decreased cerebrospinal fluid levels of neutral and basic amino acids in patients with Parkinson's disease." Journal of the neurological sciences 150.2 (1997): 123-127.
• Nakaya, Yutaka, et al. "Taurine improves insulin sensitivity in the Otsuka Long-Evans Tokushima Fatty rat, a model of spontaneous type 2 diabetes." The American journal of clinical nutrition 71.1 (2000): 54-58.
• Oudit, Gavin Y., et al. "Taurine supplementation reduces oxidative stress and improves cardiovascular function in an iron-overload murine model." Circulation 109.15 (2004): 1877-1885.
• Rahman, Mizanur M., et al. "Taurine prevents hypertension and increases exercise capacity in rats with fructose-induced hypertension." American journal of hypertension 24.5 (2011): 574-581.
• Saad, Sherif Y., and Ammar C. Al-Rikabi. "Protection effects of taurine supplementation against cisplatin-induced nephrotoxicity in rats." Chemotherapy 48.1 (2010): 42-48.
• Silva, Luciano A., et al. "Taurine supplementation decreases oxidative stress in skeletal muscle after eccentric exercise." Cell biochemistry and function 29.1 (2011): 43-49. 
• Takahashi, Yumiko, et al. "Post-exercise taurine administration enhances glycogen repletion in tibialis anterior muscle." The Journal of Physical Fitness and Sports Medicine 3.5 (2014): 531-537.
• Zhang, M., et al. "Role of taurine supplementation to prevent exercise-induced oxidative stress in healthy young men." Amino acids 26.2 (2004): 203-207.

Do the Anti-Alzheimer's Effects of Grape Seed Extract (GSE) Start in the Gut? Your Gut Bugs Could Save Your Brain

The gut may be the missing piece to the Alzheimer's puzzle.

It is well-established that an phenolic extract from the seeds of grapes (GSPE) can have significant anti-Alzheimer's and general neuroptective and anti-dementia effects (Sarkaki. 2007; Balu. 2005; Wang. 2009).

In their latest study, scientists from the University of Queensland did now, for the first time, investigate the role your intestinal microbiota may play in the metabolism and production of orally ingested and newly formed polyphenolic compounds that will then mediate the attenuation of Alzheimer’s disease β-amyloid oligomerization.

If you are concerned about brain health, keep an eye on your circadian rhythm

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While it is well-known hat the intestinal microbiota is known to actively convert many dietary polyphenols, including GSPE, to phenolic acids, there has as of now been very limited information on the bioavailability and bioactivity of GSPE-derived phenolic acid in the brain.

The latter, i.e. the ability of these compounds to actually make it into the brain, however, is of obvious importance for them to elicit any of those impressive effects that have previously been observed in the petri dish or with direct injection into the brain of rodents. To know, whether the intestinal metabolism of orally ingested grape seed polyphenol extracts (GPSEs) will impair or maybe even increase the uptake and metabolism and thus the effect of grape seed extracts is therefore of utmost importance.

No, "Microbiomes", that's no typo. We host bacteria all over and in us (Cho. 2012)

Grape seed extracts are not the only link between our microbiomes and Alzheimer's disease: Previous research clearly suggest that an unhealthy oral microbiome predisposes to dementia and Alzheimer's (Shoemark. 2015). And Hill et al. who establish in their latest review that "{t]he potential contribution of pathogenic microbes to aging and AD is becoming increasingly recognized (Miklossy, 2011; Cho and Blaser, 2012; Bhattacharjee and Lukiw, 2013; Poole et al., 2013; Heintz and Mair, 2014; Huang et al., 2014; Mancuso et al., 2014)", believe that the similarity of the pathology of Alzheimer's which includes inflammation, brain cell atrophy, immunological aberrations, amyloidogenesis, altered gene expression and cognitive deficits and the symptoms of can hardly be coincidental (Hill. 2014).

Accordingly, the same goes for what would happen to the 12 phenolic of which scientists had previously found that they would be produced by common gut bacteria when they metabolize orally administered GSPE.

Figure 1: Tentative metabolic route of GSPE PAC and molecular formulas of PAC derived phenolic acids (left | Wang. 2015); illustration of the general mechanism of action.

As the results of the study at hand show, only two of them, i.e.3-hydroxybenzoic acid (3-HBA) and 3-(3´-hydroxyphenyl) propionic acid (3-HPP) actually make it into the brains of mice who are orally gavaged with either 25mg/kg or 250mg/kg (for humans that's 160mg/day or 1,600mg/day) where they accumulate atµM concentrations that would be high enough to explain the beneficial effects scientists observed in previous rodent and huma studies.

Figure 2: The electron microscopy images show quite clearly that both GSPE metabolites inhibit the dangerous crosslinking of β-amyloid (Aβ) peptides into neurotoxic Aβ aggregates which renders originally "harmless" plague into a debilitating toxin (Wang. 2015). 

The latter is not surprising, by the way. Want et al. were after all able to show that both, 3-HBA and 3-HPP, potently interfere with the assembly of β-amyloid (Aβ) peptides into neurotoxic Aβ aggregates that play key roles in AD pathogenesis.

What does this mean? While it may at first not be relevant how exactly GPSE supplements may protect you from Alzheimer's disease, the results of the study at hand do have two very important implications:

Previous studies, likewise covered here at the SuppVersity indicate that "1.3g of Grape-Seed Extract Could Protect You From Oxidative Damage, Viral Infections, Obesity and Insulin Resistance, Reduce Your Heart Rate and Blood Pressure and Increase Your Nitric Oxide Production by a Whopping  >25%" | read more

Firstly, for medical treatments one could use ready-made supplements or injections of 3-hydroxybenzoic acid (3-HBA) and 3-(3´-hydroxyphenyl) propionic acid (3-HPP) to elicit maximal protective effects. This would probably not help us to cure, but maybe to stop the progress of dementia.

Secondly, the efficacy of GPSE supplements as Alzheimer's protectants may well depend on the "correct" make-up of your gut microbiome. Assuming you have the wrong or too few of the right bacteria, the conversion to 3-hydroxybenzoic acid (3-HBA) and 3-(3´-hydroxyphenyl) propionic acid (3-HPP) may be so compromised that the protective effect is lost. It would thus be interesting to see which bacteria, exactly are doing the trick to estimate whether or not there may be people who are at risk of getting no benefit out of GSPE supplementation... which happens to be anti-microbial (=kills bacteria) in itself (Baydar. 2006; Sivarooban. 2008), by the way | Comment on Facebook!

References:

• Balu, Muthaiya, et al. "Age-related oxidative protein damages in central nervous system of rats: modulatory role of grape seed extract." International journal of developmental neuroscience 23.6 (2005): 501-507.
• Baydar, Nilgun Gokturk, et al. "Determination of antibacterial effects and total phenolic contents of grape (Vitis vinifera L.) seed extracts." International journal of food science & technology 41.7 (2006): 799-804.
• Bhattacharjee, Surjyadipta, and Walter J. Lukiw. "Alzheimer's disease and the microbiome." Frontiers in cellular neuroscience 7 (2013).
• Cho, Ilseung, and Martin J. Blaser. "The human microbiome: at the interface of health and disease." Nature Reviews Genetics 13.4 (2012): 260-270.
• Heintz, Caroline, and William Mair. "You are what you host: microbiome modulation of the aging process." Cell 156.3 (2014): 408-411.
• Huang, Wei-Shih, et al. "Association between Helicobacter pylori infection and dementia." Journal of Clinical Neuroscience 21.8 (2014): 1355-1358.
• Hill, James M., et al. "Pathogenic microbes, the microbiome, and Alzheimer’s disease (AD)." Frontiers in aging neuroscience 6 (2014).
• Mancuso, Roberta, et al. "Titers of Herpes Simplex Virus Type 1 Antibodies Positively Correlate with Grey Matter Volumes in Alzheimer's Disease." Journal of Alzheimer's Disease 38.4 (2014): 741-745.
• Miklossy, Judith. "Emerging roles of pathogens in Alzheimer disease." Expert reviews in molecular medicine 13 (2011): e30.
• Poole, Sophie, et al. "Determining the presence of periodontopathic virulence factors in short-term postmortem Alzheimer's disease brain tissue." Journal of Alzheimer's Disease 36.4 (2013): 665-677.
• Sarkaki, Alireza, Yaghoub Farbood, and Mohammad Badavi. "The effect of grape seed extract (GSE) on spatial memory in aged male rats." Pakistan Journal of Medical Sciences 23.4 (2007): 561.
• Shoemark, Deborah K., and Shelley J. Allen. "The Microbiome and Disease: Reviewing the Links between the Oral Microbiome, Aging, and Alzheimer's Disease." Journal of Alzheimer's Disease 43.3 (2015): 725-738.
• Sivarooban, T., N. S. Hettiarachchy, and M. G. Johnson. "Physical and antimicrobial properties of grape seed extract, nisin, and EDTA incorporated soy protein edible films." Food Research International 41.8 (2008): 781-785.
• Wang, Yan-Jiang, et al. "Consumption of grape seed extract prevents amyloid-β deposition and attenuates inflammation in brain of an Alzheimer’s disease mouse." Neurotoxicity research 15.1 (2009): 3-14.
• Wang, Dongjie, et al. "Role of intestinal microbiota in the generation of polyphenol derived phenolic acid mediated attenuation of Alzheimer's disease β‐amyloid oligomerization." Molecular Nutrition & Food Research (2015).