No-Carb Foods, Artificial Sweeteners & The Cravings: In The End, It's The Glucose, Not The Taste Our Brains Crave

Despite the fact that candy is per definition (literally) made of sugar, you can buy "no carb candy" at every corner. The results of this study tell you why these aren't worth the money.

I have written extensively about artificial sweeteners in the past and would thus hope that it's not necessary to recount all the information about how they interact with insulin, potential toxicity risks, their (non-existent) effects on satiety... ah, well actually I do want to talk about the last point, because it is highly relevant to understand the implications of the results of recent Yale study (Tellez. 2013).

I know, it's just a rodent study, but I guess you will feel reminded of yourselves during your diet, when I tell you about the observations Luis A Tellez, Xueying Ren, Wenfei Han, Sara Medina, Jozelia Ferreira, Catherine Yeckel and Ivan E de Araujo made an experiment that is the first to demonstrate that the lack of glucose utilization in the brain makes artificial sweetener totally unattractive to mice.

Did you ever realize that sweeteners just won't cut it, when you're hungry?

Many of you may know that: You are dieting and you are craving - food in general, but pasta, candy and all the other carbohydrate-laden foods even more so. You've been training hard and feel that your blood glucose levels are right in the no-man's land between "just high enough to keep standing" and "already so low that you have to sit down". This is the time when you will begin to feel cold. You are sweating or getting shaky (these symptoms vary from person to person), get moody or feel like you had to run even more just to abstain from doing the one thing of which you know that it would solve all your problems (temporarily): Heading over to the kiosk next door and buying the next best Snickers or Mars bar.

Yes, Adelfo Cerame is a professed, but reformed carbophobic. Learn more about how reintroducing carbs into his diet finally got him his pro-card in this and his other guest posts

The poor critters in the study Tellez et al. conducted did not have a kiosk available. What they did have, though, was glucose and artificially sweetened water. Now, the scientists conducted the same experiment in two conditions.

• During condition one, the rodents were fed, satiated and happy (fed). 
• During condition two, however, they had been glucose deprived and were in a similar state as you may have been after the previously described workout. 

What's quite telling (and by the way new) is that the glucose availability had a major impact on their sweetener preferences. When fed and happy, the mice went for the super-sweet sugar- and calorie-free artificially sweetened water.

The disgustingly sweet but glucose-free water did however lose all its appeal once the mouse brains realized that the glucose supply was becoming tight:

"Consistently, hungry mice shifted their preferences away from artificial sweeteners and in favour of glucose after experiencing glucose in a hungry state." (Tellez. 2013)

And what's more, this deliberate(?), or probably instinctive, decision to turn their back on the fake sugars and avail themselves of the "real sweet deal" of which they new it would deliver what the mice needed was immediately rewarded. Rewarded in the most physiological sense of the word: with a whopping dose of dopamine, the very hormone that entrains stimulus < > response relationships like these.

Sugar will increase dopamine, sweeteners won't

You can tell how real this "conditioning" effect was from another observation the researchers made, when they analyzed the brain activity of their lab animals and found that a big gulp from the sugar water did not just bring the blood glucose of the sugar-deprived animals back up, it

"was [also] found to produce significantly greater levels of dopamine efflux compared to artificial sweetener in dorsal striatum" (Tellez. 2013)

When the scientists artificially disrupted the oxidation of glucose directly at the level of the dorsal striatum, which is also known as the neostriatum or striate nucleus that is activated by stimuli associated with reward and aversive, novel, unexpected, or intense stimuli, the sweetness preferences of the mice remained the same. This observation directly supports the conclusion that we are in fact dealing with a fundamental food-reward effect here; and effect, of which you can be certain that is is also involves in "past addiction" ;-)

So what does this tell you about fake foods?

Suppversity highly suggested read: "Science Round-Up Seconds: The Pro-Insulinogenic Effect of Artificial Sweeteners + Mechanisms & Consequences" | read more

As the researchers themselves point out, their results demonstrate that glucose oxidation controls the intake levels of "sweet tastants"  (=umbrella term for everything that stimulates the sweet taste receptors) by modulating the extracellular dopamine levels in dorsal striatum.

For you, this means that you know better than believe that you could get away with that low carb, sugar free candy bar, chewing gum or whatever else it may be that you are using to soothe your sweet tooth you are effectively cheating yourself. It works only in conjunction with your free will to avoid the carbs and usually only for so long as you allow yourself planned and controlled refeeds.

Note: When you are in full ketosis, things may be different; although the effects of ketones on dopamine levels are - afaik - not well researched, yet.

Let's finally try to draw some more general conclusions about carbohydrate intake in general - I mean beside the real sweet stuff, like candy, etc. Let's take the no-carb noodles you or hopefully not you, but your obese neighbor just bought, for example. They may taste just like the real deal. In the absences of the (expected) subsequent influx of glucose and its oxidation in the brain, they will yet never provide the hedonic response you are looking for. They are fake, a good one that may fool the first line of nutrient sensors, but a fake that's not good enough to reproduce the expected downstream effects on neurotransmitters.

Now, the good news is: No-carb noodles are probably non-addictive. The bad news, however, is: No-carb noodles are also highly, or I should say utterly unsatisfying replacement for real pasta, because the lack of carbohydrates, or rather the glucose that would get oxidized right in your brain, when you consume a bowl of real pasta is the critical physiological signal that makes pasta what it is: A highly addictive comfort food. For the average pasta junky, a "no-carb noodle" is thus never going to cut it, unless he or she is willing to cure him- or herself of her sugar addiction first.

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SuppVersity suggested read: "Coke vs. Diet Coke vs. Milk - The "Unhealthy Beverage Shoot-Out": Milk Reduces, Coke Increases Visceral Fat. Dreaded Diet Coke on Par With Plain Water" | read the complete article

Bottom line: Unlike "zero carb candy" or "no-carb noodles" an effective "diet aid", or let's rather say, one of the foods you should select, whenever you are trying to rid yourself of body fat (low GI starches, fruits and even vegetables (*I write "even" because the amount of carbs in some veggies borders zero)) can offer this "second line" effects in your brain; effects, none of the fake foods you buy at the supplement store, the super market and as of late even some kiosks will ever be able to produce. These real foods are the ones that will have you feel satisfied and they are the ones that should make up more than just the figurative lion's share of your diet - not the calorie, carbohydrate and nutrient free no-carb noodles and their low-carb brethren that will just have you crave the "real deal" even more.

The Neurotransmitter Depleting Effects of Branched Chain Amino Acids (BCAAs) and Their Potential Ergolytic, Anxiogenic & Depressive Downstream Effects

Oh yes, this will happen despite if not because you've taken large amounts of BCAA before the workout.

Usually you don't put the cart before the horse, but I guess you won't mind if I do so and postpone a summary of the information on magnesium from yesterday's installment of the Science Round-Up to tomorrow, when this means that we are going to take care of the "BCAA crisis" today.

Ok, maybe "crisis" is not the best word to describe the reverberations the recent publication of a study by SuJean Choi et al. should be having (=nobody buys BCAAs anymore), but I was looking for something better than the usual "the truth about..." Science, and I am not going to tire repeating that, is after all not about truth (that's what the confessional box is about), but about experimentally verifiable/verified and non-verifiable/non-verified hypothesis (Popper. 1994).

BCAAs can have ergolytic effects - A verifiable hypotheses?

Based on the observations Choi et al. made in by then decapitated lab animals (so much about the "why don't they prove this works in humans"-argument), the administration of a solution that contained either a BCAA + Arginine + Glutamine mix, or one out of two different EAA mixtures, it is safe to say that the hypothesis formulated in the subheading of this paragraph could belong to the former, i.e. the verifiable, hypothesis; and that despite the fact that the addition of glutamine and arginine to the human equivalent of 19:12:12 mg/kg body weight of leucine:isoleucine:valine (less than most BCAA products offer) would at least buffer the previously discussed performance decrements due to the accumulation of ammonia (learn more)

Table 1: Amino acid composition (mg/kg body weight) of the AA supplements tested (Choi. 2013)

In the end, the results Choi et al. present contradict both, the promises on the labels of the countless BCAA products and Newsholme's and Blomstrand's hypothesis that the inhibitory effect the BCAAs exert on the uptake of tryptophan from the blood into the brain and the way this forestalls the subsequent conversion of tryptophan to serotonin would lead to a reduction of central fatigue during exercise (Newsholme. 1996).

Figure 1: Effects of BCAA and BCAA + 100mg/kg l-tyrosine supplementation on serum and brain amino acid and neurotransmitter levels in sedentary rats; data expressed relative to vehicle (Choi. 2013)

Now, the data in figure 1 does confirm the first part of the Newsholme + Blomstrand hypothesis: The adminstration of BCAAs in an amount similar to many low dose BCAA supplements that are currently being marketed as ergogenic agents does blunt the increase in serotonin by competitively inhibiting the uptake of l-tryptophan from the bloodstream. The latter is a necessary consequence of the fact that both the BCAAs and the said 5-HTP (=serotonin) precursor are being transported by the same large amino acid transporter (think of it like a taxi that is allowed to pass the blood brain barrier) as l-tryptophan.

A note on the pro-obesity effects mentioned during the show: While some scientists invoke the increased BCAA levels in obese individuals and the subsequent blockade of serotonin (and dopamine) production in the brain to the constant insatiable cravings, anxiety and depression in these individuals (Breum. 2003; She. 2007; Coppola. 2013) a more fundemental contribution to the obesity pandemic has been proposed by Newgard et al. (2009). Their hypothesis is that a continuous presence of BCAAs in the blood will lead to a continuous overexpression of mTOR that increases the susceptibility to diet induced obesity and insulin resistance.

Now, it is also true that this will blunt the increase in 5-HTP synthesis in the brain (-48%; in the absence of exercise; see figure 1), but with the concomitant -25% decline in hypothalamic DOPA (=dopamine, the "get going neurotransmitter") in the brain after ~30min, the net ergogenic effect will, just as it was the case in the majority of pertinent rodent and human studies, be negligible, at best!

Modulatory Effects of Different Macronutrient & Stress Compositions on Serotonin (read more)

"Following oral intubation with the ‘‘BCAA’’ mixture to sedentary rats (see Table1; n=3/group), serum TRP and TYR concentrations showed non-significant reductions; the serum TRP and TYR ratios, and cortical TRP and TYR concentrations dropped markedly at 30 min. Cortical TRP and TYR concentrations remained low for the duration of the study (120 min), while the ratios began to recover at 90–120 min. DOPA and 5HTP synthesis dropped to nadir values at 60 min; DOPA synthesis remained low, while 5HTP synthesis had rebounded by 120 min (bottom panels, Fig.2).

Inasmuch as the maximal effects on DOPA and 5HTP synthesis occurred 60 min following intubation, all subsequent studies used 60 min as the experimental endpoint." (Choi. 2013)

In fact, the overall and as you've just read persistent drop in neurotransmitter levels can not only make you tired, previous research even suggests that it may be invoked in the etiology of depression / central fatigue (see previous SuppVersity post "Study Investigates Modulatory Effects of Different Macronutrient Compositions on Serotonin in the Presence and Absence of Stress" | read more).

Balancing leucine with tyrosine at a ~1:1 ratio helps

The data in figure 1 does however also tell you that you can mitigate the problem by the addition of 100mg/kg body weight of l-tyrosine to the supplement. With that being roughly equivalent to the amount of leucine in the BCAA formula (cf. table 1), this is yet far more of the dopamine precursor than your average BCAA product is going to have... after all it's a maximal leucine concentration that sells and is propagated as being "modern" and "maximal anabolic".

Figure 2: Hypthalamic DOPA and 5HTP levels after BCAA or BCAA + 100mg/kg tyrosine ingestion with / without exercise, left (Choi. 2013); effects of BCAA or l-tyrosine supplementation on time to exhaustion (Strüder. 1998)

With the addition of 100mg/kg l-tyrosine, you may yet in fact expect to see some benefits. Unfortunately, the currently available literature will put you right in a study that was conducted by Strüder et al. for example neither 21g of BCAAs nor the whopping dose of 20g of pure l-tyrosine resulted in the expected increase in the time-to-exhaustion during time trials in trained cyclists (see figure 2, right; Strüder. 1998) and Blomstrand concludes in his review for the British Journal of Sports Medicine's A-Z Supplement Review Series:

"Under certain conditions, BCAA supplementation can also improve physical performance, although the majority of studies have found no effect of BCAA on performance when supplied together with carbohydrates." (Blomstrand in Burke. 2009)

This, on the other hand, tells you that the performance enhancing effects are a mere result of the oxidation of BCAAs of which both Blomstrand, who is by the way defending his own hypothesis here, and the recently discussed by Falavigna et al. (see SuppVersity News) indicate that the ensuing increased release in ammonia production "may be detrimental to performance" (Blomstrand in Burke. 2009). If you also take into consideration that a study by van Hall et al. from 1995, i.e. before Newsholme & Blomstrand came up with the hypothesis the whole BCAA myth was built on, basically falsified the tryptophan hypothesis of fatigue, In the pertinent study the scientists were after all able to show that the provision of BCAAs as workout fuel is not superior to that of tryptophan and that despite a 8-12% reduction in brain tryptophan uptake at exhaustion with BCAAs and a 7- to 20-fold increase in response to the ingestion of a tryptophan supplement (van Hall. 1995).

Milk protein EAAs: An option, but a logical one?

If you finally take a look at the data in figure 3  you will notice that the head-to-head comparison would place an amino acid pattern as the one you can find in milk proteins, would probably be the best amino acid supplement source to resort to (don't ask me what exactly it is that makes the difference, I can't tell, but suspect it could be related to lysine which is also going to block the same small AA channel into the brain + the inclusion of non-essential amino acids in milk protein vs. pure EAAs).

Figure 3: Comparison of the the effects of BCAA, regular EAAs and an EAA amino acid mix from milk protein; composition of the mixtures see table 1 (Choi. 2013)

But let's be honest, does it really make sense to buy an additional supplement, when you already have a pouch of cheap and tasty whey and/or another fast digesting high BCAA protein such as pea protein lying around at home?

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So what's the verdict then? As you've heard on the Science Round-Up, yesterday, I personally think that this does not make sense, because ...

1. .

   

   Suggested Read: "Spiking Whey W/ EAA Will Provide Inferior Results" (read more)

   .. neither the total amount of amino acids that are obsorbed within 1h from free form EAAs, nor the the utilization speak in favor of EEAs - both have been shown to be +7% and +92% higher with slightly hydrolized whey vs. EAAs (Monchi. 1993),
2. ... nor is there any anabolic benefit to the addition of EAAs or leucine to whey, in fact "25 g of whey is better suited to increase resistance exercise-induced muscle anabolism" compared to lower amount of whey that has been pimped with additional EAAs and leucine to offer the same amount of the purpoted "anabolics" as the 25g dose of plain whey protein (click on the picture to the right to learn more; Churchward-Venne. 2012)

Contrary to Carl's jovial suggestion to simply throw away your BCAA supplements, I would suggest you keep them (unless you already have problems with anxiety, etc.), cut back on the dosage and monitor your response closely. The latter is especially true, when you take them on an empty stomach. After you've run out, train a month with nothing but cheap protein and decide afterwards whether or not your past "great training experience", "superior intensity" and whatever else the ads tell you the respective products will do was more than just another instance of the brocebo effect (learn more about brocebos).

References:

• Breum L, Rasmussen MH, Hilsted J, Fernstrom JD. Twenty-four-hour plasma tryptophan concentrations and ratios are below normal in obese subjects and are not normalized by substantial weight reduction. Am J Clin Nutr. 2003 May;77(5):1112-8. 
• Burke LM, Castell LM, Stear SJ, Rogers PJ, Blomstrand E, Gurr S, Mitchell N, Stephens FB, Greenhaff PL. BJSM reviews: A-Z of nutritional supplements: dietary supplements, sports nutrition foods and ergogenic aids for health and performance Part 4. Br J Sports Med. 2009 Dec;43(14):1088-90.
• Choi S, Disilvio B, Fernstrom MH, Fernstrom JD. Oral branched-chain amino acid supplements that reduce brain serotonin during exercise in rats also lower brain catecholamines. Amino Acids. 2013 Aug 1. [Epub ahead of print] 
• Coppola A, Wenner BR, Ilkayeva O, Stevens RD, Maggioni M, Slotkin TA, Levin ED, Newgard CB. Branched-chain amino acids alter neurobehavioral function in rats. Am J Physiol Endocrinol Metab. 2013 Feb 15;304(4):E405-13.
  
• Churchward-Venne TA, Burd NA, Mitchell CJ, West DW, Philp A, Marcotte GR, Baker SK, Baar K, Phillips SM. Supplementation of a suboptimal protein dose with leucine or essential amino acids: effects on myofibrillar protein synthesis at rest and following resistance exercise in men. J Physiol. 2012 Jun 1;590(Pt 11):2751-65.
• Monchi M, Rérat AA. Comparison of net protein utilization of milk protein mild enzymatic hydrolysates and free amino acid mixtures with a close pattern in the rat. JPEN J Parenter Enteral Nutr. 1993 Jul-Aug;17(4):355-63. 
• Newgard CB, An J, Bain JR, Muehlbauer MJ, Stevens RD, Lien LF, Haqq AM, Shah SH, Arlotto M, Slentz CA, Rochon J, Gallup D, Ilkayeva O, Wenner BR, Yancy WS Jr, Eisenson H, Musante G, Surwit RS, Millington DS, Butler MD, Svetkey LP. A branched-chain amino acid-related metabolic signature that differentiates obese and lean humans and contributes to insulin resistance. Cell Metab. 2009 Apr;9(4):311-26.
• Newsholme EA, Blomstrand E. The plasma level of some amino acids and physical and mental fatigue. Experientia. 1996 May 15;52(5):413-5. Review.
• Popper, KR. Zwei Bedeutungen von Falsifizierbarkeit [Two meanings of falsifiability]. In Seiffert, H.; Radnitzky, G. Handlexikon der Wissenschaftstheorie. München: Deutscher Taschenbuch Verlag. 1994.  
• She P, Van Horn C, Reid T, Hutson SM, Cooney RN, Lynch CJ. Obesity-related elevations in plasma leucine are associated with alterations in enzymes involved in branched-chain amino acid metabolism. Am J Physiol Endocrinol Metab. 2007 Dec;293(6):E1552-63. Epub 2007 Oct 9.
• Strüder HK, Hollmann W, Platen P, Donike M, Gotzmann A, Weber K. Influence of paroxetine, branched-chain amino acids and tyrosine on neuroendocrine system responses and fatigue in humans. Horm Metab Res. 1998 Apr;30(4):188-94.  
• van Hall G, Raaymakers JS, Saris WH, Wagenmakers AJ. Ingestion of branched-chain amino acids and tryptophan during sustained exercise in man: failure to affect performance. J Physiol. 1995 Aug 1;486 ( Pt 3):789-94.

Capsaicin - 2.56mg to Keep Your Metabolism Running on a Diet. Cold Thermogenesis - 5°C for 6kcal/h. Mobile Phones - 0.853 W/kg Pulsed EMR to Mess Up Neurotransmitters

You don't have to worry, the "guidelines" do not require you to perform either your 150 minutes of moderate cardio, or your 75 minutes of vigorous-intensity aerobic activity, and not even your two weekly full-body workouts in these shorts.

24% that's the SuppVersity Figure of the Week and it is actually not so low as I would have expected it to be, after all those 24% describe the ratio of US adults who meet the Physical Activity Guidelines for muscle-strengthening physical activity. Which guideline? Ah, you are the US guys and gals, so you should know that you are advised to

"perform muscle-strengthening activities that are moderate or high intensity and involve all major muscle groups on 2 or more days a week, because these activities provide additional health benefit" (2008 Physical Activity Guidelines for Americans)

Additional benefit? Well, it goes without saying that the 150 minutes of moderate aerobic training and the reduction of salt, as well as the use of healthy vegetable oils are the primary object for every 'true American'.

Not That Hot: Cold Thermogenesis

Figure 1: An avg. effect size of 6kcal/h, non-responders + "negative-responders"; it doesn't work for those past the 30y mark - how on earth is cold thermogenesis going to help us solve the obesity pandemic?

(Chen. 2013) In a single-blind, randomized crossover intervention 24 volunteers (14 men, 10 women) were exposed to a 5°C temperature reduction (from 24°C to 19°C). During that treatment they wre sitting in a whole-room indirect calorimeter to measure their energy expenditure and lay in a positron emission tomography (PET) scanner afterwards (results, see image to the right).

Now, based on previous SuppVersity articles on the matter, you'll know that it is not exactly easy to find people who actually harbor a "significant" (and in this case this means "any at all") amount of metabolically active brown adipose tissue to get the thermogenesis going.

And with 23cm³ and 35cm³ for the men and women participating in the study at hand, the amount of the "good fat" they were carrying around is still pretty stingy. No wonder ...

• there was no thermogenic response in the male participants, but a
• 10% increase in energy expenditure in the female participants

I already see your eyes glow in the cold, ladies, but you crow too soon - those 10% were 6kcal/h, I repeat in full words "six additional calories per hour". Or roughly as much energy as a single set of body weight squats would be burning .

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If you are looking to shed 18% fat in 21 days, increase your health and your physical appearance, turn up the heat during your workouts, clean up your diet and don't move into the fridge (learn more)!

Bottom line: Against the background that there were neither significant changes in the hormonal profile (thyroid, adrenal, etc.) and considering the fact that the effect declined with age and was hardly measurable for 5 and negative (=lower energy expenditure in the cold) for 4 subjects, I stick to previous assessment: cold thermogenesis as a means of "expending more energy to get rid", is about as stupid as the whole concept of expending more energy to lose fat and it certainly does not, as the scientists state "represent a novel environmental strategy in obesity treatment".

If you want a "environmental strategy in obesity treatment", ban all the junkfood, switch off the elevators, hand out bikes and increase the health insurance cost for everyone who refuses to get his or her ass off the couch on a regular bases. Zealous? Unrealistic? Yeah, it is - but not more unrealistic than the hilarious notion that cooling the overweight majority of the inhabitants of the Western Obesity Belt down by 5°C would solve the obesity problem.

Mobile phones mess with neurotransmitter levels

Andreassen et al. have already developed a "Facebook Addiction Scale" and found that Facebook junkies tend to be

neurotic and extraverted, but lack a reasonable amount of conscientiousness (Andreassen. 2012)

(Aboul Ezz. 2013) I am well aware that many of you don't want to hear this and will discard the results researchers from the Cairo University present in their latest paper in the European Review forMedical and Pharmacological Sciences as "just another worthless rodent study" and I freely admit, you may be right.

It is well possible that rodents are more susceptible to the pulsed electromagnetic radiation from mobile phones than humans are, but I gather you will have to agree that the chance that there are still residual effects in human beings is by no means zero... and based on my personal observations, I would even argue that you see certain abnormalities in mobile phone junkies, already. Ok, those could have psychological and behavioral roots, but ...

Before I digress even further into the abyss of the "I cannot live without my mobile" virus that has already befallen many of my real world students, let's rather take a look at the outcome of Aboul Ezz et al.'s latest experiment.

Table 1: While the first six are actually the TOP (=low SAR) phones that are currently on the market, the others are random picks of mine from the data on SARdatabase.com

In the course of the latter, the scientists exposed a group of adult rats to the pulsed electromagnetic radiation of a mobile phone having a power density of 0.02W/cm² and an average specific absorption rate (the notorious SAR-value) of 0.843W/kg for 1h/day (that happens to be a little less of what your neat iPhone5 is pumping into your brain day in and day out) and measured the monoamine levels after one, two and four months, as well as on a follow-up one month after the last exposure and found:

The exposure to EMR resulted in significant changes in DA [dopamine], NE [norepenephrine] and 5-HT [serotinine levels] in the four selected areas of adult rat brain" (Aboul Ezz. 2013)

And the Egyptian researchers add, these chance could well explain the adverse effects that have been reported in conjunction with chronic "low level" exposure to pulsed electromagnetic radiation, which are usually related to memory problems and chronic stress.

What they don't mention in the abstract though is that the changes were not really consistent. It appeared as if there was some cyclicity involved with an initial increase in 5HT, a concomittant decrease in dopamine a newly established "balance" between the two leading to an increase in norepinephrine (=chronic stress) in months four.

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Bottom line: That being said, I can only repeat that even in the absence of direct physiological effects of the EMR exposure, the constant state of "being available" to whoever wants to reach you, as well as the addictive potential of being in contact with all your (often fake) facebook friends alone should be reason enough to re-evaluate your own mobile phone use.

Capsaicin keeps fatty acid oxidation & total energy expenditure up, when you're dieting

No this is not Liza Oz after taking Mehmet's beloved RK supplements - and it is not one of the subjects from the "Kitchen Sink Approach to Fat Loss study"... although, who knows? (learn more about that study)

(Janssens. 2013) Right from the Department of Human Biology, School for Nutrition, Toxicology and Metabolism (NUTRIM) at the Maastricht University in The Netherlands comes a new study that confirms that capsaicin a long-touted "fat burner" and anti-obesity agent  that's also turning up your heat, when you consume hot peppers, will maintain your energy balance and fatty oxidation rates in the normal zone, when you are dieting.

The 15 healthy Caucasian subjects underwent four 36 h sessions in a respiration chamber, which allowed the scientists to accurately measure their energy expenditure, the ratio of glucose / fat oxidation and blood pressure after receiving a dose of 2.56mg (1.03g of red chili pepper worth 39,050 Scoville heat units (SHU)) with every meal.

Now, this wouldn’t be something we have not seen in previous studies, already. With the study at hand, however, the capsaicin intake, was not the only controlled variable. In addition to simply checking what happens, when you consume one serving of capsaicin with each meal, the scientists also assessed the influence of the baseline energy intake of the subjects, with them being randomly assigned to receive adequate amounts of energy (= 100% of the daily energy requirements), or a calorically reduced diet (=75% of the daily energy requirements) during the tests.
 
The first noteworthy observation the scientists made is the adaptiation induced amelioration of the energy deficit. Contrary to what the simply calories in vs. calories out equation would suggest, the participants who received 25% less energy than they would need ended up having an effective energy deficit of only 20.5% - in other words, the missing 4.5% were simply conserved by the dreaded metabolic downregulation that’s one of the most important reasons for weight loss plateaus.

Figure 2: Changes in energy expenditure at rest, during sleep in response to food intake and activity, as well as substrate oxidation in 15 healthy Caucasian subjects (seven women, eight men) during the supplemented (CAP) and non-supplemented (PLA) energy sufficient (100) and restricted (75) conditions (Janssens. 2013).

Now this is where the capsaicin comes into play, as the results of the study at hand clearly demonstrate, the additional provision of 2.56 mg of the hot spice with every meal can negate the reduction in diet-induced thermogenesis and restore the lowered sleeping metabolic rate the 25% caloric reduction has brought about.

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Suggested read for those looking to stacking different ingredients to propel their weight loss efforts: "Forgotten Dieting Aids: Choline, Carnitine, Caffeine and the Anti-Weight-Loss Plateau Effects of Sugar and Phosphates" (read more)

Bottom line: In view of the fact that the capsaicin supplement also increased the fat oxidation during both the calorically reduced and the normal dieting conditions, it may in fact be that we've hot a pretty "hot" fat burner here... unfortunately, just with any other "fat burner", you still got to give your body the chance to actually burn the fat. Without sweat and a slightly reduced energy intake (25% does by the way make a good rule of thumb) this is yet not going to work.

Moreover, it is also questionable, whether the effects will be that noticeable after 1-2 weeks of chronic usage. I'd bet money they will either disappear completely or be drastically reduced, but that would be the topic for another study ;-)

All that's left are... *drumrolls* the Facebook news and an awesome weekend!

You know what's coming now, right? Correct, first I will enumerate a couple of Facebook News you may or may not have seen on the SuppVersity Timline (ha! I did not write "wall", am I now going to be rewarded, Mark Zuckerberg?)

• SuppVersity Highly Suggested Read - Part II of Sean Casey's summary of the ISSN conference | read more...
• Science for Science Sake - In the current scientific environment many scientists turn to biased reporting, intrinsically flawed study design & the like to produce "break through" results that are at best irrelevant, in the worst case threaten the live of participants in follow up studies | learn more... 
• Moderate Drinking Probably Lacks Life-Extending Effects - Sociologists argue: The lifestyle and not the booze of moderate drinkers is what prolongs their lives | learn more...
• Barefoot Running is Good for Your Knees: Take your shoes off to reduce patellofemoral joint stress during running | read more ...
• Can Supplements Precipitate Headaches? At least in a recent study from China the researchers observed correlations between isoflavone-supps in men and B-complex, vitamin C and green algae supplements in women | read more...

And afterwards I am telling you to have a nice weekend and reminding you of the fact that Sunday is no "off day" here at the SuppVersity ... although, for many of you it appears to be, which is why I am actually thinking about dropping the Sunday posts completely. Whatever... enjoy your weekend!

References:

• Aboul Ezz HS, Khadrawy YA, Ahmed NA, Radwan NM, El Bakry MM. The effect of pulsed electromagnetic radiation from mobile phone on the levels of monoamine neurotransmitters in four different areas of rat brain. Eur Rev Med Pharmacol Sci. 2013 Jul;17(13):1782-8.
• Andreassen CS, Torsheim T, Brunborg GS, Pallesen S. Development of a Facebook
  Addiction Scale. Psychol Rep. 2012 Apr;110(2):501-17.
• Chen KY, Brychta RJ, Linderman JD, Smith S, Courville A, Dieckmann W, Herscovitch P, Millo CM, Remaley A, Lee P, Celi FS. Brown fat activation mediates cold-induced thermogenesis in adult humans in response to a mild decrease in ambient temperature. J Clin Endocrinol Metab. 2013 Jul;98(7):E1218-23. 
• Janssens PL, Hursel R, Martens EA, Westerterp-Plantenga MS. Acute effects of capsaicin on energy expenditure and fat oxidation in negative energy balance. PLoS One. 2013 Jul 2;8(7):e67786.
   

Dopamine, Serotonine, Creatine: Creatine Supplementation Modulates Post-Exercise Neurotransmitter Levels in Man

Can creatine beneficially influence your neurotransmitter so that you can run longer?

I guess, some of you will remember, while others will still ignore the discussion revolving around the serotonin (5-HT) depleting effects of high doses of BCAA (see news item "BCAAs inhibit serotonin metabolism"). To those who remember and may even have followed the ensuing discussion it is probably no news that the acute ingestion of ~60g of BCAAs suppresses 5-HT, raises prolactin and lowers dopamine to such a degree that it has a direct negative impact on emotional decision making in human beings (Sevy. 2006). Against that background you may probably be assuming the worst, when I am now telling you that every gymrat's darling, creatine monohydrate, does also exhibit non-negligible effects on the levels of the two important neurotransmitters.

All clear: Creatine probably won't make you depressed

Contrary to BCAAs which exert their effect irrespective of whether you do or don't exercise. The current evidence suggests that creatine does the same only in the context exhaustive aerobic exercise (I would bet it does the same with high volume training, though). In their recently published paper, Moghadasi et al. describe the dopamine, serotonin and prolactin response of 20 healthy, but sedentary male volunteers (BMI 23.5; body fat %: 20.5%) who received 4x5g creatine (standard loading protocol) for 7 days before they underwent an exhaustive aerobic exercise test, the so-called Bruce protocol, in the course of which participants are made to run on a treadmill to exhaustion, while incline and speed are increased every three minutes.

Figure 1: Dopamine and serotonin levels of the healthy, but sedentary volunteers before, immediately, 10 min and 20 min after the Bruce protocol (Moghadasi. 2012)

As you can see in figure 1 the preloading protocol  resulted in significantly different 5-HT responses to the exercise protocol and a trend towards higher, more stable dopamine levels. But this is not the only interesting observation the scientists made. Contrary to the common believe that creatine supplementation will make you look bloated in response to an increase in extra-cellular water, the participants in the creatine group of the Moghadasi study who gained a whopping 1.6kg of total mass in the course of the study period exhibited lower extracellular water levels than their peers in the control group.

Figure 2: Effect of creatine supplementation on BMI and intra- and extracellular water (Moghadasi. 2012)

The relative figures in figure 2 do obviously not exclude that the subjects in the creatine group still had a slight increase in total extra-cellular water. What's yet more important though is the more pronounced increase in the intra-cellular compartment, which has, as Moghadasi et al. rightly point out, "been identified as a universal anabolic signal, stimulating protein synthesis and net protein deposition." (Moghadasi. 2012)

Figure 3: Especially immediately after the workout the dopamine to serotonin ratio seems to suggest that there should be a significant effect. As far as the time on the treadmill was concerned there were yet no statistically significant intergroup differences in the study at hand (Moghadasi. 2012).

But all that is not new to you, I guess, so let's get back to the modified neurotransmitter response. Is that something we won't or something we don't won't? Well, from a performance perspective it turned out to be useless (just as the 5-HT blockade by BCAAs, by the way). Participants from both groups flagged after roughly 15.5-16.0 minutes on the treadmill - how accurate the Bruce Test is, specifically as a measure of central fatigue, is yet still a matter of ongoing scientific debate. Machado et al. for example have pointed out that peripheral fatigue in the legs may set in well before the purportedly 5-HT mediated central fatigues forces the study participants to jump off the treadmill (Machado. 2008), so that we cannot really tell whether the supplementation had an effect on central fatigue. After all, the leg musculature of sedentary subjects is obviously tiring faster than the fortified quads, glutes and hams of trained athletes.

The same is unfortunately true for the actual effects of the modified neurotransmitter response, while the authors are right to point out that 5-HT has been imlicated as a factor that induces mental and subsequently central fatigue, whereas dopamine is known as the "motivational neurotransmitter", previous studies by Wantanabe et al. suggested that respective cognitive benefits from creatine supplementation were facilitated by an increased oxygen utilization in the brain - not via changes in the neurotransmitter levels. And though these changes may not have reached statistical significance in the study at hand, there is actually better evidence for potential pro-dopaminergic effects of creatine, which has been shown to increase DA synthesis in the substantia nigra of mice by protecting against striata DA depletion (Klivenyi. 2003) and / or by enhancing the tyrosine hydroxylase activity and thus increasing the production of dopamine from its precursoe tyrosine (Matthews. 1999).

Much ado about nothing?

Is there a connection between creatine and prolactin: While the prolactin levels were not measured in the study at hand. The results of a 1996 study, in which Prysor-Jones et al. were able to show that the "creatine analogue" beta-guanidinopropionic acid (GPA) which is in fact a competitive inhibitor of creatine, increased the TRH induced release of prolactin. By implication this could mean that creatine will do the exact opposite. This hypothesis would also be supported by the increased dopamine levels after the workout - after all, dopamine is a natural prolactin antagonist (and vice versa).

There is however one study, by Hadjicharalambous et al. that appears to support the hypothesis that the modified 5HT-to-DA ratio may in fact figure large. The authors found that 7 days of creatine supplementation effectively reduced the central fatigue index of subjects who had to exercise in the heat. In that, they observed that the additional creatine blunted the increase in the free tryptophan-to-tyrosine ratio, which suggests that the brain 5-HT and DA levels were modulated by the supplementation protocol, as well. According to Hadjicharalambous et al. this effect was yet single-sided and related to an overall reduction in serotonin levels, while there were no significant difference between two groups as far as their dopamine levels were concerned.

Bottom  line: As it is the case in so many of the complex processes underlying human performance and the effects of proven and purported ergogenics, these insights into the effects of creatine as a potential mediator of the exercise induced neurotransmitter-response are still very preliminary. That may be surprising if you take into accaunt that millions of consumers are currently using creatine monohydrate or supplements that contain it, but in the end it's not much different from the way the same people use to train: Things that work will prevail - irrespective of whether or not the mechanisms have already been fully understood. 


References:

• Machado M, Sampaio-Jorge F, Dias, N, Knifis FW. Effect of oral creatine supplementation in soccer players metabolism. Revista Internacional de Ciencias del Deporte. 2008; 4:44-58. 
• Moghadasi M, Rahimi E, Mahani MS, Molaee, AA. Effect Of Creatine Supplementation On Brain Neurotransmitters After An Exhaustive Aerobic Exercise. Brazilian Journal of Biomotricity. 2012; 6(3):213-221. 
• Sevy S, Hassoun Y, Bechara A, Yechiam E, Napolitano B, Burdick K, Delman H, Malhotra A. Emotion-based decision-making in healthy subjects: short-term effects of reducing dopamine levels. Psychopharmacology (Berl). 2006 Oct;188(2):228-35.

Lack of Drive? Theacrine Will Get You Going - Every Day! Camellia Kucha Alkaloid Acts via Dopamine and Adenosine

Image 1: Coffee vs. tea, if it comes to the persistent dopaminergic "get going" effect it appears that a hitherto hardly known tea variety, Camellia Kucha has the edge on the #1 average westerner's #1 morning drink.

Caffeine is the #1 drug for anyone looking for that little extra of burst of energy and yet there are people who claim they would kill for their morning coffee, while others swear by having one cup right before bed to keep the blood sugar levels from dropping during the night. Whatever your personal preference may be, it probably did not escape your notice that cup no.10,000 does not exert the same magic as cup  no. 10, decades ago. The reason for that is a pretty rapid habituation effect, the extend of which varies remarkably from person to person.If you do belong to the vast majority of people for whom  the morning coffee has become more of an entrenched habit than an energizer, you will therefore probably be interested in the results of a recent study by Allison A. Feduccia and her colleagues from the Ernest Gallo Clinic and Research Center at the University of California at San Francisco, the School of Life Sciences at the San Yat-sen University in China and the Nutritional Science and Toxicology Department at the University of California (Feduccia. 2012).

Theacrine the non-sensitizing, no-tolerance locomotor activator from Camellia kucha

Feduccia et al. have been able to show that the intra-peritoneal administratoin of the human equivalent of 8mg/kg theacrine (1,2,7,9-tetramethyluric acid) a naturally occurring purine alkaloid with structural similarities to caffeine and established anti-inflammatory and analgesic (=pain reducing), as well as anti-depressant effects (Wang. 2010; Xie. 2009), boosts the physical activity of rodents by more than 130% (note: since i.p. injection have a higher bioavailability you better make the HED 10+mg/kg, if you want to see similar results; this is all the more true, in view of the fact that the lower 4mg/kg equivalent did not produce significant increases in motor activity in the study at hand).

Figure 1: Increase in locomotor activity after intra-peritoneal administration of the 24 or 48mg/kg Theacrine (human equivaled, HED: 4mg/kg or 8mg/kg; data adapted from Feduccia. 2012)

As the data in figure 1 shows the effects, which are mediated via adenosinergic (A1 and A2A) and dopaminergic (D1 & D2) pathways were pronounced yet not statistically significant in the low dose (human equivalent for 80kg ~ 320mg) group and highly significant (p < 0.01 ambulatory distance; p < 0.001 stereotypic counts) in the high dose group.

Nice, but what exactly is the advantage over caffeine?

In order to be able to give you a better idea of the actual effect size, as well as to underline the importance of the fact that even after 7 days of repeated administration, the locomotor activity counts did not change compared to day 1, I plotted data from a similar study on the effects of a low-dose of oral caffeine (HED ~280mg) on the locomotor activity of rats (Ball. 2009).

Figure 2: Ambulatory distance at day 1 and day 4 with and without daily administration of 3.5mg/kg caffeine (Ball. 2009).

As you can see in figure 2 the effects of caffeine are not only less pronounced, the sensitization effect is in fact so pronounced that after only 4 days, the rodents actually needed their daily dose of caffeine to get going - and even with it, their locomotor activity decreased by - 26% compared to baseline. Now compare that to the persistent +167% increase in locomotor activity (likewise measured by ambulatory distance) with theacrine and tell me which one would be more likely to get you through week after week of your demanding day work?

Update (05-20-2012): In response to questions on Facebook and the comment area, here on the SuppVersity, a brief summary of my formerly not mentioned, since unsuccessful attempts to identify whether or not you can buy this tea in the US or Europe. It appears as if, "Kucha" was a certain variety of the assamica variety of camellia sinensis. The latter is very commonly used in black teas, but the "Kucha" variety is probably the one with the highest theacrine content. According to Ye et al. it does contain 1.3-3.6% of the alkaloid in dried leaves - the exact content varied with season and the part of the leaves that was analyzed (Ye. 2003). If we assume a maximal extraction rate of ~80% in hot water, this would mean that a cup of tea brewed with a 2g bag could contain ~20,8-57,6mg of theacrine, which is obviously way too little to be effective. Which would make theacrine a potential candidate for a nutritional supplement - yet probably nothing you can ingest in significant amounts from your diet alone.

References:

• Ball KT, Poplawsky A. Low-dose oral caffeine induces a specific form of
  behavioral sensitization in rats. Pharmacol Rep. 2011 Nov;63(6):1560-3. PubMed
  PMID: 22358105.
• Feduccia AA, et al, Locomotor activation by theacrine, a purine alkaloid structurally similar to caffeine: Involvement of adenosine and dopamine receptors, Pharmacol Biochem Behav (2012), doi:10.1016/j.pbb.2012.04.014
• F. Wang Y, Yang X, Zheng X, Li J, Ye C, Song X. Theacrine, a purine alkaloid with anti-inflammatory and analgesic activities. Fitoterapia 2010;81:627–31.
• Xie G, Wu M, Huang Y, Cao Y, Lai-dong L, He-liangl Z, et al. Experimental study of
  theacrine on antidepressant effects. Chin Pharmacol Bull 2009.
• Ye Chuangxing, Hiroshi A, Zheng Xinqiang, Wang Xiujuan, Gao Kun, Zhang Hongda. New discovery of pattern of purine alkaloids in wild tea trees. Zhongshan da xue xue Bao. Zi ran ke xue ban = Acta Scientiarum Naturalium Universitatis Sunyatseni. 2003, 42(1):62-65

Gingko Biloba, Your Dopaminergic Brain Viagra. Plant Extract Stimulates Sexual Arousal via the Paraventricular Nucleus and the Mesolimbic System.

Image 1: Gingko biloba
trees are one of a kind, with
no close living relatives
(image Schwabe Pharm.)

I bet you got one of those Viagra spam mails, today, as well, didn't you? Well, although I assume you would not need the small blue pills, anyway, you may be interest to read that researchers from the People's Republic of China may have found a viable Viagra alternative in a longstanding (pun intended ;-) ingredient of Traditional Chinese (and meanwhile also Western) Medicine: Gingko biloba.

In order to elucidate the underlying mechanisms of previously (Yeh. 2010) observed beneficial effects of Ginkgo biloba extract on noncontact erections in male rats, Yeh et al. (Yeh. 2011) recorded both copulation, as well as non-contact erections in a group of 20 male Long-Evans (telling name, isn't it?) rats, which had been randomly assigned to a treatment (50mg/kg body weight Gingko biloba extract [EGb 761 from Schwabe Pharmaceuticals], human equivalent 8mg/kg ~ 640mg for an 80kg man) or a control group. 14 days after initiation of treatment, there was "a significant increase in the number of NCEs [non contact erections]" in the 10 rats of the treatment group. Furthermore,

[...] the expression of catecholaminergic neurons in the PVN [paraventricular nucleus] and the VTA [ventral tegmental area] was seen [to be significantly increased ...] and tissue levels of dopamine and 3,4-dihydroxyphenylacetic acid in the NAc [nucleus accubens] were also markedly increased in the EGb 761-treated animals. However, the norepinephrine tissue levels in the PVN and the NAc in the EGb 761-treated group were not significantly different from those in the controls.

In other words, the increased number of catecholaminergic neurons did not, as one might have expected, increase the total amount of the stress-related neurotransmitter /hormone norepinephrine. In agreement with previous work by Mas et al., 1990; Pfaus et al., 1990; Pleim et al., 1990;Wenkstern et al., 1993; Tsai et al., 2006, it's dopaminergenic effects in the nuccleus accubens (dopamine levels in the increased by 66%), on the other hand, had profound effects on their sexual behavior (cf. figure 1).

Figure 1: Effect of Gingko biloba extract @ 50mg/kg on non-contact erection frequency in male Long-Evans rats before and after 14 day treatment (data adapted from Yeh. 2011)

In view of the effect, that the scientist do not want to "exclude that EGb 761 treatment may also influence dopaminergic activity in other brain areas", these results may be of interest even to those among you, who do not have any trouble "getting it up".

Note: The mechanism by which Gingko biloba increases sexual desire is different from the one of PDE-5 inhibitors such as avanafil, lodenafil, mirodenafil, sildenafil citrate, tadalafil and all the other "-afils". While the systemic effect on nitric oxide induced vasolidation of Viagra and Co. will help with erection quality and quantity, Gingko biloba probably won't help if blood flow restriction in your most valuable part is an issue. The different mechanisms of action, on the other hand, would suggest the two would make an interesting stack. And in fact back in 2010 Kim et al. found that "GBE [Gingko biloba extract] could increase the relaxant potency of mirodenafil even at a minimally effective dose" (Kim. 2010).

With dopamine playing an important role in behavior and cognition, voluntary movement, motivation, punishment and reward, inhibition of prolactin production (juicers did you read that?), sleep, mood, attention, working memory, and learning, the implications of this finding reach beyond sexual function alone. Even in the etiology of the dubious central fatique syndrome, every second visitor of one of the major internet health bulletin boards claims to experience, these days, may involve dopamine or rather a lack thereof (Caldizán Uzón. 2008). That being said, the group of patients who benefit from one of the readily available over-the-counter Gingko biloba supplements may soon expand from best agers, who are concerned about cognitive decline to (pre-)andropausal men who want to regain their interest in the fairer sex and, eventually, everyone who feels he/she would benefit from some additional dopaminergic drive.

Set to Be Obese!? Dopamine Turns Out to Be Another Major Player in the Neurological Orchestra of Obesity

As I promised, I am trying my best to keep up with current research on the neurological aspects of obesity, I also talked about on Carl Lenore's Super Human Radio on March 31, 2011. While the focus of the previously mentioned study was on the less well-known relationship between inhibitory and excitatory neurons in the hypothalamus, the major player scientists from the University Medical Center at Leiden in the Netherlands studied is a rather famous one: Dopamine.

Figure 1: Basal glucose & insulin levels in DIO & DR mice after 2 weeks on placebo (P), bromocriptine (B) or haloperidol (H) (data adapted from de Leeuw van Weenen. 2011)

What de Leeuw van Weenen et al (de Leeuw van Weenen. 2011) found in the same diet induced obesity [DIO] mouse model Ravussin (Ravussin. 2011)had used in his study (cf. Follow Up on Set-Point Theories: Could Royal Jelly Help With Obesity / Diet Induced Structural Brain Changes?) were

• altered dopaminergic transmission
• exaggerated basal and feeding-evoked dopamine release
• reduced dopaminergic receptor (DRD2) activity and number of binding sites

This obesity-related modulation of DRD2 activity has been shown to have ...

[...] profound effects on energy homeostasis in humans and animals. Drugs that blockDRD2 enhance appetite and induce weight gain in animals and human. Conversely, DRD2 agonist drugs reduce body weight, increase energy expenditure, and improve glycemic control in obese animals and individuals.

To verify the efficacy of respective drugs, the researchers administered Bromocriptine (DRD2 agonist) and Haloperidol (DRD2 antagonist) to DIO and diet resistant [DR], i.e. naturally lean mice, and found that ...

It does not take Bromocriptine
for dopamine-agonism.
L-Dopa from Mucuna Pruriens
is a natural and proven
precursor to dopamine.

Haloperidol treatment reduced the voluntary activity and energy expenditure of DR mice and induced insulin resistance in these mice. Conversely, bromocriptine treatment tended to reduce bodyweight and voluntary activity, and reinforce insulin action in DIO mice.

Taken together these results / effects of reduced dopaminergic tone

• decreased insulin sensitivity, hyperglycemia
• decreased voluntary movement and slowed metabolism
• decrease in dopamine induced "reward" (satiety) after eating

further establish the unfortunate truth that the neurological abnormalities that go hand in hand with diet induced obesity eventually set you up to stay overweight or, worse, to become even more obese.

Date Palm (Phoenix dactylifera) as a Natural Test Booster and Ergogenic

A very recent study (Saddiq. 2010) published in the Journal of the International Society for Horticultural Science found that the seeds of Phoenix dactylifera can raise testosterone, norepenephrine (NE), dopamine (DA) and GABA levels and may counteract the negative effect of prednisolone administration in rats.

[...] the daily oral administration of pits of date palm caused the maximal increase in NE, DA and GABA content that was found in the brain stem after 2 weeks. The daily oral administration of methylprednisolone caused a decrease in NE, DA and GABA content found in the brain stem after 2 weeks. Moreover, the daily oral administration of pits of date palm and methylprednisolone caused an increase in NE content found in the brain stem after 2 weeks. The daily oral administration of pits of date palm and methylprednisolone caused a significant increase in testosterone level in serum blood of male albino rats.

While all this sounds promising, further studies would have to clarify whether it needs the cortisol-like effects of prednisone for the testosterone-boosting effect of the date seeds to take place or whether taking adequate amounts of pits of date palm would provoke similar (or even superior) increases in testosterone in rats and, most importantly, in men. Be that as it may, even the increase in neurotransmitters (NE, DA, GABA) certainly could provide real-world benefits for athletes, as well as people suffering from fatigue.

Barley Water: Traditional British Soft Drink Turns out to be Natural Ergogenic

A recent investigation into the effects of 4 weeks feeding of barley water (talbina), a traditional British soft drink (click here for recipe) to albino mice found remarkable neurological and endocrine changes (Bawazir, 2010):

[...] this treatment caused significant increase in, dopamine (DA), serotonin (5-HT) and gamm-aminobutyric acid (GABA) contents in different brain areas (Cerebellum, striatum, cerebral cortex, hypothalamus, brain steam and hippocampus) of male albino rats. Moreover, it caused the maximal increase in GABA content in the cerebral cortex after 4 weeks (+41.51%) and the maximal increase in DA, GABA, 5-HT and 5-HIAA content in the cerebral cortex after 3 weeks ((+62.85, +41.51, +72.73 and (+71.98%, respectively). Significant increases in cortisol (+20.09 %) and testosterone ( 46.8%) levels were found in blood after 4 weeks. The tubules of testis showed an increased active spermatogenesis with significant rise of number of mature sperms.

Before you start boiling washed pearl barley, only to pour hot water over the rind and/or pulp of the fruit, and add some fruit juice and sugar for the taste, in order have a supply of a few liters of self-made talbina for everyday consumption, you should however have a closer look at the following graph taken directly from the study (sorry for the bad image quality):

Fig.1: Changes (%) in Cortisol (left) and testosterone (right) (Bawazir, 2010)

So, even if (in the end) consumption of that brew will give you a testosterone boost the slight fall in testosterone levels accompanied by a major increase in cortisol levels in weeks 1-3 will probably give you a hard time - not so hard as in the first weeks of cold steroid withdrawal but catabolic (low testosterone / cortisol ratio), anyway.