On Short Notice: 15% Stronger With Kineso Tapes, HIIT With 30-20-10, Combined Training vs. Diabetes, Coffee vs. Scars, Peanuts & Pregnancy, Phosphate & Insulin + More!

Image 1: You like it fast? Then the novel SuppVersity column SuppVersity "On Short Notice" is right for you. So don't forget to bookmark, subscripe to the RSS feed or the email updates (see bottom right of the page) or simply start following me on facebook and/or twitter

Actually I am quite happy that most of you liked last Saturday's first installment of SuppVersity "On Short Notice" - it turned out that just writing down one of those mini-items, whenever I have a couple of minutes to spare yields more great content than a single post can hold. So, despite the fact that I have stockpiled 11 items for you in today's installment I have already written the first ones for next week's installment of this new column. Before we start with those of the past week, I would just like to remind everyone that you can simply add the RSS feed (all SuppVersity posts, only "On Short Notice" posts) to your favorite RSS reader, or start following me on facebook and/or twitter if you like those informational quickies and thus make sure that you won't miss any information from the realms of exercise science, supplementation and nutrition!

30 - 20 - 10  HIIT for maximal conditioning

As a regular at the SuppVersity you have already learned one or two things about the benefits (and in many cases superiority) of high intensity interval training (HIIT) for fat loss and cardiovascular conditioning (read all about HIIT).

Figure 1:  The 30-20-10 protocol consists of a inner 5x1min 30-20-10 'acceleration'-cycles followed by a 2min period of active rest; those 5x 30-20-10 low-, moderate-, and high-speed running + 1x 2min active rest pairs are repeated 3-4 times.

A recently published study by Gunnarson et al. does now show that even moderately trained individuals can benefit from a very simple yet intense 15-20min interval training (see figure 1) similar to the one the 3 women and 7 men in the active arm of the study performed (total number of participants N=20). And I would say that 4% higher VO2max, 21s faster 1,500-m and 48s faster 5-km running times are nothing you would want to miss, either. Specifically, if those come with a 30-20-10 decrease of systolic blood pressure and reductions in total and low-density lipoprotein (LDL) of -0.5 ± 0.2 and -0.4 ± 0.1 mmol/l, respectively - am I right? No, well you should better stick to your arduous treadmill walks in the non-existant  fat-burning zone, then.

Add strength training to your 10-20-30 aerobic regimen and rid yourself of type II diabetes

I guess it goes without saying that the exercise approach to diabetes won't work without other lifestyle interventions, such as dietary modifications and stress reduction / management (e.g. "Chronically Fatigued? Do Qigong!". After all, you would not have gotten into the mess if your nutrition had been in check and your stress-management effective - and don't give me the "bad genes excuse", I hear that from my type II diabetic grandma often enough!

Figure 2: fasting glucose and glycolosated hemoglobin levels before and after a 20-week exercise intervention consisting of either 3x per week of combined resistance and aerobic training or aerobic only training of the same volume (based on Moro. 2012)

As far as exercise goes, a recently published study has (once again) confirmed that a combined aerobic + resistance training protocol is more effective with respect to longterm (20-week) improvements in glycemia than the regular "walk" or even worse "jog an incline for 40-60min everyday" regimen - in the study at hand the aerobics regimen employed one of those classic 'ramps' starting at 15min @ 40-50% in the first week and ramping up volume + intensity to 60 min at 60-70% (Moro. 2012): What is particularly striking about the results (see figure 2) is the differential effects on simple fasting blood glucose levels and the amount of glycolosated hemoglobin, an index for the long-term (24h) glucose stability, which improved significantly more (p < 0.05) with the combined (3x split training with 3 sets à 10-12reps + 20min of light aerobic exercise afterwards), than with the aerobics only 3x per week exercise program.

Assuming that the additional strength training component is also going to help the 24 formerly sedentary participants (men and women aged 60,41 ± 7,87y) to build or at least maintain "metabolic currency" (= muscle) you can bet money that those differences would have been even more pronounced if the trial had lasted 6 or more instead of just 5 months. Remember: You are in this for life!

And if you want do get stronger, just tape your biceps

If you train in one of the gyms, where professional athletes go in and out, you will probably already have seen people come in with those blue, green or pink "package tapes" on their limbs. Usually their coaches and or physiotherapists apply those and send them to the gym, when they are still recovering from an injury and thus cannot perform their regular training sessions.

Figure 3: Concentric and eccentric elbow peak torque with and without kineseo or placebo taping ( (Fratocchi. 2012)

As the data in figure 3 goes to show, this practice could turn out to be the kinesiologic analogon to creatin... well, aside from the fact that it works instantaneously, maybe (Fratocchi. 2012). Done right, the taping can increase your concentric and eccentric peak torgue on a simulated biceps curl (performed on an isokinetic pulley machine) by 13-15%. Whether these results, Fratocchi et al. observed in trained, but not (upper body) strength trained young men and women will translate in similar pronounced strength improvement on real curls - let alone permanent gains, once you remove the tape - remains to be seen. But let's be honest, what do you have to lose? As long as you don't apply the tape wrong (see figure 3, green-framed photo), I would say that the worst thing that can happen is that people laugh at your novel 'gymwear'.

On ultra-short notice:

• Your red blood cells can produce testosterone and other androgens - Believe it or not, but according to a recent study from the Universidad de Chile in Santiago, Chile, human platelets can produce sex hormones from circulating DHEA-S (Garrido. 2012). They can also take up estrone-sulfate and convert it to 17b-estradiol (the most active form of estrogen); taking your DIM does therefore not necessarily prevent that your platelets avail themselves of the estrone your liver is spilling out and convert it back to estrogen, when they "feel that's necessary". If you don't care about that, you may be interested that DHEA can also ramp up insulin sensitivity and help you lose weight and protect your muscle against exercise induced damage - even when you train like a maniac. 

• 

  Image 2: Better smear some coffee paste onto your wound than special creams if you don' want nasty scars.

  Coffee paste applied to a closed wound could prevent scarring - Although the paper does not mention this explicitly (Perez-Aso. 2012), the discovery that the pharmacological blockade of the adenosine A2A receptor prevents scarring suggests that a paste made of/with fresh coffee should actually do the exact same thing. After all, coffee is a natural pan-(=across many)adenosine receptor antagonist. It goes without saying, though that you cannot apply the coffee onto the open wound, right? Well, I guess you can, but it is at least questionable if that would not rather increase your chance for infections that decrease your risk of developing ugly scars. Find out more about coffee!
• EPO increases muscle repair by ramping up satellite cell activity - According to Jia et al., endogenous EPO, i.e. erythropoietin that is produced by your body, plays an important role in satellite cell proliferation and thus the repair and the "structural expansion" of muscle tissue. Based on their studies in wild-type and EPO overexpressing mice, the researchers speculate that exogenous erythropoietin could thus be used to "contribute to increasing satellite cell number following muscle injury, improve myoblast proliferation and survival, and promote repair and regeneration" (Jia. 2012). Read more about EPO or sattelite cells, and the commonly overlooked role of estrogen in satellite cell replenishment and activation.
• IGF-1 from colostral whey is orally active and ameloriates high blood sugar - I have addressed the question whether the more or less complex peptides from milk (see "Colostrum & Milk"), deer antler (see "Ask Dr. Andro: Does Deer Antler Velvet Work?") & co can even work, when they are administered orally several times before - a recent discovery by scientists from the Republic of Korea does now suggest that, at least in diabetic rodents, the IGF-1 fraction in colostral whey exerts similar blood sugar lowering effects as its recombinant (artificial) human cousin (Hwand. 2011). Since this is nothing but another rodent study, the non-negligible blood sugar reductions of 11 and 33 % at weeks 2 and 4, respectively, are yet sill only something for the "ultra-short notice" section of the "on short notice" column of the SuppVersity (if you have not done so already, don't fotget to read up on the anti-diabetic effects of camel milk here).
• People with reactive hypoglycemia shouldn't follow a low carb high protein diet - I knew that from my experience with others (esp. women), but when the issue of reactive hypoglycemia surfaced again in one of the comments, I dug up a 1975 study which clearly shows that avoiding carbs altogether (50-60g /day in the study) will only add impaired glucose tolerance on top of the existing and persistent symptoms (Anderson. 1975). More on potential pitfalls with very low carbing: "Carbohydrate Shortage in Paleo Land" and "Half As Heavy, but Twice As Fat: 'Atkins-Style' No-Carb Diet + Exhaustive Exercise Compromise Body Composition"

• 

  Image 3: Craving peanut butter? The sugar (and thus increased gestational diabetes risk) is probably more of a problem than the "allergens". At least that is what the ~20% reduced asthma and allergic rhinitis risk a recent study reports based on data from the Danish National Birth cohort reports would suggest.

  Peanuts during pregnancy not a problem, but rather beneficial - While real junkies harm their unborn babies by irresponsible consumption of cigarettes, alcohol and other drugs, health junkies could be doing the same by totally avoiding exposure to any kind of potential allergens. At least this is what a recent analysis of data from the Danish National Birth Cohort would suggest. According to the results of Maslova et al., the consumption of potentially pro-allergenic pea- and tree-nuts did not only elicit any changes in terms of future allergies, it was also "inversely associated with a medication-related asthma diagnosis (OR, 0.81) and self-reported allergic rhinitis (OR, 0.80)" (Maslova. 2012) - or put simply: not the consumption, but rather the abstinence of potential pro-allergens appears to dispose unborn children to develop respective allergies in later life.
• High-normal TSH good predictor of visceral obesity; irrespective of insulin resistance - "Your TSH is somewhat high, but no reason to be concerned." If that's what your Dr. told you, you better get another one. After all, a recent study by Muscogiuri et al. shows that those "somewhat high TSH levels" are a pretty good indicator of increased visceral adiposity, and all its potentially fatal health consequences (Muscogiuri. 2012). And if you want to improve your thyroid function naturally, I suggest you read my previous post "Dietary Thyroid Treatment: Beef, Green Vegetables, Full-Fat Milk & Butter Normalize TSH in Subclinical Hypothyroidism"!
• High phosphate content of meal increases postprandial blood glucose and insulin - What are two characteristics of coke and similar soft drinks? Right: They contain tons of high GI sugar and phosphate. A combination of which a group of researchers from the Department of Clinical Nutrition at the University of Tokushima in Japan has recently shown that it leads to a profound increase in postprandial (hours after the meal) blood glucose and insulin levels compared to low GI, but also compared to high high GI low phosphate (400mg vs. 1200mg) meals in 11 young, healthy volunteers. Bottom line: If high GI is bad, high GI + high phosphorus is even worse (Taketani. 2012). I am not sure how much phosphor the sports drink I wrote about roughly two weeks ago contain, but certainly less than coke, and still the average body fat gain per energy drink was ~18g ("Fat Content Per Energy Drink 0g, Body Fat Gain Per Energy Drink 18g!").

References:

1. Anderson JW, Herman RH. Effects of carbohydrate restriction on glucose tolerance of normal men and reactive hypoglycemic patients. Am J Clin Nutr. 1975 Jul;28(7):748-55.
2. Fratocchi G, Di Mattia F, Rossi R, Mangone M, Santilli V, Paoloni M. Influence of Kinesio Taping applied over biceps brachii on isokinetic elbow peak torque. A placebo controlled study in a population of young healthy subjects. J Sci Med Sport. 2012 Jul 6.
3. Garrido A, Munoz Y, Sierralta W, Valladares L. Metabolism of dehydroepiandrosterone sulfate and estrone-sulfate by human platelets. Physiol Res. 2012 Jun 6.
4. Gunnarsson TP, Bangsbo J. The 10-20-30 training concept improves performance and health profile in moderately trained runners. J Appl Physiol. 2012 Jul;113(1):16-24.
5. Hwang KA, Hwang YJ, Ha W, Choo YK, Ko K. Oral administration of insulin-like growth factor-I from colostral whey reduces blood glucose in streptozotocin-induced diabetic mice. Br J Nutr. 2011 Oct 10:1-7.
6. Jia Y, Suzuki N, Yamamoto M, Gassmann M, Noguchi CT. Endogenous erythropoietin signaling facilitates skeletal muscle repair and recovery following pharmacologically induced damage. FASEB J. 2012 Jul;26(7):2847-58. Epub 2012 Apr 9.
7. Maslova E, Granström C, Hansen S, Petersen SB, Strøm M, Willett WC, Olsen SF. Peanut and tree nut consumption during pregnancy and allergic disease in children-should mothers decrease their intake? Longitudinal evidence from the Danish National Birth Cohort. J Allergy Clin Immunol. 2012 Jun 26.
8. Moro AR, da Rosa R, da Silva FC, Filho PJBG. Effect of combined and aerobic training on glycemic control in type 2 diabetes. Fisioter. mov. [online]. 2012, vol.25, n.2 [cited 2012-07-13], pp. 399-409.
9. Muscogiuri G, Sorice GP, Mezza T, Prioletta A, Lassandro AP, Pirronti T, Della Casa S, Pontecorvi A, Giaccari A. High-normal TSH values in obesity: is it insulin resistance or adipose tissue's guilt? Obesity (Silver Spring). 2012 Jul 3.
10. Perez-Aso M, Chiriboga L, Cronstein BN. Pharmacological blockade of adenosine A2A receptors diminishes scarring. FASEB J. 2012 Jul 5.
11. Taketani Y, Yamazaki M, Ueda H, Mori Y, Tanaka T, Horie D, Ominami H, Okumura-Yamanaka H, Yamamoto H, Takeda E. Interaction between dietary phosphate and carbohydrate on glucose and phosphate metabolism in healthy young men. Kidney Research and Clinical Practice. Volume 31, Issue 2, June 2012

On Short Notice: EPO Reduces Mitochondrial Biogenesis, Excess Zinc Raises BP + Impairs Insulin Clearance, ALA + UDCA "Cure" NAFDL, Earthing, Estrogen & Your Heart ...

Image 1: 2h of earthing would certainly solve this problem just as they seem to reduce the risk of developing blood clots,  by the way (see below)

I thought I could try something new today and just give you a brief research update on stuff that would otherwise not necessarily make it to the SuppVersity, because it is not really worth writing a whole blogpost on it. Please make sure you let me know whether or not you like this format. I am open to comments of all sorts and suggestions on whether to continue posting things like this; on the respective frequency; on whether or not you want stuff in more detail and so on and so forth... You know that I am writing this blog for no-one else, but YOU, so take this chance and give me some feedback to allow me to tailor things even more to your demands. But enough of that, let's get to the studies for today :-)

EPO treatment reduces mitochondrial biogenesis...

...in  fast twitch-muscle fibers, only! Vladimir E. Martinez-Bello and his colleagues from Spain and France (yeah, the Tour de France has just begun ;-) have found that after no more than 3-weeks of thrice weekly subcutaneous administration of 300IU of rHuEpo, the expression of PGC-1α, mTFA and cytochrome c in the fast-twitch muscles of the gastrocnemius were significantly reduced (Martinez-Bello. 2012).

Figure 1: Changes in haemoglobin, haematocrit, and reticulocytes (colored large graph) and expression of enzymes involved in the mitochondrial biogenesis pathway in gastrocnemius muscle (black-and-white small graph) before and after 21 days of rHuEpo or saline administration (Martinez-Bello.2012)

If you take a look at figure 1 you could certainly argue that this is a simple consequence of the increase in haemoglobin, haematocrit and the rediculocyte count and the subsequently increased oxygen delivery to the target muscle. Unfortunately, that does not really make sense, since that should be all the more important for the highly oxygen-depended slow twitch muscles in the soleus, where the expression of neither of the three enzymes changed. So, as Martinez-Bello et al. say "further studies are needed to address and clarify this issue as well as to establish accurate biological mechanisms". This may also explain the fact that the treatment did not ellicit any changes in maximal aerobic performance, something you would actually expect as a mechanistic consequence of the EPO-induced increase in oxygen transport.

Too much zinc can increase blood pressure by compromising kidney function 

You already know that the long-term ingestion of high doses of zinc can set you up for insulin resistance and diabetes (cf. "Zinc: 15mg Are Plenty - After 120 Days Rodents on Diets Containing 2xRDA of Zinc Develop Metabolic Syndrome"). According to another recent study from the Health Science Center, Saitama Medical University in Japan (Kasai. 2012), excessive zinc intake can reduce renal function and thus indirectly elevate in blood pressure.

Figure 2: As you can see, the compromised kindey function did not just lead to profound increases in blood pressure, it also reduced the insulin clearance by >20% and > 40% (based on Kasai. 2012)

And if you take a closer look at the effects the diets that contained 10x (for humans 10x above normal is "only" 150mg/day, something I have in face seen as a recommendation for "natural testosterone bosting" on some of the boards) and 40x the normal amount had on insulin clearance within after no more than 4-weeks, it becomes clear that in addition to the previously mentioned increased nutrient absorption the inability to clear insulin from the blood may have been an additional factor which contributed to the progression of insulin resistance, Tenaja et al. observed in their study (see "Zinc: 15mg Are Plenty"; Taneja. 2012)

400mg of ALA + 300mg of UDCA + diet = good bye NAFLD

Pretty impressive data comes from a recent human trial on non-pharmacological interventions in patients with non-alcoholic fatty liver disease (Gianturco. 2012). As the data in figure 3 goes to show the combined effects of a colorically reduced diet (1,200kcal/day for women, 1,500kcal/day for men) with a macronutrient ratio of 26% fat (5% polyunsaturated, 14% monounsaturated, and 7% saturated), 25% protein, and 49 % carbohydrates, 400mg of alpha lipoic acid (ALA) and 300mg of ursodeoxycholic acid, a bile acid that is also known as ursodiol, led to profound  improvements in all markers of non-alcoholic fatty liver disease.

Figure 3: Changes in characteristic markers of liver health after 12 months on a hypocaloric diet with and without supplementation of ALA and/or UDCA (Gianturco. 2012)

What is particularly remarkable, though, is the fact that these pronounced improvement took place in the absence of significant weight loss changes in blood glucose, insulin, HOMA-IR or triglycerides. In other words: It was not a side effect of improved weight loss, increased insulin sensitivity or the restoration of a healthy fatty acid metabolism. And what's best about all it: The treatment was side effect free!

On ultra-short notice

Image 2: It may be debatable whether or not running around in the dark is the ideal form of aerobic exercise, in terms of it's effects on your hemoglobin, platelet, etc. counts it does yet not make a difference when you train.

• Your blood does not mind, when you train - Time of the day has no effect on impact of maximal aerobic exercise on haematological parameters (hemoglobin, platelets, erythrocytes, and leukocytes) immediately after, and two hours after the exercise (Shahidi. 2012)
• "Earthing" could help reduce blood clotting - A "groundbreaking" *rofl* study by Chevalier et al. reveals that 2h of sitting quietly in a room grounded with conductive patches on the soles of your feet and palms of their hands (patches must be connected to stainless-steel rod inserted in the earth outdoors) you can reduce the zeta potential (charge of your red blood cells) and thus reduce their potential to form blood clots (Chevalier. 2012)
• Sunscreen from within? Coffee could hold the answer! - Although this is exclusively based on epidemiological data, it's interesting that Song et al. report that an increased caffeine intake appears to protect to against Basal cell carcinoma of the skin (Song. 2012). Men and women who consumed more than 3 cups/d had the lowest risk (10% and 21% lower than people who consumed only 1 cup or less). And while caffeine from other dietary sources (tea, cola, and chocolate) had similar effects, there were no benefits associated with the consumption of decaffeinated coffee.
• Estrogens protect against cardiac hypertrophy - If you are a friend of OTC or pharmacological estrogen eradication, you should be aware that the results of a recent study from the University of Colorado suggest that estrogen has preventive effects against pathological hypertrophy of the heart (Haines. 2012). And while this could explain why some of the non-aromatising anabolic steroids have more pronounced cardiovascular side-effects it should be mentioned that the study was conducted on female aromatase knockout mice and does therefore not necessarily translate 1:1 to humans, let alone men... the 2x increase in cardiac hypertrophy, on the other hand, is so pronounced that I would think twice whether or not it really is necessary to rid yourself from as much estrogen as possible, after all it appears to play an important role in skeletal muscle growth and repair, as well - see "Intermittent Thoughts on Building Muscle: Estrogen, Friend or Foe of Skeletal Muscle Hypertrophy?"

References:

1. Chevalier G, Sinatra ST, Oschman JL, Delany RM. Earthing (Grounding) the Human Body Reduces Blood Viscosity-a Major Factor in Cardiovascular Disease. J Altern Complement Med. 2012 Jul 3.
2. Gianturco Y, Troisi G, Bellomo A, Bernardini S, D’Ottavio E, Formosa V, Lo Iacono C, Verrusio W, Marigliano B, Marigliano, V. Impact of combined therapy with alpha-lipoic and ursodeoxycolic acid on nonalcoholic fatty liver disease: double-blind, randomized clinical trial of efficacy and safety . Hepatol Int. 2012 Jul 3.
3. Haines C, Harvey P, Leinwand LA. Estrogens Mediate Cardiac Hypertrophy in a Stimulus-Dependent Manner. Endocrinology. 2012 Jul 3.
4. Martinez-Bello VE, Sanchis-Gomar F, Romagnoli M, Derbre F, Gomez-Cabrera MC, Viña J. Three weeks of erythropoietin treatment hampers skeletal muscle mitochondrial biogenesis in rats. J Physiol Biochem. 2012 May 25.
5. Kasai M, Miyazaki T, Takenaka T, Yanagisawa H, Suzuki H. Excessive Zinc Intake Increases Systemic Blood Pressure and Reduces Renal Blood Flow via Kidney Angiotensin II in Rats. Biol Trace Elem Res. 2012 Jul 4.
6. Shahidi F, Alhosseini SLN, Kandi YNMP.  The Effect of a Maximal Aerobic Exercise Session in the Morning and Afternoon on Certain Hematological Factors in Young Athletes. Annals of Biological Research, 2012, 3 (6):2703-2707
7. Song F, Qureshi AA, Han J. Increased caffeine intake is associated with reduced risk of Basal cell carcinoma of the skin. Cancer Res. 2012 Jul 1;72(13):3282-9.
8. Taneja SK, Jain M, Mandal R, Megha K. Excessive zinc in diet induces leptin resistance in Wistar rat through increased uptake of nutrients at intestinal level. J Trace Elem Med Biol. 2012 Jun 8.

Ask Dr. Andro: Does the Deer Velvet Antler Spray NFL Fullback Heath Evans is Supposed to Have (Ab-)Used Work? Does it Contain IGF-1 & Can IGF-1 Be Taken Orally?

Question from Lerner: "Dr. Andro, check out the following link. It's about deer antler (which I didn't find being discussed in a search of suppversity) -- and how that supposedly contains IGF-1. I don't watch NFL football, but they do get paid big money and that motivates them to try different things for sure. Still, does it work, or is it just placebo effect?"

Image 1: Legal growth hormone
supplements in the NFL? How legit is
the deer velvet antler extract containing
'The Ultimate Spray'  (image source
official SWATS homepage)

Answer from Dr. Andro: Initially, I wanted to dismiss this one all together, because I remembered out of my head one of two peer-reviewed studies on the use of deer antler, which was not able to find any effect of elk velvet antler extract at a daily dose 560mg on exercise performance or endocrine parameters in 25 male and female rowers (Syrotuik. 2005). How on earth would the hilariously labeled The Ultimate Spray, Heath Evans is supposed to have taken, then make a difference for a high level NFL fullback?

Well, after "pubmeding" (make sure you remember this neologism of mine, it is like "googling" for smart people ;-) the missing study by Sleivert et al. (Sleivert. 2003), in which at least some of the 38 active males, who had received deer antler velvet extract in powder form concomitantly to a 10-week strength training protocol, actually gained twice as much isokinetic knee-extensor strength and endurance than the placebo group, Mr. Lerner's question suddenly had my full attention...


What is The Ultimate Spray?

A closer look at The Ultimate Spray then revealed that, other than I had expected, it was no Patrick Arnold style transdermal, but an oral preparation. Well, to be precise this is only my interpretation of the information, if you would like to call it such, on the website, of the producer SWATS, where it says, I quote:

"sparyed into the moutn, where the phospholipid spheres easily penetrate the mucosal layers of the moutn and go directly into the blood stream." [my emphasis]

So if to "spary" something "into the moutn" means to spray it into your mouth and not to smear it onto the next best mountain, I would assume that the undisclosed amount of "liposomal encapsulated" (sounds funky, no?) velvet antler extract, one serving contains, is supposed to be taken up orally - in that, I exclude sublingual delivery because a) it says that you got to spray it "into" your "moutn" and not under the tongue and b) the liposomal encapsulation would make little sense if the IGF-1, which is supposed to be in the product, would not even reach the digestive juices and enzymes of the stomach, from which the encapsulation in turn is supposed to protect it. Note: The amilase and lipase in the saliva would not harm the protein based IGF-1 peptides, anyway.

How is the product supposed to work?

Now that we know that The Ultimate Spray is a liposomally encapsulated extract from deer antler velvet that is to be taken orally as a spray, the next question we would have to answer is: How on earth does this product make Evans feel improvements in "some rest and recovery aspects" and what is the "sleep of a deeper nature" the New Orleans Saints fullback mentions all about?

A look at the purported ingredients of the product could help, but as a matter of fact, without appropriate lab analysis, we have no clue how much, if any, IGF-1, collagen, amino acids, epidermal growth factor (EGF), chondroitin sulphate, erythropoietin, glycosphingolipids, prostoglandins, phospholipids and monoamine-oxidase inhibitors The Ultimate Spray ultimately contains. What we can say for sure, however, is that IGF-1 is not "a precursor for the production of growth hormone (HGH)", as SWATS tries to tell you. It is rather a hormone whose molecular structure is very similar to insulin and which plays an important role in childhood and - you guessed it - deer antler growth.

If we leave the "amino acids", "collagen","phospholipids" and "monoamine-oxidase inhibitors" aside (you could get these in much higher concentrations from food or way cheaper supplements, anyway) IGF-1, EGF, the unspecified prostaglandines and last, but not least, every cyclist's favorite blood building 'supplement', erythropoietin, are the most likely candidates on the ingredient list which could be responsible for the beneficial effects Evans claims to have noticed. So let's see...

• Erythropoietin, commonly known as EPO, is in fact a naturally occurring glycoprotein hormone which does - as its name suggests - control erythropoiesis, or red blood cell production. The usual dosage that is used for doping purposes is 100IU/kg three times per week for the first 8 weeks, to increase red blood cell count, followed by 25-50IU/kg to maintain stable erythrocyte counts. According to Jelkmann, 1mg of pure synthetic EPO has a standardized efficiacy of 130.000 IU, while EPO from human urine has meager ~2IU/mg (Jelkmann. 2009). It stands out of question that there will be at least trace amounts of erythropoietin in the extract, since the antler of deer is supplied with blood, but even if it had an efficiacy of 50% of the purified rDNA-derived human EPO, a man like Evans who certainly weighs >160 pounds would have to get >3.500 IU or 18mg per day right into his blood stream to get the desired effects. This is something that probably is not going to happen, as the previously cited study by Sleivert et al. (Sleivert. 2003) shows that notwithstanding inconsistent beneficial effects on strength and endurance, the antler extract did not raise red cell mass or VO2max, parameters which should have been affected, if the amount of EPO in the supplement would have been adequate to elicit physiological effects.
• Prostaglandins are, in contrast to what SWATS claims not generally anti-inflammatory. The function of these locally acting messenger molecules are diverse and the blatant statement on their "anti-inflammatory" character, the producer makes here, is not worth the webspace it occupies. Whether or not Evans could have felt their effects would really depend on which kind of prostaglandins the product contains, but I bet that this is something even the SWATS team does not know.
• Epidermal growth factor (EGF) does play a role in the regulation of cell growth. Thus it is no wonder that it can be found in a constantly regrowing tissue, like deer antler (Ko. 2004 & Barling. 2005). Yet, even if it was retained in the extract, I have my doubts that it plays a major role in the ergogenic effects Evans has been talking about.

This leaves us with what the original Yahoo article on the subject also dealt with: IGF-1, a basic peptide hormone composed of 70 amino acids, which - and this has been shown by Gu et al. - is "only detectable in osteoblasts around the bone in the mid and base parts" (Gu. 2007) of deer antler. So, if the extract SWATS uses in their The Ultimate Spray was made from whole deer antler, it will in fact have IGF-1 in it. Whether this would be enough to elicit physiological effects cannot be decided without running an ELISA or HPLC test on the product to find out how much IGF-1 actually is in one serving of The Ultimate Spray (cf. Liu. 2011). But wait... being a large peptide, would the IGF-1 be able to be absorbed into circulation, even if - as the producer promises - it is protected from digestive enzymes by liposomal micro-encapsulation?

Image 1: Parts of the small intestine,
relevant for IGF-1 absorption in the
rat model used by Kimura et al.

Can IGF-1 be taken orally?

The surprising answer is: "Yes, it can." After digging through the archives of various pharmacological journals I eventually came up with a 14-year-old study by Kimura et al. (Kimura. 1997), who, in 1997, investigated the bioavailability of orally administered recombinant human insulin-like growth factor I (rhIGF-1) [the attribute "recombinant" indicates that this is synthetic human IGF-1] in adult rats (I deliberately underlined the "adult", here because in various neonatal or new-born / very young mammals the intestinal permeability is elevated to allow for the absorption of larger peptides from the mother's milk). The results of this study (cf. figure 1), I must admit, did really surprise me. If you add up (note: if you think I miscalculated, you probably just added up the percentages from figure 1 and forgot that when you absorb 35% there is obviously less IGF-1 left, of which, in a second step. another 17% will be absorbed, etc.) the amounts of IGF-1 that reached circulation (i.e. became "bioavailable") via the three different parts of the digestive tracts of the rats, the critters ended up with roughly 50% of the orally administered radio-labeled ¹²⁵I-rhIGF1 actually getting into their blood stream:

Figure 1: Bioavailability of orally administered rhIGF-1 with and without peptidase inhibitors.
(data adapted from Kimura. 1997)

As you can see, even without the addition of a peptidase inhibitor (peptidase = protease; enzyme that breaks down peptides its individual constituents and would thus "degrade" the IGF-1 before it could even be absorbed) the orally administered dose of 1.0mg/kg (human equivalent: 0.16mg/kg or 13mg for an 80kg adult human being) was absorbed at rates of ~35%, 17% and ~6% in the jejunum (middle section of the small intestine), the ileum (final section of the small intestine) and the large intestine, respectively.

This is not yet the "95% absorption" SWATS promises for a product they advertise as being "by far the best supplement for sports performance", but it is still adds up to a respectable amount of IGF-1 actually reaching circulation. To be precise, plasma concentrations peaked roughly 3 hours after administration at ~50ng/ml, ~180ng/ml and 375ng/ml for the no peptidase, the aprotinin and the casein groups, respectively. In both, the no peptidase and the casein groups, levels stayed constant for another 3h, after which they declined linearly.

I don't know about you, but when I hear about casein improving the absorption of IGF-1, I suddenly forget about dubious deer antler sprays and start thinking of colostrum - well, but I guess this would be a topic for another week ;-)

So what, Dr. Andro? Does it work?

As much as I would like to provide you with a definite answer, the only thing I can tell you for sure are the following facts:

1. there is IGF-1 in whole deer antler
2. IGF-1 survives passage through the intestines of rats even if it is not micro-encapsulated
3. non-micro-encapsulated IGF-1 can be taken up in the jejunum, the ileum and the large intestine at surprisingly high rates
4. protease inhibitors, above all, the readily available and reasonably priced peptidase inhibitor casein can improve bioavailability even further

I would yet have to speculate on

1. whether or not the deer velvet antler extract used in The Ultimate Spray was derived from parts of the antler that actually contain more than trace amounts of IGF-1,
2. how much IGF-1 actually is in one serving,
3. how effective the "natural" and probably partly bound (to IGF1 binding globulins) form of IGF-1 in the product is compared to synthetic, free rhIGF-1,
4. if the liposomal encapsulation does in fact improve and not maybe even hinder absorption,
5. and, last but not least, if the amount of IGF-1 reaching the bloodstream would aactually be able to produce physiological effects

in order to answer Lerner's question. So, now that you got the facts, its up to you, students of the SuppVersity, to make up your mind on whether or not there is more behind this lurid yahoo news-story than just a clever marketing stunt.

Teaching New Tricks to an Old Dog: Erythropoietin (Epo) "Doping" to Treat the Metabolic Syndrome!?

Figure 1: Schematic illustration of the
molecular structure of EPO (Wikipedia)

Have you ever wondered, why there are no obese competitive bicyclists? Because of the enormous calorie expenditure on "The Tour" and similar events? Well, according to the results of a recent study from the National Institute of Diabetes and Digestive and Kidney Diseases in Bethesda (Foskett. 2011), one of the "supplements" many of these athletes have been found to (ab-)use, may factor in the equation, as well.

Foskett et al. followed up on the results of recent studies which suggest a role of Erythropoietin (Epo) signaling in the regulation of body weight, fat mass, and glucose metabolism (Hojman. 2009 / Katz. 2010). They fed a group of mice the standard hypercaloric (5240 kcal/kg) "high fat" diet containing 60 kcal% fat to induce what researchers consider a good model for the metabolic syndrome, i.e. so-called "diet induced obesity" (DIO) in their lab animals. Additionally, recombinant human Epoetin alpha (Epogen) was administered subcutaneously every other day @ 1000, 600, 300, 150, and 75U/kg for 5 weeks, with saline only injected mice as sham controls. Hematocrit, body weight, body composition, glucose metabolism, food intake, and physical activity were monitored:

[...] Epo doses (1000, 600, 300, and 150U/kg) significantly reduced body weight gain and fatmass, while, only Epo doses of 300U/kg and higher significantly affected glucose tolerance. None of the tested Epo doses showed any detectable effects on food intake, and only 1000U/kg dose significantly increased physical activity [...]

What is even more intruoging is the particular effectiveness of the median dose of 300U/kg:

[...] 300U/kg Epo treatment resulted in a slightly more pronounced effect on body fat mass reduction and decreased serum insulin, with total activity levels statistically indistinguishable from the sham control, and slightly lower than those of the 1000U/kg group. [...] A question raised here pertains to the possibility of an optimum effective dose for Epo (300U/kg) in regulating fat mass and insulin levels.

As a regular visitor of the SuppVersity you know similar saturation effects from other supplements and ergogenic aids and are familiar with the fallacies of the application of our Western "the more, the better" mentality within dietary, as well as supplement related contexts.

Irrespective of the relatively small dose that is needed to produce profound metabolic effects, further (human) studies are warranted to decide, whether Epo, a pleotropic cytokine that has been discredited as a performance enhancing drug used and abused by professional athletes around the world, will have a future as a pharmacological addition to diet and exercise programs designed to help the approximately one billion overweight and obese people worldwide to shed their unhealthy body fat. Until the exact mechanisms by which Epo regulates fat mass accumulation and glucose tolerance are elucidated, its use aside from its original areas of medical application remains counter-indicated.

Eight Weeks on Moderate Doses of Erythropoietin (EPO) Build a Bigger Mitochondrial Engine and Shed Some Body Fat, but is That Really Worth Taking the Risk?

Image 1: These EPO containing Recormon vials are highly popular in the French Pyrenees ;-)

Fatty acid oxidation is certainly one of the buzzwords in the supplement industry. Interestingly enough, it is mostly used very indiscriminately for all sorts of physiological processes which are sometime more, sometimes less related to the actual process of β-oxidation, in the course of which the acetyl CoA are liberated from their original molecular bond. In fact, the majority of the currently available "fat burners" (those neat little pills with tons of fat liberating, but not burning stimulants in them) has no effect on the efficacy of this process. In previous posts, as the one on irisin and the utility of exercise induced increases of PGC1-alpha,  I have already hinted at the importance of "building a bigger engine", or, more formally, increasing the oxidative capacity of your mitochondria in your individual battle against your love handles and the global battle against obesity. Today, we are going to have a look at a not exactly kosher, but tried and proven drug everyone who has not deliberately ignored the media coverage of the Tour de France over the past couple of years will have heard of: Erythropoietin - short, EPO!

More red blood cells transport more oxygen to larger mitochondria

About two years ago, a group of researchers from the Duke University Medical Center discovered that the "blood-building" drug Erythropoietin had an unexpected yet not exactly undesirable side-effect: It activated cardiac mitochondrial biogenesis - or, to stick to the previously introduced "terminology" it tuned the lab rats engines (Carraway. 2010). Now, in the latest issue of Frontiers in Physiology a group of European researchers reproduced these results in a group of six healthy young men (21 ± 2 years, 180 ± 1 cm, weight 73± 2 kg) who participated voluntarily (no, the study does not state that those were Tour de France competitors ;-) in an 8-week trial. Over the course of the study period received an additional iron supplement (100mg; was in fact started 2 weeks prior) which, obviously in conjunction with the EPO treatment,

• 1st week: daily subcutaneous injections of 5,000IU of rhEPO
   
• 2nd-7th week: weekly subcutaneous injections of either 0, 2500, or 5000 IU, depending on the subjects' Hct level

was intended to raise their blood hematocrit (Hct) to ∼50% (which is considered still save, i.e. the risk of developing thrombosis is low, and the maximum allowed value in sports!) and to maintain that value throughout the study period. The Hct levels were controlled on a weekly basis and the rhEPO doses were adjusted appropriately:

After the 8 week intervention period, the mean Hct for the whole group was increased significantly to 51 ± 1%. Three of the six subjects received full treatment dosage with a total of 70.000 IU rhEpo over 8 weeks, while two subjects were administered 67.500 and 62.500 IU, respectively. The remaining subject exhibited a strong response to the rhEpo injections, and received a total of 50.000 IU. 

The maximal oxygen consumption of the study participants, which was measured during a standardized exercise protocol (+35W increase in resistance every 60s) on a braked cycle ergometer, increased regardless of the dosage that was required to keep the hematocrit values from 54 to 58ml/kg per minute (cf. figure 1).

Figure 1: Changes in body composition and measures of oxidative capacity in the course of the 8-week treatment period (data calculated based on Plenge. 2012)

Contrary to these 8.3% (+/- 2%) increases in VO2max, the changes in body composition, the scientists had expected based on previous rodent studies (Hojman. 2009) did not reach statistical significance, something I personally would yet not mind if my body fat percentage dropped by 2% after 8 weeks of doing nothing would set me up to shed even more fat. That is all the more true, because the statistical more than significant +22% increase in mitochondrial oxidative phosphorylation and electron transport capacity in the muscle fibers of my vastus lateralis, which are indicative of a profound increase in mitochondrial respiratory capacity, or, the aforementioned tuning of your mitochondrial engines, would set me up for further fat loss in the future.

"Cool, bro! Where can I get this EPO?"

Image 2: You better take their bikes than their drugs.

Yet although all this certainly sounds formidable and "exercise in a pill" always sells way better than real workouts, I guess I better put these results into perspective before you jump to any conclusions. After all, the 4-weeks intervention trial Jennifer L. Trilk and her colleagues from the Department of Kinesiology at the University of Georgia conducted in 2010, is only one out of many examples, which show that "artificial enhancements" like these may be highly beneficial for people performing at already superhuman levels, but comparably ineffective for the average, let alone the formerly sedentary human being (Trilk. 2010).

After all, the overweight women in the Trilk study achieved a +12% increase in VO2Max after no more than 12 HIIT sessions consisting of 4-7 30s all-out sprints on an cycle ergometer, which were seperated by four minutes rest. And let's be honest, if you'd rather take a highly expensive, potentially dangerous drug from the gray market than invest ~90min of your precious weekly TV time into some HIIT exercise, you should not wonder if you are sick and obese.