5-10% Weight Reduction From Set to Set For Hypertrophy, Heavy Leg Workouts for Cyclists, Garlic For 400% Higher Test/Cortisol Ratios & Max(!) 1g Vitamin C for Muscle Gains

7% increase in breast cancer risk for every 500g above "normal" birthweight for Scandinavian women. Weight is yet not all that counts, mommy's gestational diabetes and even a large body size also precipitate to later disease.

7% per 500g that's the increase in breast cancer risk, the female offspring of Scandinavian women will have, if they are born heavier than normal. This figure is the SuppVersity Figure of the Week and comes from a study I came across a couple of days ago (Troisi. 2013). The statistics are based on birth register data of women from Norway, Sweden or Denmark who were subsequently diagnosed with primary, invasive breast cancer (n=51419) and 10 controls for each case from the birth registries matched by country and year of birth (n = 514,190).

Contrary to what you may think, the birth weight does yet not pose as much of a risk to become obese later in life as being larger than "appropriate" for your gestational age does (Eyzaguirre. 2013). If you also consider that gestational diabetes has been linked with increased risk of metabolic syndrome in the offspring (Davis. 2013) and that obesity in itself is an independent risk factor for breast cancer (Patterson. 2013), these should be more than enough good arguments not to surrender to your occasional food cravings and laziness - pregnant or not.

It's not all in your genes, but most in your hands

Although some people would love, if this was the case, because they could blame their own misery on the mistakes other  may have made, our lives and health are not fully determined by our genes and/or the mistakes our mothers may or may not have made. As Poston and Foreyt wrote in 1999, already: "Obesity is an environmental issue." And we are lucky: It is in our hands to change the environment we are exposing ourselves to and thus influence which of our genetic disposals will become active and are  promoted and which of them won't. Now that's obviously not just the case for obesity, muscular hypertrophy would be another example. Irrespective of your genetic make-up your strength and muscle gains stand and fall with the way you train, eat and supplement... and guess what, all of these points will be addressed in today's installment of On Short Notice.

• Experimentally validated: 5-10% drop in weights per set is "optimal" for hypertrophy training (Medeiros. 2013) -- Scientists from the Laboratory of Physiology and Biokinetic at the Faculty of Biological Sciences and Health on the UNIG Campus V at Itaperuna in Brazil find: The average resistance trainee - in this case a young man aged 24.0±4.5 years with a body mass of 78.3±10.2 kg and a height of 177±7 cm - can remain in the hypertrophy range (10-12 reps to failure) for most of his sets, when he reduces the weight by 5-10% after each set.
  
  Whether this will also yield optimal gains was yet not within the scope of this 5-week study. What these results do however tell you is that you are not training hard enough if you perform all your sets with the exact same weight in the exact same rep range - well, unless you don't just like to listen to Super Human Radio, but are actually related to Superman himself ;-)

• 

  Sir Chris Hoy's legs are not as hilarious as those of the German Robert Forstemann (Robert is the right guy), but I am pretty certain their size and strength played a very important part in becoming the most successful Olympic track cyclist of all times (six gold and one silver Olympic Medal + 11 times world champion)

  Heavy leg training could make the difference between victory or defeat at the end of a cycling race (Hansen. 2013) -- In a soon-to-be-published paper, Ernst A. Hansen et al. report that the addition of 12-weeks of heavy resistance training in the form of 4 lower body exercises (3 × 4–10 repetition maximum) which had to be performed twice a week enhanced the cycling performance of highly trained cyclists by 7% compared to the training outcome of the subjects in a control group who simply followed their regular endurance-only, protocols:
  

  "Performance was determined as average power output in a 5-min all-out trial performed subsequent to 185 min of submaximal cycling. The performance enhancement, which has been reported previously, was here shown to be accompanied by improved pedaling efficacy during the all-out cycling. Thus, E+S shortened the phase where negative crank torque occurs by ~16°, corresponding to ~14%, which was more than in E (P = .002)" (Hansen. 2013)

  Since the test was conducted at the end of a 3h cycling session, it should be plain obvious that those 15% increases in torque will catapult the strength trained endurance athlete to the forefront on every final sprint.

• Human dose equivalent of ~0.1g/kg garlic per day could not just boost your testosterone and lower the high protein diet induced increases in cortisol, it could also improve the way your body utilizes dietary protein (Oi. 2013)-- Actually this is not a new study, but since Maxim was not happy with things "so yesterday" as the increases in HDL and LDL the Arabian scientists observed in the garlic study I have been talking about at the end of Thursday's SuppVersity Science Round-Up on SHR, I thought others may be as happy as Maxim will hopefully be to hear that there is more to garlic than "just" its beneficial effects on your heart.
  
  

  

  Figure 1: Higher testosterone levels, an amelioration of the high protein induced increase in corticosteroids and a 40% increase in net protein balance are unquestionably impressive results given the fact that the all those differences were brought about within 28 days and by no more than 0.1g/kg (HED) of "supplemental" garlic in form of heat dried powder that was added to the chow (Oi. 2001)

  In fact, I am almost sure that the >400% increase in the testosterone to cortisol ratio you will see if you take a closer look at the data in figure 1, is probably rather what Maxim would have liked to hear me talk about. Especially in view of the fact that this endocrine effects went hand in hand with a highly significant +60% increase in protein retention (figure 1, top right). Think about it, if only part of he protein that was now no longer excreted in the urine / feces would be used for protein synthesis this would entail exactly those hypertrophy effects you don't see with your average "scientifically proven" herb-based testosterone booster.
  
  Unfortunately, the scientists did only measure the body weight and visceral fat pads, not the actual muscle mass of the rodents,. But if you go by their ratios it is obvious that the high protein + garlic group were not just the heaviest, but also the leanest.
  
  With +11 % vs. +5% in both the medium and high protein diets, the animals on the low protein did yet exhibit the most profound benefits as far as the body weight / visceral fat ratio goes. Against the background that their net protein balance remained the same, this observation does actually suggest that the pro-anabolic effects of garlic are not solely a result of a decreased protein excretion (see figure 1).

  

  Table 1: Principal sulphur compounds of garlic preparations (Hammami. 2013)

  Warning: Don't live on garlic alone! While the provision of 0.8% garlic powder did have beneficial effects on testosterone production in the study at hand, there are a couple of studies which suggest that a diet with 15-30% of crude garlic (Hammami. 2008 & 2009), as well as the administration of Diallyl trisulphide in isolation (Qian. 1986) and raw garlic juice (e.g. 600mg/kg per day for 21 days in Fehri. 1991) can compromise testosterone production and/or testicular function. In view of the difference between 0.8% garlic powder in the diet of the rodents in study at hand and 15-30% of pure garlic in the diet of the animals in the Hamami studies, it is most likely that the effects were dose-depended, but in case you are interested in health benefits of specific sulfor compounds in garlic, the data in table 1 on the left may still come handy to pick "your" preferred form of garlic.
  Rather than that, it appears as if the human equivalent of 0.1g/kg body weight of heat dried garlic powder that contained a total amount of 5.05 mg/g of total diallylsulfide (0.05 mg of monosulfide, 1.0 mg of disulfide, 3.4 mg of trisulfide, 0.6 mg tetrasulfide) had the ability to improve the incorporation of dietary protein into muscles (and other organs).

 

• Study shows: Vitamin C supplementation does reduce skeletal muscle hypertrophy in response to chronic overload (Makanae. 2013) -- Despite the fact that it has not even been published yet, the paper by Yuhei Makanae et al. actually only confirms what more and more scientists have been speculating about within the last couple of years. The provision of high does of active antioxidants, and as it seems in particular vitamin C, blunts the hypertrophy response to skeletal muscle overload.
  
  

  

  Figure 2: 14-day of 500mg/kg  (HED 0.08g/kg) supplemental vitamin C blunt skeletal muscle hypertrophy in rodents (Makanae. 2013)

  As you can see in figure 2 the effect size was relatively small, but statistically highly significant (p < 0.01) and that despite the fact that the supplementation regimen (500mg/kg body weight; HED: 0.08g/kg body weight) was not even that much higher than what some "vitamin C enthusiasts" are taking on a daily basis in the futile (and useless) effort to boost their serum vitamin C levels to a concentrations your body does - probably not without reason - try to counter by increasing renal vitamin C clearance.
  
  As the data in figure 2 shows, the same homeostatic mechanism we know from humans worked in the rodents, as well - well, at least with respect to the serum levels. In the plantaris muscle of the supplemented group, on the other hand, there was a significantly higher accumulation of vitamin C than in the placebo group. This increase went hand in hand with an attenuation of the repressive effects the chronic overload of the muscle had on the expression of the catabolic protein atrogin-1 and the increases in the pro-anabolic protein Erk1/2 (p < 0.01) in the non-supplemented animals. Based on this observations and with reference to the results of previous studies and the fact that neither the water content of the muscle, nor a significant reduction in food intake in the vitamin C group could explain the observed differences, Makanae et al. conclude "that oral vitamin C administration attenuates plantaris muscle hypertrophy induced by chronic mechanical load." (Makanae. 2013).
  
  What the study does not answer, though, is the question whether the effects would be identical in a real-world training scenario, where the temporary, yet more intense wear and tear on the muscle could in fact be sufficient to induce skeletal muscle hypertrophy human despite vitamin C supplementation. But let's be honest in view of the fact that scientific evidence for ergogenic benefits of more than 1g of supplemental vitamin C  per day (in humans) is simply non-existent, the take away message from the study at hand should actually read: Do not escalate your vitamin C beyond the 1g per day, if you don't want to risk compromising the results of all the hard work you are investing into your training.

That's is, another installment of On Short Notice and the first day of the weekend approaching it's peak. If you still have some time before whatever your plan for Saturday night may be and feel like you could use some seconds on today's short news, I suggest you head over to the SuppVersity Facebook Wall and check out the latest news on

• 

  Ever thought about what green tea, grape seed, curcumin, cranberry, and tons of other Super Food have antimicrobial effects? Considering the LPS-influx from the gut turns out to be a major contributor to all sorts of diseases, I am curious about how much of their effects are actually mediated by the gut microbiome.

  The differential role of intramuscular lipids in trained athletes and sedentary slobs and how the difference between performance enhancement and insulin resistance it all comes back to getting your as off the coach (learn more)
• Metformin 2.0? Scientists have developed a hypolipidemic, anti-atherosclerotic, anti-obesity, and glucose lowering agent called ETC-1002 (learn more)
• Confirmed: Grape seed could be the go-to neuroprotector for diabetics - GSE administration was found to be able to ameliorate most of the biochemical altered parameters in diabetic rats (read more)
• Fermenting your own dairy? Just add some catechin rich teas and the lactobacilli will strive. Makes you wonder about the 'internal' probiotic effects of green and black teas, as well. Doesn't it? (learn more)

There will be more, don't worry - so feel free to check for updates either directly on the SuppVersity Facebook Wall or simply by taking a look at the navigation in the right under "SuppVersity Facebook Wall" from time to time. Obviously, you can also simply "like" the SuppVersity on facebook to make sure you don't miss anything.

References:

• Davis JN, Gunderson EP, Gyllenhammer LE, Goran MI. Impact of Gestational Diabetes Mellitus on Pubertal Changes in Adiposity and Metabolic Profiles in Latino Offspring. J Pediatr. 2013 Nov 10.
• Eyzaguirre F, Bancalari R, Román R, Silva R, Youlton R, Urquidi C, García H, Mericq V. Prevalence of components of the metabolic syndrome according to birthweight among overweight and obese children and adolescents. J Pediatr Endocrinol Metab. 2013;25(1-2):51-6. 
• Fehri B, Aiache JM, Korbi S, Monkni M, Ben Said M, Memmi A, Hizaoui B, Boukef K (1991) Toxic effects induced by the repeat administration of Allium sativum L. J Pharm Belg 46:363–374.
• Hammami I, Nahdi A, Mauduit C, Benahmed M, Amri M, Ben Amar A, Zekri S, El May A, El May MV. The inhibitory effects on adult male reproductive functions of crude garlic (Allium sativum) feeding. Asian J Androl. 2008; 10:593–601.
• Hammami I, Amara S, Benahmed M, El May MV, Mauduit C. Chronic crude garlic-feeding modified adult male rat testicular markers: mechanisms of action. Reprod Biol Endocrinol. 2009; 24:57–65.
• Hansen EA, Rønnestad BR, Vegge G, Raastad T. Cyclists Improve Pedalling Efficacy and Performance After Heavy Strength Training. Int J Sports Physiol Perform. 2011 Dec 2. 
• Hammami I, El May MV. Impact of garlic feeding (Allium sativum) on male fertility. Andrologia. 2013 Sep 3.
• Makanae Y, Kawada S, Sasaki K, Nakazato K, Ishii N. Vitamin C administration attenuates overload-induced skeletal muscle hypertrophy in rats. Acta Physiol (Oxf). 2013 Nov 26.
• Medeiros Jr HS, Mello RS, Amorim MZ, Koch AJ, Machado M. Planned Intensity Reduction to Maintain Repetitions Within Recommended Hypertrophy Range. Int J Sports Physiol Perform. 2013 Nov 19. 
• Oi Y, Imafuku M, Shishido C, Kominato Y, Nishimura S, Iwai K. Garlic supplementation increases testicular testosterone and decreases plasma corticosterone in rats fed a high protein diet. J Nutr. 2001 Aug;131(8):2150-6.
• Patterson RE, Rock CL, Kerr J, Natarajan L, Marshall SJ, Pakiz B, Cadmus-Bertram LA. Metabolism and Breast Cancer Risk: Frontiers in Research and Practice. J Acad Nutr Diet. 2013 Nov 2. doi:pii: S2212-2672(12)01426-8.
• Qian YX, Shen PJ, Xu RY, Liu GM, Yang HQ, Lu YS, Sun P, Zhang RW, Qi LM, Lu QH.  Spermicidal effect in vitro by the active principle of garlic. Contraception. 1986; 34:295–302.
• Troisi R, Grotmol T, Jacobsen J, Tretli S, Toft­Sørensen H, Gissler M, Kaaja R,Potischman N, Ekbom A, Hoover RN Stephansson O. Perinatal characteristics and breast cancer risk in daughters: a Scandinavian population­based study. Journal of Developmental Origins of Health and Disease, Available on CJO 2013.

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

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

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

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

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

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

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

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

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

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

Table 1: Prevalence of infectious processes in the control group and study group (Solivellas. 2013)

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

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

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

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

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

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

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

• Protection against skin cancer  and related pathologies - PL protects the melanocytic nevi in your skin from forming sporadic melanoma in response to UV radioation, dark eyed patients with higher UVR sensibility (lower basal minimal erythematous dose) would benefit most (dosage 1080mg of PL; Aguilera. 2013). Similar results in rodents, where 300mg/kg of PL 5 days before UVR exposure "reduced the number of proliferating cells by 13%, increased the number of p53(+) cells by 63%, enhanced the antioxidant plasma capacity (ORAC) by 30% and reinforced the network of dermal elastic fibres" (Rodríguez-Yanes. 2013). Also helps against photo aging, polymorphic light eruption, idiopathic photodermatosis, UV-B induced immuno-suppression in the skin,
• Prevention of hyperpigmentation (and psoriasis) - Hydroquinone has been a cornerstone for the treatment of hyperpigmentation; however, concerns regarding adverse effects have prompted a search for alternative agents, one that was suggeted only recently is Polypodium leucotomos (Konda. 2013). Ameliorative effects have also been observed in psoriasis patients, although it appears that more research would be necessary to make any recommendations (Middelkamp-Hup. 2004)
• Remission of subacute cutaneous lupus erythematosus (SCLE) - SCLE is an uncommon autoimmune disease that results in substantial photosensitivity of affected patients. Eruptions often are triggered or exacerbated by UV light (UVL) exposure and a recent case in Cutis shows that while the disease was at best "moderately controlled" with hydroxychloroquine sulfate, "near total remission of disease" was achieved after the addition of oral Polypodium leucotomos supplement (Breithaupt. 2013).
• Amelioration of atopic dermatitis, reduction of antihistamine requirements - Scientists have only shown recently in a phase IV randomized, double-blind, placebo-controlled, multicenter trial involving 105 patients aged between 2 and 17 years who were receiving topical corticosteroids to treat moderate atopic dermatitis that PL administered for 6 months led to a statistical significant reduction in oral histamine use of  4.5% (for those interested, patients received Anapsos 120 mg manufactured by Especialidades Farmacéuticas; Ramirez-Bosca. 2013).
• Prevention of the shift in Th1/Th2 (immune characteristics) in response to trauma - In 2007 already researchers from the University of Zaragzoa found that PL blocked the postoperative (day 1) increases in IL-6 and IL-10 in rats undergoing fracture..On postoperative day 7, "rats undergoing fracture showed an increase of IL-6 levels", the latter was not observed in the PL supplemented rats who had increased levels of the "good" inflammatory cytokine IL-12 on postoperative day 7, instead (Navarro-Zorraquino. 2007)

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

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

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

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

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

References:

• Aguilera P, Carrera C, Puig-Butille JA, Badenas C, Lecha M, González S, Malvehy J, Puig S. Benefits of oral Polypodium Leucotomos extract in MM high-risk patients. J Eur Acad Dermatol Venereol. 2013 Jul 31.
• Argilés JM, Meijsing SH, Pallarés-Trujillo J, Guirao X, López-Soriano FJ. Cancer cachexia: a therapeutic approach. Med Res Rev. 2001 Jan;21(1):83-101.
• Breithaupt AD, Jacob SE. Subacute cutaneous lupus erythematosus: a case report of Polypodium leucotomos as an adjuvant therapy. Cutis. 2013 Apr;89(4):183-4.
• Konda S, Geria AN, Halder RM. New horizons in treating disorders of hyperpigmentation in skin of color. Semin Cutan Med Surg. 2013 Jun;31(2):133-9.
• Middelkamp-Hup MA, Pathak MA, Parrado C, Garcia-Caballero T, Rius-Díaz F, Fitzpatrick TB, González S. Orally administered Polypodium leucotomos extract decreases psoralen-UVA-induced phototoxicity, pigmentation, and damage of human skin. J Am Acad Dermatol. 2004 Jan;50(1):41-9.
• Navarro-Zorraquino M, García-Alvarez F, Martínez-Fernández AR, Pastor C, Larrad L, Salinas JC, Lozano R. Pharmacological immunomodulation of surgical trauma. J Invest Surg. 2007 Sep-Oct;20(5):283-9. 
• Ramírez-Bosca A, Zapater P, Betlloch I, Albero F, Martínez A, Díaz-Alperi J, Horga JF; Grupo de Anapsos en Dermatitis Atópica y centros de realización del estudio. Polypodium leucotomos extract in atopic dermatitis: a randomized, double-blind, placebo-controlled, multicenter trial. Actas Dermosifiliogr. 2013 Sep;103(7):599-607. Epub 2013 May 3.
• Rodríguez-Yanes E, Juarranz Á, Cuevas J, Gonzalez S, Mallol J. Polypodium leucotomos decreases UV-induced epidermal cell proliferation and enhances p53 expression and plasma antioxidant capacity in hairless mice. Exp Dermatol. 2013 Aug;21(8):638-40.
• Solivellas B, Martin TC. Polypodium leucotomos Extract use to prevent and reduce the risk of infectious diseases in high performance athlete. Infection and Drug Resistance. 2013 Oct 15.

On Short Notice: Oxytocin to Boost Testosterone & Block Cortisol? Exercise for Life-Extension? Which Tea for Metal-Chelation? Which Fat to Reduce Calorie Intake by ~30%?

Image 1: This is still my preferred way to boost oxytocin - regardless of possible ergolytic effects ;-)

Due to the sudden heat-wave over here in good old Germany I thought, I'd use these early morning hours to get another installment of "On Short Notice" on it's way before my brain dries out (or I drown in the public swimming pool ;-). I hope you enjoy the four items on the recent interest in intranasal the hormone modulating effects of oxytocin, it's effect on cortisol and progesterone, estradiol and (I know you were waiting for that ;-) testosterone, my early morning / late evening (depending on whether you see this from my or Wyatt's perspective) 'intellectual' exchange on the potential longevity effects of exercise and why it probably is not life-extending in the literal sense, the different antioxidant potency of green, black and white tea and their ability to chelate metals (=help to remove all not just "bad" metals from the body) and the best fat, DHA or MUFA to blunt appetite and help you stick to your diet.

Don't forget to come back later today (or maybe early tomorrow for some of you ;-), for a third installment of "On Short Notice", which will hopefully suffice to "get rid" of the stock I have... ah, I did not forget about the Circadian Rhythm Series, by the way, it's just that the SuppVersity rhythm got slightly out of sync ;-)

• 

  Figure 1: Effects of 26IU of intranasal oxytocin at rest on progesterone, estradiol and testosterone in healthy men (large; based on Gossen. 2013); effects of 24IU or 48IU of intranasal oxytocin administered before a steady state cardio session on cortisol levels in healthy young men (small; from Cardoso. 2013)

  Intranasal oxytocin to block cortisol & boost testosterone A whole series of studies has been published recently; all of them have one thing in common, they investigate the various physiological and psychological effects of oxytocin. Of these, the two studies by Gossen et al. and Cardoso et al. are yet probably of greatest interest for the average physical culturist. After all, the researchers from the Centre for Research in Human Development at the Concordia University in Quebec (Canada) were able to show that the administration of 24IU (not the higher dose of 48IU, though;see figure 1) effectively reduced the increase in cortisol in a 70% HRmax steady-state cardio session in 17 healthy young men (aged 18–3; mean ± SD; 23.1 ± 3.5), in the experiment they describe in their Aug 2013 paper in Psychoneuroendocrinology (Cardoso. 2013).
  And even though the German scientists from the University of Aachen report minimal, but statistically significant increases in testosterone in 8 young men (mean age 26.4 ± 2.6 years) at rest, 210min after the (likewise) intranasal administration of a minimally higher dose (26IU) of oxytocin (Gossen. 2013). Both of these observations are not just very similar to what your average natty test booster is supposed to do, their real-world effects are probably also as insignificant. Also, did you ever try to tear down the gym and rep out a couple of PRs a couple of minutes after having sexual intercourse? If so, you should actually be aware why oxytocin probably ain't the ideal pre-workout supplement - in this regard it is also somewhat unfortunate that Cardoso et al. did not do a real performance test (suggested read: "Will Sex Before A Competition Hamper Your Performance"; note: this is not about sex minutes before the competition ;-).
  And when it comes to building muscle, previous research from Phillips lab at McMasters University appears to suggest that blocking cortisol is a hilarious idea, anyway. After tall, cortisol was the only endocrine hormone the elevation of which in the vicinity of resistance training sessions showed a positive correlation (r=0.29, P=0.03 cf. West. 2011) with increases in lean muscle mass in the large-scale by West et a.
• Exercise gets rid of the junk in your body, but will it help increase your lifespan? Basically this could be the headline to an interesting exchange of thoughts, I just had with Wyatt Brown on the SuppVersity facebook wall - one I believe is well worth being "recorded" as a short news item. The discussion came about in response to me posting the link to a study by He et al. who found that the way exercise induces autophagy (=natural, healthy cell death) contributes to its beneficial effects in the prevention of all sort of ailments, above all cancer and neurological problems such as Alzeimer's & co, because it allows your body to get rid of the debris and junk that's accumulating from just living your life (no matter how healthy or unhealthy that may be). Since exercise is not the only thing that can ramp up autophagy, and caloric restriction (as in starving yourself to live longer) can do the same, Wyatt mused about whether or not you could achieve the same (more or less; for animals vs. humans) proven benefits of life-long caloric restriction by exercise.

  

  Image 2: Twin studies are one of the ways to identify whether genes or lifestyle are the fundamental determinants of how old we get. One of the consistent findings of the numerous pertinent studies is that lifestyle factors (diet, exercise, but also our outlook on life, friends and family!) determine how well we are able to use the time that our genes (or whoever you want) has granted us on earth. Not more, but not less, either: If 100 years are what we got, all exercise and healthy eating will allow us to make it to that age with great ease, not more... and let's be honest, if that was the biblical age of 100y, wouldn't it be ungrateful to ask for more?

  A very good question, indeed and one I do not have a definite answer to. In view of recent reviews of the role of exercise in the longevity of centenarians (the oldest of the old; cf. Venturelli. 2013), it does however seem more likely that exercise does not have direct effects on the life-span, but, as Huffman states, "[e]pidemiologic evidence in humans supports exercise as a strategy to reduce the risk of morbidity and mortality" (Hufmann. 2010). Unfortunately, a low mortality won't help you to make it past the 100 ± X years your genes have in stock for you. The insights into the genetic determinants from pertinent studies into single-nucleotide polymorphisms (SNPs ~ single gene variations) does support this notion (Sorensen. 2013): The oldest of the old don't stick out, because their genes protect them from premature death, but simply because their genes allow for more cell cycles to occur before the 'natural reserve'. We already know that telomere length is a fundamental determinant of this 'reserve', so that it is not really surprising that telomere length at birth is one of the most reliable predictors of longevity (Heidinger. 2013)!
  Now, if we just use a totally random number to use basic math to make us understand, what this means, we could say that your telemore length at birth may be sufficient to make it to age 100, assuming that it is not prematurely shortened or you are dying from whatever other "natural" (not accidents etc.) cause, such as cancer, metabolic syndrome, CVD etc., exercise will of course help you to make it to those 100 years, but when the say 100,000 total turn overs that your telomeres allow for are done, you are done as well - no matter how "healthy" you eat and how much you exercise in the 99.99 years before. If you complement this "preventive" (=mortality reducing) effect by literally living on the slow lane, i.e. downregulating all your metabolic processes by starving yourself, you will obviously slow down the turn-over rate, as well. For simplicity of the calculation we assume that all these processes are linear (which I can guarantee they are not) and you are eating so little that you achieve a 50% slow down. That would mean that your turn-over rate would be reduced from 1,000 / year to 500 / year. Your reserves would last 2x longer and, assuming you eat and exercise and thus decrease your mortality risk, will allow you to make it to the ueber-biblical age of 200years! Great? Well you decide...

• 

  Image 3: If you want to get rid of metals, white tea should be your tea of choice, if you are already low on iron, copper, zinc & co. you should at least drink it away from your meals, though.

  Different tea preparations different effects antioxidant activity and metal chelation ability  It is nothing new that green and black tea will have differential effects on your physiology. What is yet a novelty is a comparison of the antioxidant and metal chelating activity the exact same hand plucked leaves of a specific cultivar (in this case PC108, bred in Malawi, typically used for black CTC tea production) will have when it is used for the production of either white, two black (Orthodox and CTC; both methods produce leaves of fannings or dust grades that are commonly used in tea bags, CTC = crush + tear + curl is processed by machines, while orthodox usually involves a mixture of mashine and manual processing) or two green (w/ and w/out caffeine) teas - a comparison like the one Patricia Carloni and her colleagues present in their latest paper in Food Research International (Carloni. 2013).
  As you will probably have expected the least processed green tea exhibited the greatest, while the most processed CTC black tea the least antioxidant activity (green ≥ low-caffeine green > white ≥ black Orthodox > black CTC), what may come as a surprise though is the superiority of white tea in the metal chelation essay the scientists performed. Closely followed by the orthodox black tea, the CTC tea (<50% of the white tea metal chelating activity) and the two green teas (<25% of the white tea metal chelating activity).

• 

  Figure 2: Reduction in calorie intake on standardized breakfast 20min after the ingestion of 6ml of a lemon flavored oil emulsion and in the course of the day compared to no oil control (based on Harden. 2013)

  Fat satiety effects: DHA > Olive Oil (MUFA) > regular diet That would be the ranking according to the satiety effects of the different fatty acids, as elucidated in a recently published study in the British Journal of Nutrition (Harden. 2013). For their study, the researchers had recruited 18 healthy normal-weight men. In a single-blind, three-way crossover study design the subjects received a single 6ml dose of either DHA or oleic acid (olive oil is 60-80% oleic acid, alternatives would macadamia ~60% and high-oleic acid sunflower oil >82%) with lemon flavor. The day before, the subjects had consumed standardized diets. 20min after the ingestion of the emulsion, they had a standardized breakfast, went home and went about their regular daily business for the rest of the day.
  The telephone interviews the researchers conducted on the next day showed that the ingestion of the DHA emulsion had exerted an, as the researchers argue cholecystokinin (CCK) dependent, decrease in energy intake of -20% and -29% for the breakfast and the total daily energy intake, respectively. That would make DHA a pretty effective tool to stick to my often-suggested -20% caloric deficit when you're dieting - at least for healthy individuals. Whether this will work for the obese, let alone morbidly obese with their deranged satiety signaling remains to be seen, though.

As I mentioned in the introduction, already. This was not the last "On Short Notice" item for this weekend. So, digest this, have some sex to calm down (unless you are about to work out, obviously), and drink a cup of tea to increase your chance to make sure that your end is not arriving before it's time and you can come back for more ;-)

References

• Cardoso C, Ellenbogen MA, Orlando MA, Bacon SL, Joober R. Intranasal oxytocin attenuates the cortisol response to physical stress: A dose-response study. Psychoneuroendocrinology. 2013 Aug 10. 
• Carloni P, Tianob L, Padellab L, Bacchettic T, Customud C, Kayd A, Damian E. Antioxidant activity of white, green and black tea obtained from the same tea cultivar. Food Research International. 2013.
• Gossen A, Hahn A, Westphal L, Prinz S, Schultz RT, Gründer G, Spreckelmeyer KN. Oxytocin plasma concentrations after single intranasal oxytocin administration - A study in healthy men. Neuropeptides. 2013 Aug 9. 
• Harden CJ, Jones AN, Maya­Jimenez T, Barker ME, Hepburn NJ, Garaiova I, Plummer SF, Corfe BM. Effect of different long­chain fatty acids on cholecystokinin release in vitro and energy intake in free­living healthy males. British Journal of Nutrition. 2013; 108:755­-758
• He C, Sumpter R Jr, Levine B. Exercise induces autophagy in peripheral tissues and in the brain. Autophagy. 2013 Oct 1;8(10).
• Heidinger BJ, Blount JD, Boner W, Griffiths K, Metcalfe NB, Monaghan P. Telomere length in early life predicts lifespan. Proc Natl Acad Sci U S A. 2013 Jan 31;109(5):1743-8. Epub 2013 Jan 9.
• Huffman DM. Exercise as a calorie restriction mimetic: implications for improving healthy aging and longevity. Interdiscip Top Gerontol. 2010;37:157-74. Epub 2010 Aug 10. 
• Soerensen M. Genetic variation and human longevity. Dan Med J. 2013 May;59(5):B4454.
• Venturelli M, Schena F, Richardson RS. The role of exercise capacity in the health and longevity of centenarians. Maturitas. 2013 Aug 7.
• West DW, Phillips SM. Associations of exercise-induced hormone profiles and gains in strength and hypertrophy in a large cohort after weight training. Eur J Appl Physiol. 2013 Jul;112(7):2693-702. Epub 2011 Nov 22.

On Short Notice: Ghrelin & GH Boosting Fats for Intermittent Fasting, 4-AD, 5-AA, Testosterone & Co in "Pod", Too Much Vitamin D for Your Prostate, Estrogens in Milk & More

Image 1 (fidged-group.co.uk): Being average may not be sexy, but one thing I did not mention in the summary of what you are going to learn today is that an average amount of body fat (not the new average American though ;-) could hold the key for a longer life - ah, I almost forgot: This is only valid if it comes with an appropriate amount of lean mass, which is still the best predictor of a long and healthy life!

Somehow these On Short Notice posts become increasingly longer... I had to "outsource" a couple of items, to reduce today's installment to a manageable length, but don't worry a couple of them will turn up in the next installment or make it into the regular news in the days to come. For now you will have to settle for valuable and at least in part surprising insights into the broad range of effects different types and loads of dietary fat can have on your appetite, metabolism and your, or rather your bacterial subtenants' methane production. You will also learn what TAC means and why you want more than 1,080 units of it in every 100g of whatever you are stuffing down your pie-hole. You will be surprised to hear that SuppVersity student FatFree instinctively chose the low estrogen variety of dairy, when he "downed 1l of raw goat's milk" from his local farmer earlier today (see respective comment) and you will attend another lesson of the "what's good for your obese neighbor, is not necessarily good for you" class. All that will be topped of with some testosterone laden, WADA prohibited "pod", too much vitamin D for your prostate to handle and a glass of bone-conserving wine for the habitual drinkers among the ladies ;-)

Fat Interactions - MUFA, PUFA, SUFA and How They Influence Your Metabolism

The idea that "not all fats" are created equal is meanwhile broadly accepted. What is still a matter of constant debate, though, is which of the three main classes, i.e. saturated, mono- and polyunsaturated fatty acids exert beneficial and which of them detrimental effects on our health. A recently published on the differential effects of butter (saturated fat), olive oil (mono-unsaturated; oleic acid + a relative high amount of omega-6), fish oil (polyunsaturated; high omega-3) and soybean oil (polyunsaturated; mainly omega-6 + some omega 3) on the expression of the purported "hunger hormone" ghrelin (note: acetylghrelin, which was measured in this study, is the "active" variety of ghrelin) may yet help to get a better grasp of what exactly we should be looking for (Saidpour. 2013), when it comes to the downstream metabolic effects of high amounts of certain fatty acids - and no, it is not for maximal ghrelin suppression.

Figure 1: Food intake (in g, left), body weight (relative to control group on regular diet, middle) and acetylghrelin levels in the fasting and fed state during the 8-week experimental period (data based on Saidpour. 2013)

As the data data in figure 1 shows, the 5-week old male Wistar rats who had been randomly assigned to either standard rodent chow or calorically identical (3.98kcal/g of food) high fat diets who were fed ad libitum every other day only to maximize the ghrelin response) for 8 weeks did not, as common sense would suggest, eat the least and gain the least on the saturated fat (butter) diet with its long lasting satiety effect (as evidenced by the lowest fasting ghrelin levels).

In fact, the exact opposite was the case: The acute satiety effect of the fish oil and olive oil diets (as evidenced by the plummeting acetylghrelin levels in the fed state) turned out to be the main determinant of the amount of food the rodents, who were effectively intermittently fasted (though with a pretty long fasting window of 24h), consumed.  And while the low ghrelin levels in the fed state reduced the food intake, the fasting induced rise of acetylghrelin to 23% higher levels than in the butter fed animals has probably given them the metabolic advantage of elevated growth hormone levels. At least this is what we must expect based on the ability of ghrelin to directly bind to the GHS receptor and induce the release of the fat annihilating 191-amino acid, single-chain polypeptide from the lateral wings of the anterior pituitary gland (Kojima. 1999).

Bottom line: While this is certainly only another small piece to the oftentimes puzzling effects of fatty acids (check the "On Very Short Notice" items in this installment for more "puzzling" effects ;-), it does not only provide another mechanism by which the original "Mediterranean diet", which is rich in both fish and olive oil and by no means as fat free as its latest mainstream interpretation would suggest, could in fact provide a metabolic edge. And though the "intermittent fasting" feeding pattern may reduce the significance of the results for the "average" inhabitant of the Western hemisphere, who can hardly go 2h without a Snickers bar or at least a sugar-laden coffee, it does suggest that all the "lean gainers" and "intermittent fasters" out there could derive great benefits from a huge piece of salmon and couple of tablespoons of high MUFA olive, macadamia or artichoke oil in their "feeding windows".

A Diet High in Dietary Antioxidant Keeps you Lean & Healthy

Image 2: Clover is among the most potent antioxidant foods.

You know that I am very critical when it comes to the supply of exogenous antioxidants (cf. "Multivitamins, a question of Faith?!"; more on multivatmins), but would never even remotely consider limiting the supply of whole foods that are rich in antioxidants. I was thus not very surprised, when I read that the consumption of high amounts of dietary antioxidants was associated with statistically significant lower body weight and abdominal fat gain in a 3-year longitudinal (this is where scientists analyze data from the same persons on different time-points) study from the University of Medical Sciences in Teheran (Bahadoran. 2013).

Foods	TAC
Cloves (see image), Cinnamon, Oregano, Tumeric, Acai (all dried or grounded)	300,000 -100,000
Cacao, Parsley, Basil, Currry, Sage, Peppercorns, Mustard, Ginger, Marjoram	100,000 -25,000
Rice bran, Chili, Pecans, Paprika, Choke berries, Elderberries, Kidney Beans (dried), Oregano, Walnuts	25,000 -10,000
Hazelnuts, Cranberries, Artichoke hearts, Blueberries, Prunes, Pistachios, Blackcurrant, Artichokes, Plums, Blueberries (cult.) Lemon balm (fresh) Blackberries, Garlic, Coriander,	10,000 -5,000
Raspberries, Basil (fresh), Almonds, Apples, Dates, Strawberries, Figs, Peanuts, Raisins, Cherries, Asparagus, Spinach	5,000 -2,500
Cornflakes, Red Cabbage, Gooseberries, Cashews Avocado, Pears, Peaches, Oranges, Oats, Macadamia, Tangerines, Broccoli, Potatoes, Grapefruit, Red grapes	2,500 -1,500
Carrots, Olive oil, Green grapes, Mango, Lettuce, Radish Eggplant, Kiwi, Banana, Red pepper, Pineapple, Artichoke, Nectarines, Pine nuts, Cauliflower, celery	1,250 -500
Leeks, Lettuce, Baby carrots, Tomatoes, White wine, cantaloupe, Honeydew, Watermelon, Cucumber	500 -100

In particular, Zarah Bahadoran and her colleagues found that the consumption of foods with an average total antioxidant capacity equal to 1,080µmol TAC essay units per 100g - something your would get from oats + blueberries or a handful of pecans and an apple - was associated with a -38 % decrease in the risk of central obesity (note: The TAC essay is an experimental measure of the total antioxidant capacity of food and is independent of whether it's phenols, vitamins, thiols or whatever that contribute to the antioxidant effects of a food; the clear disadvantage of this method is that it does not really tell you what exactly the compounds will do outside of a petri dish, but, but this is the topic for another blogpost ;-)

And while some of the confounding factors have been eliminated from the above hazard risk calculations, it is still worth to take note of the fact that...

• people with the highest antioxidant intake consumed food with the lowest energy density (so they cannot be eating nuts and chocolate only ;-)
• women consumed significantly more antioxidants than men, with +10% more women in Q3 (959-1080µmolTE/100g) and +15% more women in the critical Q4 (>1,080µmol/kg) quartiles
• the more leisure time the subjects had, or I should say allowed themselves, the higher was their antioxidant intake
• high antioxidant consumers were also dairy lovers with 81% more dairy consumption in the highest quartile, exactly those people, thus, who consumed the >1,082 µmolTE/100mg diets
• needless to say that people who are reckless enough to smoke also consumed the least antioxidants

Aside from these significant differences, the non-existence of other differences people often take for granted, such as the notion that education and job activity, or different macronutrient compositions would have an impact on the total amount of antioxidants you consume, is certainly worth mentioning.

  On Very Short Notice

• 

  Figure 2: "Pod" contains a hell lot of steroids. Unfortunately, most of them will be dumped by right into the urine specimen for the WADA agents (data based on Thevis. 2013)

  "Pod" doping could get you banned, but probably won't increase your performance - While I cannot tell you what the swimmers at the Olympics have been taking to break world record after world record (some even in consecutive races on the same day), I can tell you that it were not the reddish-brown musk grains from the dried secretion from the preputial follicles of the male musk deer , which are located in the "pod", a small sac in close proximity to the preputial orifice (see figure XYZ, upper right), because none of these athletes would have passed the WADA doping controls had he or she taken a couple of grams of those steroid-containing staples of Traditional Chinese Medicine.
  Now, despite the fact that we do see "classics" such as 4-AD, Androsterone, Epiandrosterone, DHEA and even minuscule amounts of the "Big T" (1-6µg/g with the highest level in the pod from the zoo animals from Leipzig, Germany - read more about testosterone's ability to build muscle in the "Intermittent Thoughts on Building Muscle") testosterone , the total amount of those compounds which could actually induce noticeable performance increases may be high enough to show up during doping controls as the five cases during the last FIFA Women World Cup show(cf. Thevis. 2013), it does not appear reasonable to assume that the rumored performance enhancing effects of musk (pod) extracts would stand the test in a placebo controlled supplementation trial.

• 

  Figure 3: When administered at a HED of ~750mg/day sodium salicates reduce the glucose (left axis) and insulin (right axis) levels in response to a standardized intraperitoneal glucose injection in obese mice, they do the opposite in lean mice (based on Nixon. 2013).

  Salicates block cortisol expression in fat cells and increase insulin sensitivity in obese mice, but... as we have seen for alpha lipoic acid (see "ALA? You are Better of Without the Purported Nutrient Repartitioner") and tons of other "wonder-supplements", things that are good for your obese neighbor will rarely work out for lean folks like, yourself; and thus it should not come as a surprise that the blockade of adipose tissue 11-beta-HSD, the enzyme that converts cortisone, the inactive form of cortisol into it's active twin, exerts no, if not the exact opposite effect (see figure 3; adapted from Nixon. 2013).
  So, if you are lean and want to stay lean, leave the aspirin, the 7-ketos and other overpriced 11-beta-HSD inhibitors or "cortisol blockers" to those who need them - inflamed, overweight (pre-)diabetics.
• Purportedly anti-carcinogenic high vitamin D levels increase risk of prostate cancer - Swedish scientists found a statistically significant trend towards an increased risk of developing prostate cancer with rising vitamin D levels. In the 7th and 8th decile which corresponds to plasma vitamin D levels of 91-97 nmol/L the calculated risk of developing prostate cancer was 67% higher than in the lowest decile (Brändstedt. 2013). Other than previous studies which reported associations between high calcium intake and prostate cancer risk, Brändstedt et al. observed an association between high serum calcium levels and prostate cancer levels only among men aged 55-65 who had a BMI < 25. It is thus very unlikely that the underlying reason of the pro-carcinogenic effects was an increase in calcium absorption... hmm, I don't have to remind you of (a) the antagonism between vitamin D and vitamin A and (b) last weeks news on the anti-carcinogenic effects of the latter, do I?

• 

  Image 3: Although the scientists controlled the compliance by measuring the serum concentration of fatty acids instead of using unreliable food logs, there are still  a lot of uncontrolled confounding variable, here. Hower, the same can be said of those studies on which the concept of the pro-inflammatory omega-6s is based. Anyway, I will still eat butter, not margarine and if olive oil is one of staple sources of dietary fat, you will be getting plenty of omega-6 from this purported GH booster (see previous new item)

  High omega-6 diet reduces insulin, total/HDL-cholesterol ratio, LDL cholesterol, and triglycerides - Helena Bjermo and her colleagues from the Uppsala University in Sweden report that feeding 67 abdominally obese patients (15% were diabetic) either a butter-based high saturated fat diet or a diet that was particularly rich in linoleic acid (omega-6 mainly from sunflower oil; 15% of the total energy intake) for 10 weeks had very differnt effects on the hepatic fat content an other highly relevant markers of metabolic health. Despite the fact that both diets were isocaloric, the butter-based high saturated fat diet increased the hepatic fat content of the study participants (measured by MRS) by 10% while the subjects in the high PUFA group were able to reduce the fat content of their livers by -35%. Similarly, the basal insulin level, triglycerides, as well as total and LDL cholesterol increased in the butter eaters and decrease or remained the same in the 15% linoleic acid group.
  The results are honestly not what I had expected, but in essence only further evidence there is still a lot to learn about the shades of grey that exist between the dichotomous black and white that is still so characteristic of the way we think about fats.
• Goat's milk is the better choice for people concerned with limiting their intake of exogenous estrogens - According to analyses that were conducted at the Laboratory of Proteomics and Analytical Technologies in Frederick (Farlow. 2013), cow's milk contains significantly more estrogens (estrone and 17beta-estradiol) than goat's milk and that irrespective of whether it was organically produced or not. Bad news for the reproductive health of the North Americans and Europeans, where the consumption of cow's milk exceed that of goats milk by several magnitudes and good news for the fertility of the rest of the world, where goat's milk still is the "milk of choice".

• 

  Image 4: Looks like this was not the only potential side effect of methane producing bacteria in your gut.

  High fat diets increase the ratio of methane producing to other bacteria and thus increase obesity risk - Most of you will probably remember the finding that mice without gut microbiome are more or less resistant to dietary induced obesity. A recent study does now suggest that (as it was to be expected) not all bacteria are created evil.. ah, pardon... equal ;-) In the lab mice of Ruchi Mathur and his colleagues, the tendency to develop obesity correlated with the amount of gastrointestinal (GI) methanogens, including Methanobrevibacter smithii, and was independent of the presence of other bacteria (Mathur. 2013).
  With the pro-methanogenic (=allows those little bastards to grow) effects of high fat diets Mathur et al. may in fact have found another potential co-founder in the development of the metabolic syndrome. Interestingly enough Methanobrevibacter smithii is also the predominant methanogen in patients with constipation-dominant IBS and methane breath (Kim. 2013) - so if that is you, this could be one of the few cases where the use of a broadband antibiotic could save you from a lot of ailments, because you would thus not have to care about contradictory results from Million et al., as well as dozens of other studies, each of which identifies another type of bacteria as 'the root cause' of the obesity epidemic - in Million's case the name of the scapegoat is Lactobacillus reuteri, by the way (Million. 2013).
• Mediocrity guarantees a long life - At least when it comes to body fatness being too lean and being too fat are equally detrimental to the life expectancy of male 65+ agers (Toss. 2013). If you are women, though, the results Fredrik Toss and his colleagues published in the latest issue of Age and Ageing suggest that being on the chubbier side of things can actually be life-saving, as long as you carry the fat in the gynoid and not the abdominal area. Most importantly, however, lean mass, or as my buddy Carl Lanore calls it, "metabolic currency" is yet still the most significant predictor of survival in older subjects - in other words: Don't even think of emulating the skinny fat celebrities with their starvation diets and endless cardio sessions if you intend to live your grand- and grand-grand-children, better check out yesterday's news on the "Iranian HIIT Solution for Improved Insulin and Leptin Sensitivity".

• 

  Image 5: If you are concerned about bone health, menopause is not the best time to stop drinking... unless you start weight lifting, of course ;-)

  Don't stop drinking alcohol in menopause! At least if you don't want to increase bone-resorption, i.e. the leeching of calcium from your bones. This is the surprising result of a recently published study by Jill A. Marrone and colleagues, who had  investigated the effects of total abstinence from alcohol in 40 healthy postmenopausal women (mean ± SE age, 56.3 ± 0.5 y) who consumed the alcohol equivalent of ~1 glass of wine per day (Marrone. 2013). Interestingly, the bone formation marker osteocalcin and the resorption marker C-terminal telopeptide (CTx) returned to their normal values, once the women resumed their former drinking habits.
  In view of the fact that there was also a significant correlation between baseline bone-density, as measured dual-energy x-ray absorptiometry, and the extent of mild to moderate alcohol consumption, these results raise the question whether "bone health" would be another factor to add to the list of the "minimalist approach" to alcohol consumption.

References:

• Bjermo H, Iggman D, Kullberg J, Dahlman I, Johansson L, Persson L, Berglund J, Pulkki K, Basu S, Uusitupa M, Rudling M, Arner P, Cederholm T, Ahlström H, Risérus U. Effects of n-6 PUFAs compared with SFAs on liver fat, lipoproteins, and inflammation in abdominal obesity: a randomized controlled trial. Am J Clin Nutr. 2013 May;95(5):1003-12. 
• Brändstedt J, Almquist M, Manjer J, Malm J. Vitamin D, PTH, and calcium and the risk of prostate cancer: a prospective nested case-control study. Cancer Causes Control. 2013 Aug;23(8):1377-85.
• Farlow DW, Xu X, Veenstra TD. Comparison of estrone and 17β-estradiol levels in commercial goat and cow milk. J Dairy Sci. 2013 Apr;95(4):1699-708.
• Kojima, M., Hosoda, H., Date, Y., Nakazato, M., Matsuo, H., Kangawa, K. Ghrelin is a growth hormone releasing acylated peptide from stomach. Nature. 1999; 402, 656-660.
• Mathur R, Kim G, Morales W, Sung J, Rooks E, Pokkunuri V, Weitsman S, Barlow GM, Chang C, Pimentel M. Intestinal Methanobrevibacter smithii but Not Total Bacteria Is Related to Diet-Induced Weight Gain in Rats. Obesity (Silver Spring). 2013 Jun 7. 
• Marrone JA, Maddalozzo GF, Branscum AJ, Hardin K, Cialdella-Kam L, Philbrick KA, Breggia AC, Rosen CJ, Turner RT, Iwaniec UT. Moderate alcohol intake lowers biochemical markers of bone turnover in postmenopausal women. Menopause. 2013 Jul 9.
• Million M, Maraninchi M, Henry M, Armougom F, Richet H, Carrieri P, Valero R, Raccah D, Vialettes B, Raoult D. Obesity-associated gut microbiota is enriched in Lactobacillus reuteri and depleted in Bifidobacterium animalis and Methanobrevibacter smithii. Int J Obes (Lond). 2013 Jun;36(6):817-25.
• Nixon M, Wake DJ, Livingstone DE, Stimson RH, Esteves CL, Seckl JR, Chapman KE, Andrew R, Walker BR. Salicylate downregulates 11β-HSD1 expression in adipose tissue in obese mice and in humans, mediating insulin sensitization. Diabetes. 2013 Apr;61(4):790-6.
• Saidpour A, Kimiagar M, Zahediasl S, Ghasemi A, Vafa M, Abadi A, Daneshpour M, Zarkesh M. The modifying effects of fish oil on fasting ghrelin mRNA expression in weaned rats. Gene. 2013 Jul 25.
• Thevis M, Schänzer W, Geyer H, Thieme D, Grosse J, Rautenberg C, Flenker U, Beuck S, Thomas A, Holland R, Dvorak J. Traditional Chinese medicine and sports drug testing: identification of natural steroid administration in doping control urine samples resulting from musk (pod) extracts. Br J Sports Med. 2013 May 6.
• Toss F, Wiklund P, Nordström P, Nordström A. Body composition and mortality risk in later life. Age Ageing. 2013 Jul 20.

Double Your Workout Volume With 3,4-DA - Chlorogenic Acid Metabolite, Dihydroxycinnamic Acid, Makes Rats Run 60% Longer, 30% Faster 90% Further!

Image 1 (sodahead.com): Another reason to supersize your cup of coffee; no not the girl, or ... well ;-)

Those of you who can no longer be without their well-deserved daily dose of SuppVersity news will probably remember the amazing weight loss effects an extract from green coffee beans yielded in a 2013 trial by Vinson et al. (cf. "GCB Another Fatloss Acronym: Green Coffee Bean Extract Helps Pre-Obese Men and Women Shed 16lbs in 22 weeks"; Vinson. 2013) and while I am still not convinced that you would see similar results in non-obese individuals, another recently published study by Novaes et al. does suggest that even those of you who don't think that they have another lbs of body fat to spare, could largely benefit not just from the caffeine, but also from the 0.5-1.0g of chlorogenic acid and the subsequent conversion of the latter into 250-500mg of 3,4-Dihydroxycinnamic acid (3,4-DA) even 400ml of regular coffee do contain (Chung. 2004; Novaes. 2013).

3,4-DA is like legal gear from the brown brew

Compared to placebo and vitamin C (25mg/kg), the hydrolyzed chlorogenic acid molecule, of which the 8-week-old male Wistar rats in the Noves study received either 5mg or 25mg per kg body weight (HED for 80kg human being: 65mg or 324mg) had almost incredibly potent "ergogenic" effects:

Figure 1: Time to fatigue (TTF), speed, workload and total distance covered (secondary axis) during exhaustive treadmill running after oral supplementation with placebo (control), vitamin C or 4,5 DA at doses of 5mg/kg and 25m/kg (based on Novaes. 2013)

As you can see in figure 1 the rodents in the high dose group ran 60% longer, 30% faster, 90% further and performed overall twice as much work (42 vs. 21 kg*m) than the rodents who had received the human equivalent of ~325mg vitamin C before a forced running test on a motor-driven treadmill.

Less ROS = Increased efficacy?!

Interestingly, the lactate levels of the 3,4-DA rodents were significantly lower and the remaining liver glycogen levels were significantly higher than in the placebo and vitamin C group (see figure 2).

Figure 2: Serum triglyceride (group effects non-significant) and lactate levels, hepatic glycogen content and protein arbonyl and malondialdehyde levels after the exercise (based on Novaes. 2013)

As Novaes et al. point out this suggests that the effect is partly mediated by a higher metabolic efficiency. The latter is probably a direct result of the profound reduction in reactive oxygen specimen, which have been associated with impairments of the cellular metabolism and subsequently reduced aerobic energy production (Atalay. 2002) - a hypothesis that would be supported by the reduced levels of protein carbonyl and malondialdehyde in the liver of the 3,4-DA treated rodents.

But don't we need ROS?

Image 2: Don't worry those love handles will go away - rather with the antioxidant + caffeine power of coffee than without it!

These observations are also quite revealing as the offer an alternative explanation for the previously mentioned possibly negative effects of antioxidants on the exercise-induced improvements in glucose metabolism (cf. "Update on Antioxidants & Exercise - Neither Vitamin C Nor E Have ANY Effect on the Response to Intense Exercise"): If high doses of other anti-oxidants have the same beneficial effects on metabolic efficacy, it stands to reason that even weaker antioxidants than 3,4-DA would spare liver (and muscle) glycogen and thus reduce the exercise-induced expression of AMPK of which you may remember from posts like "AMPK II/III: Leucine, HMB and a Glimpse on Other AMPK Modulators" that it is expressed in response to intracellular glucose, or more specifically ATP depletion, and the subsequent increase in glucose (re-uptake).

A huge cup of coffee before your workout will therefore neither hamper the weight loss, nor the health effects of your workout, as long as you do actually make use of its ergogenic effect and train 60% longer, 30% faster, 90% further and perform overall twice as much work... just kiddin', if you train regularly you should be more concerned about keeping the amount of inflammation at bay - some is probably necessary, too much counter-productive, but that would the topic of another SuppVersity post. I for one am now going to get myself a nice cup of coffee...yummy!

Suggested reads on coffee:

• GCB Another Fatloss Acronym: Green Coffee Bean Extract Helps Pre-Obese Men and Women Shed 16lbs in 22 weeks.
• Warding Off Holiday Weight Gain 2.0: The Anti-Diabesity Effect of Coffee Goes Beyond its Caffeine Content.
• Only "Real", Not Decaffeinated Instant Coffee Increases Fatty Acid Oxidation. Revisited: Caffeine's Dose-Dependent Effects on Testosterone & Cortisol Response to Exercise
• Study Identifies Caffeic Acid Induced AMPK-α2 Activity Behind the Fat Burning, Insulin-Sensitizing & Life-Extending Effects of Coffee. Plus: Why Creatine & Coffee Don't Mix!

• all about coffee

References:

1. Atalay M, Laaksonen DE. Diabetes, oxidative stress and training. Journal of Sports Science and Medicine 2002 Jan; 1 - 14.
2. Chung TW, Moon SK, Chang YC, Ko JH, Lee YC, Cho G, Kim SH, Kim JG, Kim CH. Novel and therapeutic effect of caffeic acid and caffeic acid phenyl ester on hepatocarcinoma cells: complete regression of hepatoma growth and metastasis by dual mechanism. FASEB J. 2004 Nov;18(14):1670-81.
3. Novaes RD, Gonçalves RV, Peluzio Mdo C, Natali AJ, Maldonado IR. 3,4-dihydroxycinnamic Acid attenuates the fatigue and improves exercise tolerance in rats. Biosci Biotechnol Biochem. 2013 May 23;76(5):1025-7.
4. Vinson JA, Burnham BR, Nagendran MV. Randomized, double-blind, placebo-controlled, linear dose, crossover study to evaluate the efficacy and safety of a green coffee bean extract in overweight subjects. Diabetes Metab Syndr Obes. 2013;5:21-7. Epub 2013 Jan 18.