Showing posts with label thyroid. Show all posts
Showing posts with label thyroid. Show all posts

Sunday, December 22, 2013

Natural Sildenafil & Testosterone Alternatives: Pedalium Murex & Paederia Foetida +150% Testosterone and +200% Erectile Function. Plus: Icariin, Aromatase & Stronger Bones. Probiotics, Phytosterols & Thyroid Activity.

If the Aliens have seen these Bugarash apocalypse pilgrims, they have probably turned tail and fled ;-)
I guess the SuppVersity figure of the week was a date "12/21/2013", I mean this is a once in a life-time event! Or do you really believe there will be another chance for mankind to be snatched from the jaws of extinction?

Ok, enough of the sarcasm, the world is still there and the SuppVersity is still operating, so let's get to the not so short On Short Notice items for today.

If there had been more room in the headline I would probably have labeled it "Endocrine Special" and I guess once you have gone through the posts, you will agree that this would certainly have made sense.

  • Traditional treatment of osteopenia with Epimedium brevicornum works, 'cause it's a potent aromatase promoter (Yang. 2013) -- When a group of researchers from the Chengdu Institute of Biology, Chinese Academy of Sciences and the School of Chinese Pharmacy, Chengdu University of Traditional Chinese Medicine in Chengdu, China, set out to investigate the mechanism behind the anti-osteoporotic effects of the dried leave extract from Epimedium brevicornum, they already suspected that it would probably be related to some sort of endocrine modulation.

    Figure 1: In vitro effect of Forskolin and Icariin on aromatase expression in KGN cells (Yang. 2013)
    With estrogen deficiency being the major cause of osteoporosis, a disease which does by the way affect over 200 million people worldwide (Riggs. 1998), being their the most likely mechanism behind the bone building and bone mineral density (BMD) protective effects, it was obvious to study, whether there was some sort of interaction between the extract and the data in figure 1 shows that Yang et al. were right to do so (note: the cell line used in the study was a KGN granulosa cell that's closely associated with the developing female oocyte, so effects could vary from one tissue to the other)

    Now all that certainly sounds as if this was bad stuff no sane male human being should be taking. Luckily, for many of you, my fellow men, who may have been exposed to Epimidium / Icariin from various supplements, this is not the case. Why? Simply because estrogen is not the enemy and Epimidium has not only been found to have anti-aging effects (whole extracts; Yan. 2009), it also prevents neurotoxicity from beta-amyloid plague the key feature of Alzheimer's and similar diseases (Zeng. 2010; listen to Thursday's Science Round-Up for other amyloid beta inhibitors / protectant's) and the neurotoxic effects of excess corticosteroids (Liu. 2011). In addition, Epimidium pubescen flavenoids have been shown to reverse the negative effects even passive exposure to cigarette smoke may have on the bone mineral density of male rats (Gao. 2013) and Icariin the common denominator in all of the members of the Epimidium family exerts direct proliferative and thus pro-fertility effects on the sertoli cells in male rodents (Nan. 2013).

    Table 1: Analysis of Chinese Epimidium species (MDida. 2010)
    Ah, and last but not least the beneficial effect Horny Goat Weed (likewise one of the members of the Epimidium family) has on male libido are likely partly a result of the increased aromatase activity, as well. If it works for you, your estrogen levels are probably pretty low to begin with (this reasoning is based on the profound beneficial effects of estrogen on male libido in men expressing little to no aromatase enzyme; Carani. 1999).

  • Pedalium murex Linn. fruits may not be as potent acute libido and erectile performance enhancers as sildenafil, but the effects accumulate and persist just as its unique testosterone boosting effects (Sharma. 2013) -- In case taking a potential proestrogenic compound like Horny Goat is nothing you feel would do anything good for your libido, you may want to use some Pedalium murex Linn. in traditional Indian medicinea herb that has been used in traditional Indian medicine for centuries to treat male sexual dysfunction and impotency.
    Figure 2: Effects of different doses of an ethanolic extract from Pedalium murex (P.m.) and Sildenafil citrate (5mgkg) on penile erection scores and post ejaculatory interval (time it takes to be able to have sex again) exrpessed relative to saline treated control (based on Sharma. 2013)
    As the data in figure 2 shows, its effects on erectile performance are slightly less pronounced than those of sildenafil citrate, but at an appropriate dosage and after some time, it will probably do its job sufficiently for most men with respective problems. What's really exiting though, is that the data in figure 3 clearly shows that it does so not by simple nitric oxide effects (P. murex at 10 mg/
    ml exhibited a relative nitric oxide release of 15.3 mM as compared to a nitric oxide release of 39.3472.7 mM with sildenafil citrate), but probably (also) by boosting testosterone levels. 

    Figure 3: Serum testosterone levels during and after Pedalium murex or Sildenafil citrate administration expressed relative to saline control (Sharma. 2013)
    Since the testosterone levels remained elevated for 14 days after the treatment was seized these observations make P. murex a potential candidate for the next best natty test booster.to be powered by advertisement lines like "up to 125% increase in testosterone that last for more than 2 weeks" even when you take some time off. I guess, the only serious downside here is the close relation of P. murex to the notoriously useless Tribulus, which does also contain furostanol glycosides. Luckily Magnle and Jolley found another potentially active ingredient in P. murex fruit. The compound goes by the name diosgenin and appears to be a direct precursor for the synthesis of sex hormones including testosterone (Mangle. 1998).

    Since I don't think you will have to wait very long until the first major players in the supplement business will jump on this bandwagon - you know that a single rodent study is enough to make fortune until people realize that this stuff does not work, at all - you will probably soon be able to test it on yourself. In case you intend to do that, you should certainly look for a standardized ethanolic extract with ~20%+ of diosgenin (that was the content of the extract Sharma et al. used) and a serving size of 16.2mg/kg per body weight, the HED of the 100mg/kg group (that would be 1,300mg /day of the extract for an 80kg adult).

  • Paederia foetida Linn. (P. foetida) yet another Indian libido and testosterone boosting herb (Soni. 2013) -- If you like the appeal of exclusiveness a climbing plant found in the Central and Eastern Himalayas, at elevations of up to 5000 ft, you may prefer the an ethanol extract of Paederia foetida Linn. (P. foetida) leaves over the previously discussed Pedalium murex fruit extract.

    Figure 4: Penile erection index and testosterone levels of rats after 15 and 28 days on P. foetida, data expressed relative to saline control (Soni. 2013)
    According to a recent study from the same group of Indian scientists (yet a different lead author), the effects of P. foetida and P. murex are in fact virtually identical. While the general protocol was very similar (in this done on rat, not mice) the positive control was not Sildenafil citrate, as in the previously mentioned experiment, but an intramuscular injection of 0.5 mg/kg body weight of testosterone suspension in arachis oil twice a week. It's actually a pity the scientists didn't measure the actual testosterone levels in the animals in the testosterone group. I would be curious how the 2.5x increase in the high dose group (200mg/kg, human equivalent ~2,600mg/day) would compare. When it comes to the erection quality, it did at least easily top the results of injectable testosterone (see figure 4), which is yet allegedly not the best erection booster, anyway. And if we went by the data on body weight and the weight of the testes, seminal vesicles, prostate glands and epididymis, it even appears to be more anabolic than testosterone; after all the body weight gain in the PF groups were 15%. 23% and 34% higher than in the control group and comparable if not higher to those that were induced by testosterone (+29%).

    And for all the supplement producers and fans of stacks it may be important to know that the leaves of P. foetida, which is also used as carminative, antiinflammatory, astringent, spasmolytic, antidiarrhoeal, diuretic and antilithic do contain a whole host of well- and lesser known compounds, e.g. iridoid glycosides, sitosterol, stigmasterol, campesterol, ursolic acid, hentriacontane, hentriacontanol, ceryl alcohol, palmitic acid and methyl mercaptan, but no diosgenin. So Ayurvedabol (TM) or whatever name ending on -bol, -drol or -ripp-off has not been used by the creepy competition, already, could benefit from having both Paederia foetida and Pedalium murex in it ;-)

  • Combination of probiotics and phytosterols ramps up thyroid function and (re-)establishes a healthy lipid profile (Awaisheh. 2013) -- While I could offer you a minimum of two additional libido enhancing, potentially pro-anabolic testosterone booster, I know that not all of you are into these products (am I right ladies?), so I thought it prudent to close this installment of On Short Notice with a study on thyroid metabolism, which could be is of interested for all of you.

    Which phytosterols are there and where can I find them? The major phytosterols in the human diet are sitosterol (high in nuts, amaranth, avocados, grape leaves), stigmasterol (high in coriander, chocolate and soy), campesterol (high in various vegetable oils, spec. conola / rapeseed) and brassicasterol (high in cabbage, broccoli, other brassica, but also coriander, seafood and rapeseed oil).
    Contrary to some previous studies and anecdotal reports on the Internet, a recent paper by scientists from the Department of Food Science at the Al-Balqa Applied University, in Salt, Jordan, suggest that phytosterols don't have thyroid inhibiting, but promoting effects.

    In their latest study Awaisheh et al. investigated the effects of a probiotic stack containing two strains of each of Lactobacillus acidophilus, Lactobacillus casei, Lactobacillus gasseri, and Lactobacillus reuteri and a phytosterol supplement on the lipid metabolism in rodents. Their results show that the addition of the phytosterol supplement promoted the already pronounced effects the probiotics had on the hypercholesterolemia of the rodents who were fed with a high-fat-high-cholesterol basal diet for 8 weeks. In addition, the phytosterols, yet not the probiotics alone, elevated the levels of serum total thyroxine (TT4), total triiodothyronine (TT3), and free triiodothyronin (fT3), which could have exerted additional benefits on the non-measured triglyceride levels.

    These results do actually come as a surprise and I would like to see more research - specifically in human trials - before I would buy products from producers who seize the scientists suggestion that this renders probiotics and phytosterols potential candidates for "functional foods" - I mean, let's be honest ever since the first "functional foods" hit the market people have been getting sicker: Do you really believe that's because they don't eat the "good" cholesterol lowering margarine instead of their beloved Kerrygold butter? I don't think so.

That's it for today.. well, aside from the promise to include the other testosterone and libido boosting herb studies in another SuppVersity post and a selection of the latest  SuppVersity Facebook News, of course:
  • Iron deficiency makes H Pylori go on a rampage - Iron deficiency enhances H. pylori virulence and increases risk of gastric cancer (read more)
  • Danish folk medicine for depression? Not really, but there are a couple of promising natural MAO-A inhibitors the Danes have been using for centuries (read more)
  • Strength training equally heart healthy as aerobics - 6-weeks of strength training show particular beneficial effects in African American men (read more)
Since I it's still pretty early and I am certainly not going to the city, before the shops close and all the people who believed they wouldn't need Christmas presents this year, since the world would *put whatever apocalyptic catastrophe you like here*, have gone home, I may be adding some more news later. Until then, I hope you have some fun with what's already there and are looking forward for the 2nd installment of the "Making HIIT a Hit" series that will be published tomorrow.

    References:
    • Awaisheh SS, Khalifeh MS, Al-Ruwaili MA, Khalil OM, Al-Ameri OH, Al-Groom R. Effect of supplementation of probiotics and phytosterols alone or in combination on serum and hepatic lipid profiles and thyroid hormones of hypercholesterolemic rats. J Dairy Sci. 2013 Nov 22.
    • Carani C, Rochira V, Faustini-Fustini M, Balestrieri A, Granata AR. Role of oestrogen in male sexual behaviour: insights from the natural model of aromatase deficiency. Clin Endocrinol (Oxf). 1999 Oct;51(4):517-24.
    • Gao SG, Liu H, Li KH, Liu WH, Xu M, Jiang W, Wei LC, Zhang FJ, Tian J, Xiao WF, Yang Y, Song Y, Lei GH. Effect of Epimedium pubescen flavonoid on bone mineral density and biomechanical properties of femoral distal end and femoral diaphysis of passively smoking male rats. J Orthop Sci. 2013 May;17(3):281-8.
    • Liu B, Zhang H, Xu C, Yang G, Tao J, Huang J, Wu J, Duan X, Cao Y, Dong J. Neuroprotective effects of icariin on corticosterone-induced apoptosis in primary cultured rat hippocampal neurons. Brain Res. 2011 Feb 23;1375:59-67. 
    • Mangle MS, Jolley CI. HPTLC studies on Tribulus terrestris (Chota ghokru) and Pedalium murex (Bada ghokru). Indian Drugs. 1998; 35:189–194.
    • MDidea Extracts Professional. Horny Goat Weed or Epimedium Herb: Botanical Origin, Archeology, Traditional and Pharmacological findings of Epimedium species, fractions and isolated components. 08th, Oct. 2010. < http://www.mdidea.net/products/herbextract/icariin/data10.html > retrieved on 12/21/2013. 
    • Nan Y, Zhang X, Yang G, Xie J, Lu Z, Wang W, Ni X, Cao X, Ma J, Wang Z. Icariin stimulates the proliferation of rat Sertoli cells in an ERK1/2-dependent manner in vitro. Andrologia. 2013 Nov 7.
    • Riggs BL, Khosla S, Melton LJ 3rd. A unitary model for involutional osteoporosis: estrogen deficiency causes both type I and type II osteoporosis in postmenopausal women and contributes to bone loss in aging men. J Bone Miner Res. 1998 May;13(5):763-73. 
    • Sharma V, Thakur M, Dixit VK. A comparative study of ethanolic extracts of Pedalium murex Linn. fruits and sildenafil citrate on sexual behaviors and serum testosterone level in male rats during and after treatment. J Ethnopharmacol. 2013 Aug 30;143(1):201-6.
    • Soni DK, Sharma V, Chauhan NS, Dixit VK. Effect of ethanolic extract of Paederia foetida Linn. leaves on sexual behavior and spermatogenesis in male rats
    • Yan S, Wu B, Lin Z, Jin H, Huang J, Yang Y, Zhang X, Shen Z, Zhang W. Metabonomic characterization of aging and investigation on the anti-aging effects of total flavones of Epimedium. Mol Biosyst. 2009 Oct;5(10):1204-13.
    • Zeng KW, Ko H, Yang HO, Wang XM. Icariin attenuates β-amyloid-induced neurotoxicity by inhibition of tau protein hyperphosphorylation in PC12 cells. Neuropharmacology. 2010 Nov;59(6):542-50.

    Sunday, December 15, 2013

    Complete Meals & GI (Non-)Sense, Glutamine & GLP-1, Low Thyroid & High Trigs, N-3 vs. N-6 Interactions, Optimal DHA Dosage in Kids W/ NAFLD, Selenium vs. Aluminum Toxicity

    While this is not the exact combination of chicken breast, mashed potatoes and salad in the first one of today's news items, it's more than likely that the predicted GI (and thus probably what you would find if you looked it up in a table) overestimates the postprandial glucose response to this meal by ~50% and says absolutely nothing about the insulin response. It looks like complex meals and over-simplified theories, don't mix well, at all ;-)
    78% that's the SuppVersity Figure of the Week and actually part of the additional information I provided on one of today's On Short Notice items. It's the increase in coronary heart disease risk women with subclinical hypothyroidism have compared to their peers with spot on TSH levels of 0.5-1.5mU/L (Asvold. 2013). In conjunction with other more or less recent studies, such as Mitchel's, Hsu's and Sahai's paper confirming the previously often talked about but not well-established 2-fold increase in congenital hypothyroidism from the early 1990s to the first years of the new millennium (Mitchel 2011), the predictive value of high TSH levels in the first trimester (early pregnancy hypothyroidism) for adverse pregnancy outcomes (Schneuer. 2013), the 30% risk increase in all-cause mortality in both women and men with subclinical hypothyroidism Tseng et al. reported in their paper earlier this year or the impairment of spatial working memory (Yin. 2013), Asvold's results only add to the evidence that the potential pitfalls of an increasingly prevalent metabolic dysfunction may have been ignored way too long.

    • More GI lovin' - On the menu today: Mashed potaoes with chicken, rapeseed oil or both (Hätönen. 2011) - I thought a mini-follow-up on Friday's post on the GI would be nice, 'cause some of you have not without reason been complaining that not everyone would eat pure white bread, like my students do.

      Figure 1: The real (=measured) GI of a meal does differ significantly from the theoretical prediction. So, even if the concept was worth bothering, the GIs of complete meals simply wrong, if they are not measured (Hötönen. 2011).
      Moreover, the mere fact that the scientists from the Department of Lifestyles and Participation at the National Institute for Health and Welfare in Helsinki, Finland, found that the addition of chicken breast, rapeseed oil and a salad, individually and in combination, had the GI of a meal containing six mashed potatoes (this was the parameter that was held constant) induced more than twofold changes in GI, with the addition of chicken breast having the greatest deviation from the predicted value in this group of 11 (initially 12) healthy subjects, three men and nine women, aged 36.2 (SD 14.1) years with a BMI of 21.3 (SD 1.7) kg/m² and normal glucose tolerance (see figure 1).

      Now given the fact that most data on the GI of complete meals has never been measured, but is actually based on the same predictions the scientists used, it stands to reason that...
      [...] this highlights the problems encountered when predicting the GI values of mixed meals. The protein com-ponent of the mixed meal evoked the largest insulinaemic responses and markedly increased the II of the mixed meal containing protein. However, introducing fat into the meal decreased the effect of protein on the insulinaemic responses (Hätönen. 2011)
      So, this does not simply bust the idea that you could calculate the GI, it does likewise show you that people who are still overtly scared of insulin (which is hillarious as long as you are insulin sensitive) are doing he exact wrong thing, when they make food-choices based on GI: Whey protein would in that case be in as much a no-go as simply eating a chicken breast with your mashed potatoes would be, because other than what most people believe, it does increase the insulin spike and thus reduce the glycemic index by allowing your body to clear the glucose more efficiently from the circulation.

      Suggested reads: The red box in the "Whey is More Insulinogenic than White Bread" post on the partitioning effects of BCAAs and yesterday's Facebook post on the anti-Alzheimer's effects of insulin.

    • Suggested read: Amino Acids for Super Humans the purported ergogenic effects of l-glutamine
      30g of oral glutamine have similar effects on GLP-1 as 75g of glucose (Greenfield. 2008) - Still a follow up on the GI discussion, I think you may be interested in. If you are someone who follows the questionable practice of ingesting large boluses of glutamine in the futile believe that this would increase your gains or speed up recovery, you may be pleased to hear that only 30g of oral l-glutamine produced an increase in the "Fat Burning Satiety Hormone GLP-1" (read more on GLP-1) that's on a gram to gram basis more pronounced than in response to insulin (0.41pmol/L per gram glucose vs. 0.75pmol/L per gram of glutamine; in 8 healthy subjects).

      Before you go and buy tons of glutamine, you should however consider that GIP, the pro-insulinogenic peptide and glucagon (ramps up gluconeogenesis in the liver) were likewise increased by the ingestion of this bolus of glutamine. It is therefore no wonder that glutamine has never been shown to be a "fat burner". Nonetheless, a 1999 study by Bowtell et al. would suggest that it may come handy to replenish liver and muscle glycogen after a workout (8g alone did increase glucose storage after a workout to a similar degree as a 18.5% glucose polymer solution and additional 25% glucose storage mostly in the liver, when both were coingested; cf. Bowtell. 1999). And if you don't care about that - your gut integrity could also be a reason to consider supplementation in the vicinity of particular strenuous or length workouts (see "Shedding Some Light on the Leaky Gut <> Exercise Connection") 

    • Practical relevance? Based on data from a 12-year longitudinal study, even women with subclinical hypothyroidism have 76% risk for coronary heart disease (p = 0.005), than women with spot on TSH levels of 0.5-1.5mU/L (Asvold. 2013). And even women well within in the "normal range" (TSH of 1.5-2.4mU/l) have a 41% higher risk of heart disease, although this is only borderline significant (p = 0.08). For men the TSH level alone had not predictive value. Spec. w/ regards to T3, there are also reports of increased incidence of ventricular disfuntion (Cassetti. 2009), increased cardiac death in CVD patients (Iervasi. 2003) and impaired recovery after a stroke (Alevizaki. 2007). We do yet have to be cautious, here as "low T3" syndrome could as well be the consequence of overall inflammation and the association does not tell us anything about what's the chicken and the egg.
      Low thyroid, high triglyceride (Hashimoto. 2013) -- If you are wondering why on earth your trigs won't come down, it may well be that it's the absence of sufficient amounts of thyroid hormone. I a soon-to-be-published paper in Endocrinology scientists from the Gunma University in Maebashi, Gunma, Japan, report that thyroid hormone regulates the expression of a Stearoyl-CoA desaturase-1 (SCD-1) which controls the production of trigs from carbohydrates.

      Surprisingly the 75% increase due to hypothyroidism and the 75% decrease in SCD-1 mRNA expression (both compared to a euthyroid state) the scientists observed in rodents in response to the administration of T3 were not mediated by receptor binding, but simply as a down-stream effect of direct modifications of the SCD-1 gene promoter between -124 and -92 bp by T3.

      On a related side note: It is actually the last mentioned mechanism which is the major new finding in the study at hand and not the fact that T3 can reduce the conversion of carbohydrates to triglicerides that is the actual news here. After all, the latter is something scientist should know, but obviously like to forget about ever since the late 1999s (Waters. 1997)

    • Omega-6 intake and not low omega-3 intake is the problem (Liou. 2007) -- Another older study, but one I am posting in response to a discussion some of you are having about omega-3 (ALA) intake in the post about safflower oil and DHT, because I simply feel that it's necessary to shed some light  on the erroneous assumption that by simply upping your intake of omega-3s or fish oil intake you could get away without decreasing your omega-6 intake, which in and out of itself will already increase the amount of anti-inflammatory omega-3 fatty acids (supplementation of DHA can still be advisable, specifically if you are a vegetarian).

      Figure 2: Effect of 4 weeks of high (red) vs. 4 weeks of low (green) linoleic acid (n-6) intake on short and long-chain omega-3 plasma phospholipid content in healthy men (Liou. 2007)
      In 2007, already Liu et al. conducted a very interesting experiment in the course of which they fed healthy men diets with identical amounts of omega-3 fatty acids (1% of the total energy intake), but two different amounts of linoleic acid (omega-6) and found that the high omega-6 intake (10.1% vs. 3.8% of the total energy intake) alone decreased the total amount of EPA among the plasma phospholipids (the major long-chain omega-3 fatty acid in fish oil), not just the ratio of omega-3 to omega-6, in the blood of their 29-45 year-old subjects by more than 25% (see figure 2). The paradoxical effect on DHA, on the other hand, would warrant further investigation, and underlines how reliant we are - if anything on the intake of pure DHA, which dropped in consequence to the test diet, which was devoid of fatty fish, while the original diet of the non-vegetarian subjects had fish in it.

      In this context, I would also like to point out that DHA is exactly where real fish is far superior to fish oil caps, because it has a way more favorable EPA:DHA ratio than fish oil caps. Salmon fillets for example have - depending on the fatty acid source in the diet 8.5g : 13.8g, 4.4g : 7.8g and 1.5g : 2.9g (all values per 100g) when the feed contains fish oil, fish and rapeseed and fish + rapeseed and rapeseed, only.

      And while the ratios are similar regardless of the chow, the data from the Seierstad et al. clearly shows that the fatty acid content of the diets can induce almost 5-fold differences in terms of the total DHA content and the omega-3 to omega 6 ratio (fish oil diet: 6.5, fish oil + rapeseed: 1.7, rapeseed: 0.6) of salmon fillets (Seierstad. 2003). 

    • It does not take much: 500mg DHA not more effective than 250mg  (Nobili. 2013) -- At least if it comes to its beneficial effects against liver steatosis in children  (mean age 11 years; BMI 26.6kg/m² and 24.4kg/m², in the low and high dose groups respectively with with NAFLD, the amount of DHA does not appear to be so important. According to the results of their 2-year registered controlled trial, both 250mg and 500mg of Docosahexaenoic acid lead to identical and profound reductions in the odds ratio of developing more severe steatosis during the study period.

      Figure 3: Odds ratio (comparing DHA supplement vs. placebo) of more severe vs. less severe liver steatosis determined every 6 months during the 24-month study period (Nobili. 2013)
      If you take a closer look at the data in figure 3, you will even have to concede that the lower dosage did a better job - while the mean odds ratios were only marginally lower in the 250mg DHA group, the extremely high standard deviations in the 500mg DHA would suggest that the 250mg dose appears to be more reliable. In this regard it may be interesting that the increase in serum DHA did mirror the dosages. With a 0.65% and 1.15% increase in DHA those were about 2x higher in the 20 boys and girls in the high dose group compared to the 20 kids in the control group who received a 290 mg linoleic acid germ oil supplement "placebo" (by the way, a monosaturated fatty acid placebo would have been more of a placebo than 290mg of omega-6)

      In view of the fact that the changes in triglycerides, ALT, HOMA-IR and BMI (which was not even different from the placebo group) were likewise identical, it does not appear as if anything that goes beyond the amount you will find in 2x cheap fish oil caps, or 10g even of the cheapest salmon fillet (see last paragraph of previous item) would be necessary to ellicit the anti-steatosis effect of fish oil - since those kids weight on average 55kg, an adult may want to add in another fish oil cap to get up to 360mg DHA per day or simply eat his fatty fish once or twice a week.

      • Selenium ameliorates aluminum toxicity (Viezeliene. 2013) -- With the whole upheaval about the potential negative side effects of the aluminum in vaccines, the formerly overlooked yet well-known neurotoxic (Exley. 1992; Gupta. 2005), hepatotoxic (Abubakar. 2003; Perez. 2005) and nephrotoxic metal (Geyikoglu. 2013) has all of a sudden returned to the center of public interest.

        Therefore I thought that you will be interested in the results of a study that's going to be published in the next issue of the Journal of Trace Elements in Medicine and Biology - irrespective of whether you believe, like Tomljenovic and Shaw that
        "the possibility that vaccine benefits may have been overrated and the risk of potential adverse effects underestimated, has not been rigorously evaluated in the medical and scientific community"(Tomljenovic. 2011)
        After all, vaccines are not the only potential source of aluminum in our environment, so that the ameliorative effects (all values remained normal in the aluminum exposed group, while there were 30%, 55% and 42% increases in GSH in the animals who received only the selenium injection) the co-administration of supplemental selenium had on the GSH reductions in liver, kidney and brain of Balb/c mice weighing 20–25g who were exposed (by i.p. injection)to AlCl3 (25 mg Al(3+)/kg body mass) for 16h could be important, regardless of whether you do or don't intend to get vaccinated.

        There is more about selenium at the SuppVersity, for example on its pro-fertility effects, and its anti-corrosive effects in the brain.
        That said, the dosage requirements necessary to maintain healthy GSH levels are probably much lower than the hillarious (for a healthy individual) in the study at hand 1,250µg/kg body weight of sodium selenite (Na2SeO3). Considering the elemental selenium content in Na2SeO3, the latter would equal to ~3,650µg - unquestionably WAY too much (remember this was a one-time dosage that was specifically co-administered w/ the aluminum). Even the 'no observed adverse effect' level for a 70kg man of intake which is ~1000µg/d (Whanger. 1999) appears unnecessarily high, so that the consumption of a handful of brazil nuts once or twice a week and/or other high selenium foods such as tuna, cod, oysters, shrimp, but also eggs, meats, poultry, mushroom and onions on a regular should suffice to get what you need, to fortify yourself against the constant assault of heavy metals.

        What would be interesting, though, is a study into the effects of adding selenium to the "safe" aluminum in vaccines. I mean, you cannot seriously tell me that we could not afford doing that and if it reduced any toxicity issues, why not?

      That's about it for today, I did not post all too many new facebook news as of yet (I mean, come on, it's Saturday ;-), but if you are into medicinal horror-stories, you will certainly like the story about the flesh eating killer fungus. If you prefer microbes over fungi, you are probably better off with the latest insights into the associations of certain gutbacteria with the incidence of stroke. And if you are more into other aspects of the digestive tract you may be interested in the effects of gastric emptying time on postprandial gylcemia and insulin release.

      If none of those news is to your liking, I suggest you either wait for me to post something else (could be happening within the next hours at www.facebook.com/SuppVersity), or simply enjoy the weekend and come back tomorrow when you are rested for another (hopefully) enlightening SuppVersity post.

        References:
        • Abubakar  MG,  Taylor  A,  Ferns  GA.  Aluminium  administration  is  associated  with enhanced  hepatic  oxidant  stress  that  may  be  offset  by  dietary  vitamin  E  in  the rat. Int J Exp Pathol 2003;84:49–54.
        • Asvold BO, Bjøro T, Platou C, Vatten LJ. Thyroid function and the risk of coronary heart disease: 12-year follow-up of the HUNT Study in Norway. Clin Endocrinol (Oxf). 2013 Dec;77(6):911-7.
        • Bowtell JL, Gelly K, Jackman ML, Patel A, Simeoni M, Rennie MJ. Effect of oral glutamine on whole body carbohydrate storage during recovery from exhaustive exercise. J Appl Physiol. 1999 Jun;86(6):1770-7.
        • Cassetti G, Pinelli M, Bindi M, Bianchi M, Castiglioni M. [Low T3 syndrome and left ventricular diastolic function]. G Ital Cardiol (Rome). 2009 Aug;10(8):553-7. 
        • Exley  C,  Birchall  JD.  The  cellular  toxicity  of  aluminium.  J  Theor  Biol 1992;159:83–98.
        • Geyikoglu  F,  Turkez  H,  Ozhan  Bakir  T,  Cicek  M.  The  genotoxic,  hepa- totoxic,  nephrotoxic,  haematotoxic  and  histopathological  effects  in  rats after aluminium chronic intoxication. Toxicol Ind Health 2013;15.
        • Greenfield JR, Farooqi IS, Keogh JM, Henning E, Habib AM, Blackwood A, Reimann F, Holst JJ, Gribble FM. Oral glutamine increases circulating glucagon-like peptide 1, glucagon, and insulin concentrations in lean, obese, and type 2 diabetic subjects. Am J Clin Nutr. 2009 Jan;89(1):106-13.
        • Gupta  VB,  Anitha  S,  Hegde  ML,  Zecca  L,  Garruto  RM,  Ravid  R,  et  al.  Alu- minium  in  Alzheimer’s  disease:  are  we  still  at  a  crossroad?  Cell  Mol  Life  Sci 2005;62:143–58.
        • Hashimoto K, Ishida E, Miura A, Ozawa A, Shibusawa N, Satoh T, Okada S, Yamada M, Mori M. Human Stearoyl-CoA Desaturase 1 (SCD-1) Gene Expression Is Negatively Regulated by Thyroid Hormone without Direct Binding of Thyroid Hormone Receptor to the Gene Promoter. Endocrinology. 2013 Dec 7.
        • Hätönen KA, Virtamo J, Eriksson JG, Sinkko HK, Sundvall JE, Valsta LM. Protein and fat modify the glycaemic and insulinaemic responses to a mashed potato-based meal. Br J Nutr. 2011 Jul;106(2):248-53. 
        • Iervasi G, Pingitore A, Landi P, Raciti M, Ripoli A, Scarlattini M, L'Abbate A, Donato L. Low-T3 syndrome: a strong prognostic predictor of death in patients with heart disease. Circulation. 2003 Feb 11;107(5):708-13.
        • Liou YA, King DJ, Zibrik D, Innis SM. Decreasing linoleic acid with constant alpha-linolenic acid in dietary fats increases (n-3) eicosapentaenoic acid in plasma phospholipids in healthy men. J Nutr. 2007 Apr;137(4):945-52. 
        • Mitchell ML, Hsu HW, Sahai I; Massachusetts Pediatric Endocrine Work Group. The increased incidence of congenital hypothyroidism: fact or fancy? Clin Endocrinol (Oxf). 2011 Dec;75(6):806-10.
        • Perez  G,  Pregi  N,  Vittori  D,  Di  Risio  C,  Garbossa  G,  Nesse  A.  Aluminium  expo- sure  affects  transferrin-dependent  and  -independent  iron  uptake  by  K562  cells. Biochim  Biophys  Acta  2005;1745:124–30. 
        • Schneuer FJ, Nassar N, Tasevski V, Morris JM, Roberts CL. Association and predictive accuracy of high TSH serum levels in first trimester and adverse pregnancy outcomes. J Clin Endocrinol Metab. 2013 Sep;97(9):3115-22.
        • Seierstad SL, Seljeflot I, Johansen O, Hansen R, Haugen M, Rosenlund G, Frøyland L, Arnesen H. Dietary intake of differently fed salmon; the influence on markers of human atherosclerosis. Eur J Clin Invest. 2005 Jan;35(1):52-9.
        • Waters KM, Miller CW, Ntambi JM. Localization of a negative thyroid hormone-response region in hepatic stearoyl-CoA desaturase gene 1. Biochem Biophys Res Commun. 1997 Apr 28;233(3):838-43. 
        • Whanger P, Vendeland S, Park Y-C & Xia Y. Metabolism of sub-toxic levels of selenium in animals and humans. Annals of Clinical Laboratory Science. 1996;26, 99-113.

        Sunday, September 15, 2013

        194 Bananas in 3 Weeks, Same Liver Fat & Lower Body Fat 6 Months After; Nigella Sativa Boosts Testosterone & Fertility; Sugar Dampens Caffeine Rush + Thyroid & Body Comp.

        Three weeks of +1,000 kcal carb overfeeding (approx. 194 bananas!): Does it supersize your liver fat? This and more in today's installment of On Short Notice
        As promised in yesterday's first part of the weekly written news-round up aka On Short Notice, we won't waste any time on lengthy introductions (the "short" items themselves are already long enough ;-) and get right down to business! For today this means that we are going to take a peak at the latest studies on
        • the reality of thyroid hormone metabolism
        • the dampening effects of sugar on high dose caffeine
        • the sugary truth about the reversibility of early NAFLD
        • the pro-testosterone, pro-fertility effect of black cumin
        as well as the latest data on US drug sales and an upcoming blogpost discussing "training for anabolism" - enjoy!
        Just in case you feel that's not enough, I suggest you listen to this week's installment of the SuppVersity Science News Roundup (click here to download) on Super Human Radio, as well!
        • Figure 1: The more energy reserves a metabolically healthy and euthyroid person has and the more he or she eats (though this was not quantified we can probably assume that the heavier participant also consumed more energy on a daily basis), the less energy efficient is his metabolism going to be - the margin is yet not unlimited, eat 40% more and get fat regardless of what type of food those calories come from (generated based on Roef. 2013)
          Levels of thyroid hormone associated with greater body weight and body fatness I know this sounds surprising, but int he end the latest results from the Department of Endocrinology at the Ghent University Hospital in Belgium only confirm what I keep preaching here at the SuppVersity over and over again: The main reason that the calories in vs. calories out calculations don't work is that the "calories out" part of the equation depends on both the "calories in" and the "calories stored", as well as the "accessibility of the calories stored" parameters, and [...].
          Put differently, the reason that the 941 generally healthy and euthyroid (=normal thyroid function) male siblings (25-45 yrs, median BMI 24.6) with the highest body weights and the greatest body fat mass also had the highest levels of leptin, free and total T3 & T4, as well as thyroid binding globulin is simple: In the presence of ample energy supply their bodies will treat their resources more wasteful, than those of the skinny or wanna-be-skinny, ah... I mean "ripped" guys who undereat and overtrain.
          The opposite is the case for the more muscular study participants, whose greater lean mass and muscle cross-sectional area were associated with lower (F)T3, (F)T4 and TBG levels (p ≤0.0003). They simply cannot afford (you could also say that they don't need) to ramp up their already higher fatty acid oxidation and overall energy expenditure, even further. Lastly, there was a clear-cut association with higher free T3 levels and lower insulin sensitivity, and - I had almost forgotten to mention that - "[n]o associations between TSH and body composition or metabolic parameters were seen."
          I suggest you print the finding about TSH levels and ask your doctor if he judges the speed of his car by looking at the gaspedal (TSH is more or less the gas-pedal that will tell your thyroid how hard it's got to work, but won't tell you how much of active thyroid hormone it is capable of producing) rather than the speedometer, when he is too cheap to order a full thyroid panel the next time you ask him to do so ;-)
        • Figure 2: While the initial caffeine spike is blunted by the ingestion of a sugar-laden breakfast, the area under the curve (bottom, right) a similar, yet less pronounced effect and both, the reduction of the initial spike in serum caffeine, as well as difference of the total influx over time are dose dependent (Skinner. 2013)
          Sugary breakfast reduces early rise in serum caffeine levels by up to 90% That's at least the result of a recent study by Tina Skinner and her colleagues from the University of Queensland in Down-Under. The high carbohydrate meal, in this case a toast with jam, cordial, and an energy bar ("Vanilla Crisp" PowerBar Performance Bar), the scientists served their 14 healthy active male participants (age 24.8 ± 3.7 yrs, body mass 74.6 ± 8.5 kg, height 184.0 ± 8.5 cm; mean ± SD) who had reported fasted, well hydrated and 48h after they had consumed their last caffeinated beverage at the lab (Skinner. 2013). It does not really take a rocket scientist to see that the absence of the initial onslaught of caffeine as a result of the pre-ingestion of the sugary "breakfast" will probably diminish, if not totally blunt the stimulating effects of coffee.
          In view of the fact that this effect was particularly pronounced during the "high dose" (=9mg/kg body weight; ~540-900mg; equiv. to 3-4.5 large cups of strong coffee), it is yet probably of greater importance for stim junkies and athletes looking for the pre-workout edge before they hit the gym, than for the average white color worker who needs to get his daily buzz, if he does not want to miss his bus (or train ;-)
        • Liver-fattening effects of carbohydrate overfeeding are genetically dispositioned, but the recently published data from a study that was conducted by scientists from the Minerva Foundation Institute for Medical Research, the University of Helsinki and other Finnish research facilities shows that an appropriate diet can reduce increased liver and body fat levels, reduce body fat levels and improve lipid and glucose metabolism, regardless of the genotype (PNPLA3-148II = disadvantaged vs. PNPLA3-148MM) of the subjects.
          But let's take on thing after the other. After some standard baseline tests, the 16 subjects (mean age 54 year; BMI at baseline 30.6kg/m²; 5 men, 11 women) were "overfed" with a high carbohydrate diet from the "every low-carbers worst nightmare" category:
          Figure 3: Change in body composition from due to 3-week overfeeding (blue), 6 months dieting (compared to post overfeeding - red; Sevastianova. 2013)
          "The subjects were instructed to continue their normal diet and in addition to consume an extra 1000 kcal/d with 98% of energy from carbohydrates. The extra diet consisted of candy (Oy Karl Fazer Ab), pineapple juice (Tuko Logistics Oy), sugar-sweetened soft drinks (Oy Hartwall Ab), and/or carbohydrate-loading drink (Squeezy Sports Nutrition GmbH) and was provided free of charge from the research unit to the study participants." (Sevastianova. 2013)
          As you will probably have expected the highly insulinogenic, additional 21,000kcal from glucose and fructose (~5250g or 194 bananas, medium size to be precise ;-) did leave "their marks" on the waist and hips of the subjects, but probably not to the extend you may have anticipated (see figure 1). Even more suprisingly, the short term overfeeding did not deteriorate any of the blood glucose parameters (all changes had p-values way beyond what would be statistcally significant, the glucose clearance over 2h did even improve! - statistically likewise non-significant, though).
          Most importantly, however, the body composition, triglyceride levels (-6%), HDL (+11%) and all the important body composition measures (see figure 3) improved and the liver fat returned to baseline in the course of the 6-months "diet period", which consisted of - mark my words - nothing but making a switch to a diet with more vegetables, less simple sugars, white flour, and alcoholic drinks and dietary counseling wrt to food types and appropriate (=moderate) portion sizes. No extreme low carbing, no drastic calorie reductions, just healthy whole foods - regardless of "your bad genes"!
        • Nigella sativa, aka black cumin, jacks up testosterone and makes tired sperm get a move on Being well aware that you cannot go without a weekly post about at least one natural testbooster,  you will probably be relieved to hear that Rahmatollah Parandin, Namdar Yousofvand and Rostam Ghorbani have published a paper in the latest issue of the Iranian Journal of Reproductive Medicine in which they describe the fertility and testosterone boosting effects of 200 and 400mg/kg of an alcoholic extract from Nigella sativa seeds (Parandin. 2013).
          *Reminder: Regardless of whether we are dealing with rodents or humans, a "testosterone booster" that works in sick animals or humans does not necessarily work in healthy ones, as well. It is much more likely, that the effects on testosterone are secondary to the effect of the effect the herb or whatever else has on the overall health of the lab animals / participants, so that someone who is not sick in the first place won't see any (or at best minimal) improvements.
          The seed extract that was administered to healthy*  male Wistar rats 60 days contained a mix of various active ingredients
          • 30-48% Thymoquinone,
          • 7-15% P-cymene, 
          • 6-12% Carvacrol, 
          • 2-7% 4-terpineol, 
          • 1-4% T-anethole, and 
          • 1-8% Sesquiterpene,
          of which Prandin et al. state that Thymogquinone is currently considered to be be the pharmacologically active constituent of N. sativa (cf. Padhye. 2008) - keep that in mind, when you cannot resist giving this stuff a try ;-)
          Now, the ~23% increase in testosterone is certainly nothing like the "140% increase in testosterone" certain supplement companies state one of the testers had (without any peer-reviewed data whatsoever, by the way), but as mediocre as it may seem, it was achieved from a healthy baseline level and it went hand in hand with improvements in all sperm parameters, of which I picked the sperm count and plotted it together with the latest human data from the University Department of Growth and Reproduction at the Rigshospitalet of the University of Copenhagen in Denmark in the second graph in figure 3 (Jørgensen. 2013).
          Figure 4: Yeah, Nigella boosts testosterone by 20% (left), but there are other things in life... what about it's effect on sperm count (right) for example? The increase the rodents in the high-dose group experients would catapult the infertile Danish men almost into the normal zone (based on Jørgensen. 2013 & Parandin. 2013)
          Now this is certainly by no means scientific evidence and I am not suggesting that it will help solve potential fertility problems (not just because sperm count is only one out of a dozen parameters, but also because we don't know whether what works in healthy rodents will work in sick people; see red box above for the other side of the coin). What I found quite important though, is to give you an idea of what those abstract numbers could eventually mean. Contrary to the 20% increase in testosterone which will hardly help you to build significantly more muscle mass, a similar bump in sperm count (and other fertility parameters) could very well make the difference between fertile and infertile!
          So, at whichever Internet source you may be able to dig up a respective extract and regardless of whether you want it for fertility or futility, ah... I mean "testosterone boosting" issues, make sure that it has a high Thymoquinone content and that you have enough of it to hit the human dose equivalent (click here to learn how to calculate HEDs) of 65mg/kg or 4-5g per day!
        Figure 6: US Drug sales 2010 & 2011 as posted on the SuppVersity Facebook wall earlier today (based on Lindsay. 2013).
        The End - for today, at least. I guess I won't take too much away, if I tell you that there was actually another item scheduled for today... a post about "High or Low, Long or Short, Heavy or Light what are the Best Set Numbers and Rest Times,Weights and Rep Schemes, When You're Training for Anabolism" - and while this is "anabolism" in the old and actually sort of outdated sense of more testosterone and less cortisol, I'm pretty confident that the muscle-heads among you would have liked it, if it did not get longer and longer, so that I decided to polish it up a little and put you on the rack for another two days or so ;-)

        So, in case that's driving you crazy, you may want to consider asking your Dr. for a script for an antipsychotic, currently the #5 on the 2011 (=the latest) US drug sale ranking (see figure 6; remember the data is $-based not script-based), I posted along with a handful of other interesting news-items earlier today on the SuppVersity Facebook wall.

        References:
        • Jørgensen N, Joensen UN, Jensen TK, Jensen MB, Almstrup K, Olesen IA, Juul A, Andersson AM, Carlsen E, Petersen JH, Toppari J, Skakkebæk NE. Human semen quality in the new millennium: a prospective cross-sectional population-based study of 4867 men. BMJ Open. 2013 Jul 2;2(4).
        • Lindsley CW. The top prescription drugs of 2011 in the United States: antipsychotics and antidepressants once again lead CNS therapeutics. ACS Chem Neurosci. 2013 Aug 15;3(8):630-1.
        • Roef G, Lapauw BM, Goemaere S, Zmierczak HG, Toye K, Kaufman JM, Taes Y. Body composition and metabolic parameters are associated with variation in thyroid hormone levels among euthyroid young men. Eur J Endocrinol. 2013 Sep 6.
        • Padhye S, Banerjee S, Ahmad A. Mohammad R. Sarkar FH. From here to eternity- the secret of Pharaohs: Therapeutic potential of black cumin seeds and beyond. Cancer Ther 2008; 6: 495-510
        • Parandin R, Yousofvand N, Ghorbani R. The enhancing effects of alcoholic extract of Nigella sativa seed on fertility potential, plasma gonadotropins and testosterone in male rats. Iran J Reprod Med. July 2013; 10(4): 355-362.
        • Sevastianova K, Santos A, Kotronen A, Hakkarainen A, Makkonen J, Silander K, Peltonen M, Romeo S, Lundbom J, Lundbom N, Olkkonen VM, Gylling H, Fielding BA, Rissanen A, Yki-Järvinen H. Effect of short-term carbohydrate overfeeding and long-term weight loss on liver fat in overweight humans. Am J Clin Nutr. 2013 Sep 5.
        • Skinner TL, Jenkins DG, Folling J, Leveritt MD, Coombes JS, Taaffe DR. Influence of carbohydrate on serum caffeine concentrations following caffeine ingestion. J Sci Med Sport. 2013 Sep 7.

        Sunday, July 21, 2013

        On Short Notice: Testosterone - 12% Drop /W 75g Glucose? Fat Loss - Adzuki, Leucine + B6 or HiMaize? Thyroid - T3↓ + rT3↑, Is Blood Sugar to Blame and Can TUDCA Help? +More!

        Image 1: It's quite funny, I am piling up so many of these interesting mini-news that I actually had to drop a few or postpone them to next week to keep the size of this post manageable without a direct brain transmission device like the one you see in this picture ;-)
        "On short notice" is the name of the new 'saturdaily' SuppVersity column and therefore I will try to make it short: After all, you've got a hell lot to learn today and unless you have just crawled out from beneath your sheets, your testestorone levels and with it your cognitive abilities will aready have declined - that's not you? Well I guess you have the hubris of a boxer, then, or you did simply sleep so little that even your increased energy consumption could not make up for the memory dysfuction that's been brought about by the sleep deficit. Let's just hope that your cell mass is at least so high that your basal energy expenditure is sufficient to burn those serotonergic carb binges off, because I am pretty sure that the leucine + B6 combo from NuSirt Science won't do that for you... what? You don't understand a word? Don't worry, you will, once you are done with today's installment of "On Short Notice"...

        Adzuki bean extract - just another fat binder or more?

        Image 2: Those Adzuki beans look pretty much like kidney beans, don't they? Ah, btw. you did know that kidney beans contain a "carb blocker" (a molecule that hampers carbohydrate digestion; cf. Mosa. 2008) - did you?
        I am really no a fan of those "anti-fat absorption agents", as most of them will have immediate or long-term consequences on your supply of fat soluble nutrients which could in fact be worse for your overall health than the few additional lbs of body fat you may be carrying around. That being said, you may still be interested in the latest results from Tomoko Kitano-Okada and his colleagues from the Department of Food Science, Obihiro University of Agriculture and Veterinary Medicine in Inadacho, Obihiro, Hokkaido, Japan. In a combined in-vivo (rodent) and in-vitro study, the researchers found that control and high fat diets with 1% adzuki bean extract, despite having only non-significant effects on the high fat diet (HFF) induced weight gain, did not just ameliorate the HFD induced deteriorations in serum low-density lipoprotein (LDL) and triglyceride (TRIG) levels, but lead to marked improvements in LDL and TRIG in the rodents on the standard diet (55% cornstarch + 10% succrose, 20% casein, 5% soybean oil), as well.

        Figure 1: Absolute total cholesterol and triglyceride levels, as well relative (expressed in percent of respective values for animals on control diet) liver and faecal matter weight and lipid content in male Fischer rats after 4 weeks on control (high carb) or high fat diets (data based on Kitano-Okada. 2013)
        This is interesting as it appears to confirm the hypothesis that the Adzuki beans do not work their anti-hyperlipidemic (=cholesterol and triglyceride lowering) effects solely via their ability to increase the fat content of the excrements, but also via other mechanisms of which Kitano-Okada et al. identified the reduction of inflammatory cytokines (e.g. 24–51% IL-6 reduction following treatment with Adzuki bean extract containing polymerised polyphenols) and the likewise dose-dependent profound reduction in glycerol-3-phosphate dehydrogenase, an enzyme that is necessary to generate glycerol (fatty acids) from carbohydrates, in in-vitro cell studies with human adipocytes by up to -50%!
        Implications: Just in case you are now interested in popping some of those beans you should be aware that the product that was used in the study contained 16% polyphenols (including 470 mg anthocyanidins, 20.7 mg catechins, 2.33 mg caffeic acid, 2.62 mg ferulic acid, 44.5 mg quercetin, and 102 mg protocatechuic acid), that the human dose equivalent would ~5-6g /day and that you should try to get an extract with polymerized (=interconnected) phenols, as those were roughly 2x more active in the in-vitro essays (although it is questionably if this translates into better real world results).

        Marathon running is for the metabolically efficient!

        Image 3: Marathoners have nothing to lose!
        Just in case you have ever wondered what makes a good marathon runner a very good marathon runner, the results of a study that was published in the latest issue of Sport Sciences for Health could hold the answer: Marathon champions have a surprisingly high metabolic efficiency (Andreoli. 2013), or put more simply, they are carrying little to no (for their goals!) useless ballast like profane fast-twitch muscle fibers and only so much fat as it takes to optimally protect their organs (in percentages this is yet still way more than the guys with the "profane" fast-twitch fibers are carrying around)

        As the data in figure 2 goes to show, their body cell mass (BCM), a more accurate measure of the amount of metabolically active tissue in their body than "lean mass" (Moore. 1963), is about equal to the one of division 1 football players (data compiled from Andreoli. 2003 and Andreoli. 2013), but their lean mass is much lower (as mentioned before they have no use for heavy type I and type IIX muscle fibers).
        Figure 2: Body composition data (fat free  mass, body cell mass, body fat percentage) in different athletes and control (left), as well as correlation between BCMI (BCM / height) with marathon running time (right; data compiled from Andreoli. 2003 and Andreoli. 2013)
        In conjunction with higher metabolic rates, of which Andreoli et al. found that they are the 2nd best predictor of marathon times (correlation r = -0.69 vs. BCMI = BCM / height with r = -0.73), a high amount of "oxygen-exchanging, potassium-rich, glucose-oxidizing, work-performing cells" (=what the BCM measures ;-) and correspondingly high resting energy expenditures (r = 0.77) do thus make the difference between victory and defeat.

        Sounds strange, when you come to think about it - right? "People with higher energy expenditures make good marathon runners?" Well, I guess you better think of it differently: Bigger engines need more fuel and as we have seen yesterday, a very welcome side effect of "mitochondrial biogenesis that's induced by Chitooligosaccharide supplementaton" was an increase in endurance - that those big engines have to be fueled adequately, by the way, does also explain why people like Michael Phelps do in fact have to eat like a horse - that he really needs 12,000-15,000 calories per day is yet probably just another of those urban legends.
        Implications: Interestingly enough, the necessity of having a "big engine" (=huge metabolically active cell mass) does also implicate that the formerly obese, who appear to flock around marathon or at least endurance running, with their slabs of metabolically unactive tissue and suppressed metabolic rates due to months or years of undereating and overtraining have little to no chance of ever winning a marathon race, which  - and this may be the most surprising finding of the study - is not the prerogative of the person who "burns the less fuel"  - at least not as long as nobody takes away their 30 bananas a day and the highly concentrated energy gels marathoners use on their 42-km run, I guess ;-)

        Can 75g of Glucose Reduce Testosterone by 10% Within Minutes?

        In a recently conducted trial, Lisa M. Caronia and her colleagues from the Massachusetts General Hospital in Boston observed an astonishing -12% drop in total testosterone within 30 min of the ingestion of an 75g of glucose - the same amount you would ingest in every regular oral glucose tolerance test (OGTT) and even less than some hilarious "expert suggestions" will tell you would need to optimally replenishing your allegedly depleted glycogen stores after an intense workout.
        Figure 3: Glucose, insulin, SHBG, lepin, LH and testosterone levels in response to the oral ingestion of 75g glucose in 74 young men; data expressed relative to baseline (data adapted from Caroni. 2013)
        If you take a closer look at the exact data in figure 3 you will probably be as startled with respect to the underlying mechanism behind this reduction as the researchers were. Aside from the drop in testosterone, the only statistically significant changes (indicated by * in figure 3) the scientists observed, were a profound drop in leptin and the explosive increase in glucose and insulin - both of which, the decrease in leptin and the increase in insulin, have yet been shown to augment testosterone production in previous studies (Adashi. 1982; Giovambattista. 2003). At least with respect to the drop in leptin, Caronia et al. do yet point out, that it could be a mere conseqence of "circadian fluctuations in leptin that are unrelated to glucose administration" (Caronia. 2013; those fluctuations, by the way, have been observed by e.g. Panarotto. 1999)

        Symptoms of low Testosterone
        • Lean muscle loss, agitation/motor dyskinesia, decreased appetite
        • Depression, guilt, low-self esteem, anhedonia, decreased cognitive capacity
        • Increased stress, general fatigue, sleep disturbances
        • Decreased libido, decreased spontaneous erections, decreased ejaculate, erection dysfunction, decreased sexual fantasies, anorgasmia
        Furthermore, neither cortisol (not shown in figure 3), a potential suppressor of testicular testosterone production, nor luteinizing hormone (LH), which stimulates testicular testosterone production and should actually increase in response to the drop in testosterone, did budge in the course of the 120 min after the 74 men (age range: 19-74 years, mean: 51.4 ± 1.4) who reported to the lab after a 12-hour overnight fast had ingested the 75g of glucose.

        As Caronia et al. point out, the non-existent response of the luteinizing hormone (LH) levels to the reduced testosterone levels, is probably the only clue we have as far as the underlying mechanism of allegedly glucose-induced reduction in testosterone levels is concerned, because "one would anticipate that the decreased negative feedback of T would lead to increased LH levels" (Caronia. 2013). And though Caronia et al. are certainly right that this and the fact that this was not the case and that the effect occured in healthy, in insulin resistant and in diabetic subjects (where it was slightly more pronounced, though; data not shown), clearly "suggests an additional central component", the latter should actually, as it was observed by  Iranmanesh et al. only recently involve a drop in luteinizing hormone (Iranmanesh. 2013).

        After thinking about that for a couple of minutes I was just about to write in the implications that this would be another good reason not to go overboard on fast carbs, when I remembered my previous research on all things testosterone for the "Intermittent Thoughts on Building Muscle" Series and what the scientists themselves had said about the declining leptin levels - well, let's take a look at what the testosterone levels of both young and old men do between 8:00am and 12:00pm, i.e. during the exact time the subjects in the Caronia study ingested their allegedly anti-androgenic bolus of 75g of glucose:
        Figure 4: An analysis of the natural diurnal testosterone rhythm in young men (dotted line in graph in the background; Diver. 2003) reveals that the "drop" in testosterone in response to the OGT is likely only a consequence of the pronounced diurnal rhythmicity of the total testosterone levels - in older men we see the exact same phenomenon, but the effect is about 50% less pronounced.
        The data from the Diver study in figure 4 does not leave a slight doubt that the OGTT, or rather the 75g of glucose the subject had to consume probably had no independent effect on the level of testosterone and that the decline Caronia et al. observed is simple a result of the natural diurnal rhythm. This does not exclude that the latter is per se connected to food intake as the availability / influx of energy is, beside light, probably, the most important setscrew for our clock-genes.
        Image 4: Conclusions are rarely 100% conclusive.
        Implications: There are actually two important take home messages from this study and "carbs are so bad for you" is not one of them:
        1. draw your own conclusions, and don't trust those of others blindly regardless of their "credentials"
        2. make sure that you don't ignore the diurnal rhythmicity of testosterone, and are thus fooled to believe that short term changes in the +/- 50% range would make you build or lose muscle, let alone your virility
        The second take home message is also of great importance when you test your own testosterone levels and/or read about the testosterne boosting magic of the latest supplement scam (aka "natural testosterone booster"). As you can see, you can easily achieve a  70-80% increase or decrease in testosterone by simply measuring at different points in the day.

        On Very Short Notice

        • Figure 5: Changes in fatty acid metabolism (top) and inflammatory markers (bottom) in response to 4 weeks of thrice daily NuFit (250mg leucine + 30mg vitamin B6) supplementation to 20 obese men and women (based on Zemel. 2013)
          Astonishing improvements in RQ & fatty acid oxidation from 2g of leucine and 30mg vitamin B6 - Although you need to be somewhat cautious with a study that was financed by NuSirt Sciences the producer of the 750mg leucine + 10mg pyridoxin supplement under scrutiny (Zemel. 2013), the effect the ingestion of those caps had on the fatty acid metabolism and moreover the expression of inflammatory markers in 20 overweight or obese subjects was literally marvelous (I leave the interpreation of this term up to you ;-). A decrease in respiratory quotient (=greater fatty acid, lower glucose oxidation), an increase in total fatty oxidation per day and more importantly and probably causally the decreases in TNF-alpha and CRP are changes I would not have expected to see within 4 weeks on 2.25g of leucine and 30mg of vitamin B6. After all,  you should see similar effects with almost every cheap (or expensive) BCAA supplement on the market - aside from even greater amounts of leucine most of them contain at least 10mg of additional B6.
        • Fat burning machines can't have orange juice for breakfast - The additional 210kcal the subjects of a 2013 trial by scientists from the Children’s Hospital Oakland Research Institute consumed in form of "healthy" orange juice were not just more or less empty calories, they also reduced the postprandial fatty acid oxidation by whopping 25%. This lead Stookey et al. conclude that "independent of a state of energy excess, [drinking] a caloric beverage instead of drinking water with a meal [will decrease] the amount of fat consumed in the meal before their next meal." (Stookey, 2013) If you want to become / stay a fat burning machine (and in my humble opinion even if you just want to stay lean and healthy) you better eat your fruit and never drink it (let alone other caloric beverages, see "Fat content per Energy Drink 0g, Fat Gain Per Energy Drink 16g").
        • Image 5: The first hit on google says HiMaize will cost 8$/340mg; mimicking the dosage used in the study would thus be ~1$ per day; relatively cheap if you consider that it is not necessary a supplement, but can also be used for baking & co
          Resistant starch could stop and reverse developing diabetes - scientists from the University of Surrey and the venerable Imperial College in London were able to show that their 12 overweight (BMI 28.2±0.4 kg/m2) prodiabetic subjects' first-phase insulin secretion, which is the one that determines whether you do or don't go hyperglycemic right after the ingestion of a meal, by improved by ~35% after only 4 weeks of consuming a mildly resistant (60% resistant / 40% digestible) maize starch. Probably as a direct result of this early pro-insulinogenic effect, the HiMaize260 RS2 starch produced a -10% reduction in fasting blood glucose, compared to a regular tapioca starch of which the subjects in the control group consumed only 27g to assure that they would ingest equal amounts of glucose (Bodinham. 2013).
          Despite the fact that WM HDP is an artificial restistant starch, of which even less will be digested and absorbed as glucose in the small intestine, these results do confirm what we have already seen in the WM HDP studies and what some of the latest blogposts bordering on dietary fiber have hinted at, as well (e.g."Weightloss Threesome"): The effects of these not, or only partially digestible fibers and carbohydrates go way beyond simply filling you up or being non-insulinogenic (=not causing an insulin spike as even the low GI starches do). There is however, as Carolin L. Bodinham and her colleagues rightly point out, need for "further studies [...] to confirm these findings and to elucidate the mechanisms" and, as I would add, to identify whether or not this could work for people who have already developed type II diabetes, as well.
        • Counter-intuitive effects of high glucose-dependent insulinotropic polypeptide (GIP) levels in form of increased insulin and reduced obesity: While the hitherto published studies on WM HDP (see previous bullet point) clearly suggest that part of its fatburning effect is mediated by a reduced, even almost non-existant GIP (and subsequently insulin response), a recent study from Canada clearly suggest that whenever you do consume regular starch a more pronounced incretin response will not just avoid hyperglycemia (due to the more pronounced release of insulin from the pancreas), but also improve / prevent adipose tissue inflammation, hepatic steatosis (non-alcoholic fatty liver disease) and even weight gain - remember: we are talking about higher insulin responses, here (Kim. 2013)! Unfortunately, the anti-obesity effect Su-Jin Kim and his colleagues observed in their experiments with GIP-overexpressing rodents, were mostly a direct consequence of reduced energy intakes and that those hardly ever translate into the real world is something I believe I don't have to tell you, right?
        • Figure 6: If your body does not convert T4 into T3 adequately taking levothyroxin (T4) may even worsen many of the symptoms of hypothyroidism due to increased conversion to r-T3 and an even more sluggish metabolism that certainly won't help to get blood glucose back under control (see also "Natural Thyroid Treatment with food")
          Low T3 syndrome (pseudo-hypothyroidism) or diabetes? This is an "oldie, but goldie", i.e. a study I happen on while doing research on this and that... in this case I do not even really know how this study appeared on my radar, but according to Kabadi et al. high blood sugar in type II diabetes does reduce the conversion of the "inactive" form of thyroid hormone, T4, to its active cousin, T3 and increases the conversion of T4 to rT3 (reverse T3). The latter is believed to act similar to a receptor blocker, which hinders T3 do to its metabollically activating job. The statistically highly significant (p < 0.0001) correlation (r = 0.611) the scientists observed between rT3 and fasting blood glucose would suggest that improper blood glucose management could be the root course of the heavily lamented high rT3 levels of thousands of posters on various bulletin boards all across the Internet (Kabadi. 1982). Now, the good news is that the researcher found that by controlling blood glucose levels you can return your rT3 and T3 levels back into the normal zone. 
        • Tauroursodeoxycholic (TUDCA) and 4-phenylbutyric (4-PBA) increase T3 to T4 conversion - The chemical chaperones TUDCA and 4-PBA, of which the former has as of late been hailed as the new "milk thistle", i.e. the go-to-supplement for liver health among athletes who use oral anabolic steroids, could turn out to be a valuable tool not just to escape from the aforementioned vicious circle of low T3 and high rT3 levels, but also as a means to kickstart your metabolism. Although this hypothesis is based on data from a combined in-vitro + in-vivo rodent study (da-Silva. 2011), the shift away from glucose and towards fatty acid oxidation, as well as the doubled activity of the fat burning brown fat and the profound improvements in glucose tolerance, da-Silva et al. observed in their high-fat fed rodents certainly won't harm your physique.
        • Figure 7: Narcicistic personality traits of kickboxers, freestyle and  Greek Roman wrestlers, Boxers and Weightlifters (based on Tazegül . 2013)
          Weight lifters and boxer are the most narcissistic athletes - At least among the five groups the Turkish scientist Ünsal Tazegül analyzed for his recently published paper, the 17-19-year old male boxers and weight lifters had the most pronounced narcissistic character traits. While the boxers were the most exhibitionists and pretentious, the weight lifters were the most rebellious, inadaptable, spiteful, disrespecting (subsumed under exploitation) and ambitious, power-thirsty and spiteful among the subjects who participated in this study. Interestingly enough, the freestyle wrestlers appeared to be the guys with whom you would probably get along best. So what does that tell you? Nothing... and that's why this study is only on very short notice ;-)
        • If you don't sleep yourself smart, you got to binge yourself half-smart: Just in case you have already forgotten what you read a few paragraphs above, the reason could be sleep deprivation. And while cognitive deficits due to sleep deprivation is nothing essentially new, another thing, namely the effectivity of increased daytime energy intake to recover your mental capacity, is something a recent study by Nina Herzog et al. has investigated for the first time (Herzog. 2013). Unfortunately, binging rescues only the procedural part of your memory (where you store how to brush your teeth before you go to bed ;-), it will not compensate for the detrimental effects a lack of adequate sleep will have on your declarative memory. If you also  take into account that it is going to make you fat and sick, I would thus suggest you go to bed now, after all you havale already done the single most important thing of the day - you've gotten your daily dose of SuppVersity news! And let's be honest, you don't want to forget any of these valuable lessons, do you ;-)
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