Get Lean & Stay Lean Quickie: Add Cinnamon to Cereals. NPY Detrimental? Melatonin Beneficial! 50,000IU Vitamin D3 Useless. Phtalate DHEP Dangerous! PPAR, AKT & GLUT-4 Agonist From False Black Pepper Surprisingly Potent!

In 1998 the Consumer Union wrote a letter to the FDA complaining about the occurrence of DEHP and other "endocrine disrupting chemicals" in cheese and dairy of which they suspected that they were partially emitted from the plastic wrappings (read more)

Those of you who are following the SuppVersity news on Facebook very closely, will be aware that I announced yesterday, already that there was going to be another installment of On Short Notice, today... another "Quickie", so to say with a couple of selected news on getting and staying lean. Something I know is pretty much a pain in the a** of most of us and if you take a closer look at the news about phtalates it is actually no wonder. I guess on their own those nasty plasticizers would probably not even be a problem, but together will all the other byproducts of our convenient lives, they form a perfect storm.

And you know what's worst, simply wrapping all those plastics that 'infect' even organic foods with the 'P-Virus' around your waist while you're working out will probably make things worse, not better.

Let's get down  to business ;-)

Enough of that! Are you ready for today's quickie -- Note: The next installment of the Athletes' Triad is scheduled for next week. I am honestly sorry for these delays, but I just have "real" work to do on the weekends at the moment and no time to do the respective research that would be necessary to provide you with not just any, but actually useful information. In the mean time I hope you like this post, as well.

• 6g of cinnamon stretch postprandial glucose response to cereals over more than 2h. That's the result of the latest study from the Ball State University in Muncie (Magistrelli. 2013). Interestingly the effects of 6g of ground Cassia Cinnamon were independent of the body weight and metabolic health of the thirty-seven 18 to 30 year-old normal-weight and obese study participants.
  
  

  

  Figure 1: Postprandial blood glucose with plain cereal containing 50g  carbs and the same cereal with cinnamon in all subjects, normal-weight and obese; by the way if you go by the AUC I doubt there is a benefit, after all the glucose does not drop base to baseline within 120min (Magistrelli. 2013).

  There is however one slight downside to this study: The scientists measured the blood glucose response for only 120min. If you take a look at the graph in figure 1 you will immediately notice that the co-ingestion of 75g of "Cream of Wheat", an instant farina cereal, with 6g of regular cinnamon did lead to a 24% reduction in the area under the glucose curve, but only if you discard what happened after the 120-min period the scientists used to measure. After all, the co-administration of Cassia cinnamon did not do anything that could not be ascribed to a mere reduction in glucose uptake - there is no evidence for an improvement of insulin sensitivity here. On the other hand, the absence of spikes in blood glucose will protective effects against the development of type II diabetes, esp. in the presence of a diet that's overall high in carbohydrates where one blood sugar spike chases the other.
  

  "To date, no study has documented cinnamon's influence on postprandial blood glucose after a mixed meal. Although preliminary in nature, the available research suggests cinnamon supplementation can significantly reduce short-term glycemic response in healthy adults." (Magistrelli. 2013)

  The last information is actually pretty surprising. Personally I expect the effects to be less pronounced with mixed meals, but since we still don't really know the underlying mechanism it's difficult to predict what exactly is going to happen, when you eat a spoon full of cinnamon right before your steak with rice. This as well as the previously discussed prolonged elevation of blood glucose (see figure 1)  actually raise some doubts about the real-world usefulness of eating tons of cinnamon if you don't actually like it, just as a way to manage blood glucose - specifically if you are not a type II diabetic (or on your way to become one) and avoid "food" like cereals and similar junk, anyways.
• Neurpeptide Y (NPY) does not protect against obesity -- Based on the results of a recent rodent study from the University of Turku in Finland, it seems that the exact opposite is the case. In that it does not seem as if it would fail to make you satiated and happy. Rather than that it appears to put your metabolism in "high efficacy" mode, so that you gain weight despite the fact that you are not eating more.
  
  The Finish researchers exposed two strains of mice to a typical Western type diet (high energy, high fat, high carbohydrate) for seven weeks. One strain, the OE-NPY(DBH) mice, had 'naturally' high amounts of NPY in the noradrenergic neurons of the brain, the other were normal wild type mouse. Actually, the scientists had expected that the high NPY expressing mice would gain less weight than their wild-type peers, but much to their surprise, the exact opposite was the case.
  
  

  

  In 1990 Kaye et al. conducted post-mortem analyses on the brains of patients with anorexia nervosa and found highly elevated levels of NPY. These results do actually stand in line with those of the study at hand, after all anorexic patients don't feel any exuberant hunger (in the later stages of the disease) and their bodies are running in a mode that is meant to conserve even the smallest amount of energy they consume.

  And as if that was not already strange enough, the scientists also found that female OE-NPY(DBH) were much more prone to gain significantly more weight and larger white and brown fat depots with no difference in UCP-1 levels, hyperphagia (=overeating) or decreased activity. And the weight gain was not without consequence, as these mice
  

  "...also displayed impaired glucose tolerance and decreased insulin sensitivity. OE-NPY (DBH) and WT males gained weight robustly, but no difference in the degree of adiposity was observed." (Ruohonen. 2013)

  Now what's interesting is that similar effects were only observed in 40% of their male counterparts and in exactly none of the wild type males on the Western type diets. These observations lead Ruhonen et al. to the conclusion that ...
  

  "[...] increased NPY release may predispose females to a greater risk of weight gain under high caloric conditions." (Ruhonen. 2013)

  And if you asked me this must be mediated by whatever gender-specific direct effect on feed efficacy and the changes in brown adipose tissue morphology the researchers observed in the NPY overexpressing mice. This would be good news, since brown fat figure much less in human beings than in rodents. Unfortunately, with identical body temperatures and UCP-1 expression in all animals that is at best one of the causative factors. It can hardly explain all the profound weight and fat gains in the non-hyperphagic (not overeating) OE-NPY mice.
  
  Now, at least for me this raises the question if this is not yet another instance, where the artificially increased NPY levels in the absence of the natural confounding factors, such as increased GLP-1 levels, for example (click here to learn more about GLP-1), couldn't be the actual reason and any conclusions with respect to pro- or anti-obesogenic effect of NPY based on the results at hand would be as unwarranted as the usage of drugs that target this and other neuropeptides in isolation.

• 

  Just in case you have missed the Circadian Rhythm Series, this would be the right time to read about how to boost / not hamper melatonin, live by your internal clock and get healthy and lean (and stay the same) - light and foods timing are key, here (learn more).

  Thiazolidinediones + melatonin, a dynamic duo vs. insulin resistance -- A group of researchers from the Indira College of Pharmacy in Tathawade, India, have just published a study on the combined effects of PPAR agonists and melatonin as a means to ameliorate dexmethasone (artificial cortisol) induced insulin resistance in rodents (Ghaisas. 2013).
  
  The data of the study casts a particularly good light on melatonin which does, contrary to the potentially fattening PPAR agonists pioglitazone and rosiglitazone, not entail a simple increase in glucose storage within the adipose tissue. The combination treatment did also normalize the levels of superoxide dismutase, catalase, glutathione reductase and lipid peroxidation in liver homogenates, an effect the scientists partly ascribe to the antioxidant effects of melatonin , as well (the reduced blood glucose is obviously another factor) 
• 50,000 IU of vitamin D per week improve 25OHD in previously vitamin D deficient subjects but don't produce the expected improvements in insulin sensitivity. Contrary to one of the most underrated dietary supplement, namely melatonin (see previous news item), the most overrated, namely vitamin D3, does not do anything for insulin sensitivity -- even when the subjects are deficient to begin with and their 25OHD levels do actually respond to supplementation (Simha. 2013).
  
  Despite a weekly dose of 50,000 IU of vitamin D3 and a + 42% increase in 25-OHD levels (to be fair it must be said that the levels were still relatively low and nowhere near where some experts want to see it), the researchers from the Department of Internal Medicine at the Texas Tech University Health Sciences Center at Permian Basin did not observe any improvements in glucose uptake after 8 weeks of supplementation in their 12 healthy subjects with baseline plasma 25-hydroxy vitamin D (25OH-D) levels of less than 20 ng/mL.
• More about DEHP and its occurrence in your environment: Prepackaged foods are among your best sources to get your detrimental dose of DEHP every day. Belgian children have been shown to get up to 80% of their DEHP and other phtalates from school lunch. And bread was the worst offender (Sioen. 2013) - probably because it's packed 'sandwich style' in plastic containers of which Cirillo et al. were able to demonstrate that these and other plastic packagings leech the phtalates right into the food (Cirillo. 2011). It is therefore no wonder that the packaged hopsital foods are full of it (Teresa. 2013).
  

  Apropos, having a venyl flooring in either schools or hospitals will only increase the DEHP load due to the emission of the plasticizer into the air (Yu. 2013) and the DEHP content of the bags with blood transfusions are so high that the anti-doping agencies use it as a marker of illegal blood transfusions (Monfort. 2013). Moreover, phtalates leech into milk and dietary products fat-enriched food such as cheese and cream during processing and storage (Kappenstein. 2013); vegetable oils in plastic containers are likewise full of it (Wu. 2013).

  Cooking seems to remove some of the phatalates, but that does not work for vegetables for example (Fierens. 2013). No wonder foods are still the #1 source, followed by bottled water and indoor air of phatalate exposure in Westerners (Martine. 2013).
  

  Unfortunately, the negative effects of DEHP and its metabolites are not restricted to obesity or the prenatal period, they also induce insulin resistance and metabolic syndrome later in life (Rajesh. 2013) - effects which can be ameliorated by increased vitamin C + E intakes. DEHP has also been shown to reduce progesterone and lead to apoptosis of the ovarian granulosa cells and subsequent infertility (Li. 2013a). Similar detrimental effects have been seen in male rodents (Li. 2013b).
  Natural metabolite of ubiquitous plasticizer DEHP sets you and your unborn kids up for obesity DEHP is used in a wide range of soft PVC products ranging from lifesaving medical devices such as medical tubing and blood bags, to footwear, electrical cables, packaging, tarpaulins for lorries, flooring, stationery and roofing. According to a recent study that's been published in Bioscience Reports its natural metabolite MEHP [mono-(2-ethylhexyl) phthalate] has the potential of turning you into a fat, sick slob:
  

  "In the present study, we show the dose-dependent effects of MEHP on adipocyte differentiation and GPDH (glycerol-3-phosphate dehydrogenase) activity in the murine 3T3-L1 cell model. MEHP induced the expression of PPARγ as well as its target genes required for adipogenesis in vitro. Moreover, MEHP perturbed key regulators of adipogenesis and lipogenic pathway in vivo. In utero exposure to a low dose of MEHP significantly increased b.w. (body weight) and fat pad weight in male offspring at PND (postnatal day) 60. In addition, serum cholesterol, TAG (triacylglycerol) and glucose levels were also significantly elevated. These results suggest that perinatal exposure to MEHP may be expected to increase the incidence of obesity in a sex-dependent manner and can act as a potential chemical stressor for obesity and obesity-related disorders." (Hao. 2013)

  In the latest risk assessment of the EU and the DEHP Information Center it is of course 100% save... which bags the question, whether the guys working there simply consider being obese normal, so that anything that makes you even fatter is "save" and does not pose any more of a health threat than life in general, or if they just deliberately ignore that molecules rarely go in and out of our bodies unmetabolized and thus settled for a set of totally meaningless petri dish experiments, before they concluded:
  

  "The use of DEHP has been carefully considered by EU scientists and it is already well regulated by European legislation relating to toys and childcare articles, cosmetics, food contact materials and medical devices." (DEHP Information Center. 2009)

  Hallelujah! Unfortunately it's metabolite MEHP [mono-(2-ethylhexyl) phthalate] obviously is not such a nice guy :-/  

• 

  Figure 2: Serum markers and adiposity, as well as mRNA expression in adipose tissue of male and female mice after 14 weeks on "high fat" diets (based on Estrany. 2013)

  High fat diets (Western style) for women only? I know, this is once again a rodent study, but it is still intriguing that scientists from the Universitat de les Illes Balears in Palma de Mallorca and the Instituto de Salud Carlos III in Madrid, Spain, found that male rodents become insulin resistant and obese, when they are fed a high fat diet (30% fat, in other words high fat + high carb), the female rodents, on the other hand, switch to a 'fat burning mode' or as the scientists state they ...

  "[...] counteract excessive fat intake by improving their ability to use lipid fuels, which limits adiposity and maintains insulin sensitivity." (Estrany. 2013)

  Just as in a previous study neither the male nor the female rats showed the usual symptoms of hyperphagia (overeating), and the body weight gains in all groups were normal.
  
  "Normal" body weight gain and insulin resistance? That should actually ring a bell. Correct! "Normal-weigh obesity" or being skinny fat! And in fact, the underlying reason for Estrany et al.'s observations seems to be that the diet increased the inflammation in the male rats, while it did not do so in the female rodents. What exactly it was that made the difference here, will yet still have to be elucidated, but my best bet is estrogen, which is by no means just the bad guy as which it is portrayed within the fitness community.
• Molecule in false black pepper aka Embelia ribes turns out to be natural GLUT-4 + PI3K/AKT activator, PPAR-gamma agonist and anti-diabetic. What's particularly exciting about the embelin the active ingredient in Embelia ribes Burm, a member of the species Myrsinaceae, which is widely distributed in India and and has a documented history of being used as a diabetes 'medication' in the Ayurvedian traditional medicine system, is that it increases insulin sensitivity without predisposing to further weight gain and adiposity, as the standard Thiazolidinediones (TZDs) such as rosiglitazone and pioglitazone do.
  
  Using the same streptozotocin (STZ) induced rodent model of type II diabetes you have encountered in numerous other studies that have been covered here at the SuppVersity a group of researchers from the Loyola College in Chennai and the University of Madras (Gandhi. 2013), have found that 50mg/kg body weight of embelin that had been extracted from fresh E. ribes fruits by drying and eluting the raw material in benzene...
  

  • 

    Figure 3: Effects of embelin vs. rosiglitazone on insulin levels and rel. expression of antioxidant enzyme activity (Gandhi. 2013)

    reduced body weight gain, blood glucose and plasma insulin in treated diabetic rats,
  • modulated the altered lipid profiles and antioxidant enzymes,
  • exerted cytoprotective effects on the β-cells of the pancreas,
     
  • increased the PPARγ expression in epididymal adipose tissue,
  • inhibited adipogenic activity (=fat gain),
  • mildly activated PPARγ levels in the liver and skeletal muscle, and
     
  • regulated insulin mediated glucose uptake in epididymal adipose tissue through translocation and activation of GLUT4 in PI3K/p-Akt signaling cascade.
  And best of all, contrary to most natural anti-diabetes, these effects were no mere downstream effects of the antioxidant effects of Embelin, but can be ascribed to direct receptor binding: The active ingredient from false black pepper does not only show a high binding affinity for PPARγ, in the experiments Gandhi et al. condcted, it also had stable binding affinities for the active sites of PI3K, p-Akt and GLUT.
  
  
  Embelia ribes in Ayurveda The false black pepper is no newcomer to the scene of natural medicine / health supplements. Embelia ribes has been used in Ayruveda for centuries as an appetiser, laxative, carminative, anti tape-worm cure, to ameliorate / protect from snake bites, against skin deseases, bronchitis and urinary discharges, versus dyspepsia, liver ailments, jaundice, and glatulence.
  The results certainly are exciting, specifically in view of the fact that emeblin could be interesting not just for type II diabetics and individuals with insulin resistance, but also for lean mean women who are looking for a tool that would optimize their insulin sensitivity without the pro-obesogenic effects that render most other "insulin sensitizer" at best useless. And if we assume that similar effects on PI3K and p-AKT do occur in skeletal muscle, as well (this was unfortunately not measured in the study at hand), embelin could even help you build some muscle. Just as its general efficacy in human beings the last hypothesis does of course still require experimental verification... but don't worry, you know that I will keep you posted on any future studies!

That's it! What? You want more? But that's what a quickie is supposed to be it's the frequency that makes it worthwile not the length... ah, I guess I better wish everyone a happy Sunday before I am starting to go into further details here ;-)


References:

• Cirillo T, Fasano E, Castaldi E, Montuori P, Amodio Cocchieri R. Children's exposure to Di(2-ethylhexyl)phthalate and dibutylphthalate plasticizers from school meals. J Agric Food Chem. 2011 Oct 12;59(19):10532-8.
• DEHP Information Center. DEHP Fact Sheet (revised). June 14, 2013. <  www.dehp-facts.com/upload/documents/webpage/ECPI%20-%20factsheet%20DEHP%20revised%20-%20140609.pdf > retrieved on Nov. 03, 2013.
• Estrany ME, Proenza AM, Gianotti M, Lladó I. High-fat diet feeding induces sex-dependent changes in inflammatory and insulin sensitivity profiles of rat adipose tissue. Cell Biochem Funct. 2013 Oct 30.
• Fierens T, Vanermen G, Van Holderbeke M, De Henauw S, Sioen I. Effect of cooking at home on the levels of eight phthalates in foods. Food Chem Toxicol. 2013 Sep 14;50(12):4428-4435.
• Ghaisas MM, Ahire YS, Dandawate PR, Gandhi SP, Mule M. Effects of Combination of Thiazolidinediones with Melatonin in Dexamethasone-induced Insulin Resistance in Mice. Indian J Pharm Sci. 2011 Nov;73(6):601-7.
• Gandhi GR, Stalin A, Balakrishna K, Ignacimuthu S, Paulraj MG, Vishal R. Insulin sensitization via partial agonism of PPARγ and glucose uptake through translocation and activation of GLUT4 in PI3K/p-Akt signaling pathway by embelin in type 2 diabetic rats. Biochim Biophys Acta. 2013 Oct 24. doi:pii: S0304-4165(12)00302-9.
• Hao C, Cheng X, Xia H, Ma X. The endocrine disruptor mono-(2-ethylhexyl) phthalate promotes adipocyte differentiation and induces obesity in mice. Bioscience Reports. 2013; 32:619–629.
• Kaye WH, Berrettini W, Gwirtsman H, George DT. Altered cerebrospinal fluid neuropeptide Y and peptide YY immunoreactivity in anorexia and bulimia nervosa. Arch Gen Psychiatry. 1990 Jun;47(6):548-56.
• Li N, Liu T, Zhou L, He J, Ye L. Di-(2-ethylhcxyl) phthalate reduces progesterone levels and induces apoptosis of ovarian granulosa cell in adult female ICR mice. Environ Toxicol Pharmacol. 2013 Sep 1
• Li XW, Liang Y, Su Y, Deng H, Li XH, Guo J, Lian QQ, Ge RS. Adverse effects of di-(2-ethylhexyl) phthalate on Leydig cell regeneration in the adult rat testis. Toxicol Lett. 2013 Oct 11. 
• Martine B, Marie-Jeanne T, Cendrine D, Fabrice A, Marc C. Assessment of Adult Human Exposure to Phthalate Esters in the Urban Centre of Paris (France). Bull Environ Contam Toxicol. 2013 Oct 23.
• Magistrelli A, Chezem JC. Effect of ground cinnamon on postprandial blood glucose concentration in normal-weight and obese adults. J Acad Nutr Diet. 2013 Nov;112(11):1806-9. 
• Monfort N, Ventura R, Balcells G, Segura J. Determination of five di-(2-ethylhexyl)phthalate metabolites in urine by UPLC-MS/MS, markers of blood transfusion misuse in sports. J Chromatogr B Analyt Technol Biomed Life Sci. 2013 Sep 21. doi:pii: S1570-0232(12)00560-0.
• Rajesh P, Sathish S, Srinivasan C, Selvaraj J, Balasubramanian K. Exposure to diethyl hexyl phthalate (DEHP) to adult male rat is associated with insulin resistance in adipose tisssue: Protective role of antioxidant vitamins (C & E). J Cell Biochem. 2013 Sep 18.
• Ruohonen ST, Vähätalo LH, Savontaus E. Diet-induced obesity in mice overexpressing neuropeptide y in noradrenergic neurons. Int J Pept. 2013;2013:452524. doi: 10.1155/2013/452524. Epub 2013 Oct 18. 
• Simha V, Mahmood M, Ansari M, Spellman CW, Shah P. Effect of Vitamin D Replacement on Insulin Sensitivity in Subjects With Vitamin D Deficiency. J Investig Med. 2013 Oct 29.
• Wu P, Yang D, Zhang L, Shen X, Pan X, Wang L, Zhang J, Tan Y, Feng L, Ying Y. Simultaneous determination of 17 phthalate esters in edible vegetable oils by GC-MS with silica/PSA-mixed solid-phase extraction. J Sep Sci. 2013 Nov;35(21):2932-9.
• Xu Y, Liu Z, Park J, Clausen PA, Benning JL, Little JC. Measuring and Predicting the Emission Rate of Phthalate Plasticizer from Vinyl Flooring in a Specially-Designed Chamber. Environ Sci Technol. 2013 Oct 23.

BPA & Phtalate News for the Plasti-Nation. The Endocrine Contribution to Muscle Growth. Magnesium & Testosterone Increase in Parallel. Anabolic Vibes on the Lat Pull & More

You still have a couple of milli- or centimeter too much on your waistline? Let's hope this spring will provide ample time to work out in the sun, after all that's the energizing way to work out, something even virtual reality indoor exercise cannot compete with (Plante. 2006)

The SuppVersity figure of the week is "90". That was the average total amount of sunshine hours we got here in North-Rhine-Westphalia within the winter months (DWD. 2013; and there were places with only 40h!). A pretty depressing figure, in the literal sense. If you listened to the last installment of the Science Round Up (click here to download the podcast), you may remember that I was actually somewhat surprised to hear that this was the darkest Winter ever since the sunshine hours have been recorded - after all, I got my 45min of "artificial sunshine" in, every morning. So, just in case you are still wondering how it's possible to write a blogpost everyday, the data from a 2013 series of studies in Dutch schools would support that it's all about the right lighting (Sleeges. 2013).

Apropos news, here is your weekly serving of short news on all sorts of things... you are missing the exercise related news? Well, I saved those for a round-up and one or two individual posts in the course of the next week ;-)

• Fiber renders mammalian guts colon proof (Nagy-Szakal. 2013) -- As a recent rodent study from the Baylor University suggest, it can hardly be too early to keep an eye on fiber intake. The mice in the pertinent study that had been randomly assigned to a low-cellulose (indigestible fiber that's present in fruits, veggies, whole grains etc.) diet had little to no protection against experimentally induced cholitis.
  
  

  

  Semisynthetic non-fermentable viscous fiber Hydroxpropyl-Methylcellulose is imported pound-wise from China and ends up as E464 from in all sorts of food - obviously at too low dosages to do the anti-obesity trick, though (learn more).

  Murine pediatric cellulose supplementation, on other hand, induces transient trophic and  anticolitic effects, which is - and that's important (!) - dependent on a continuous supply of adequate amounts of dietary fiber. The same goes for the benefifical changes in the diversity of the gut microbiome which did largely  decline after only 10 days.
  
  The protective effect on the epithelial cell lining and the increase in surface area in response to cellulose supplementation should also facilitate the uptake of those vitally important nutrients, people with Crohn's etc. are lacking - a result that may well be significant for those of you who are trying to make the most of the nutrients and not just the energy in their diets.
  
  Edit: As George Henderson rightly said, the study at hand does not talk about cancer protection, I simply inferred that from previous human studies such as Mendez (2007), Terry (2001) or Roth (2001), without mentioning that, my mistake, sorry for that. I still changed the headline to reflect the contents of the study and want to point out that George also makes a valid point stating that (a) fiber often replaces other less healthy nutrients in the diet and (b) that (my addition) "once the baby has been thrown out with the bathtub" and you already have Crohn's and co different rules may apply.

• The diabesity syndrome - Is it the soda, or the bottle it's packaged in? (Indumathi. 2013) I am well aware that the doses of BPA we are supposed to get from our "diets" is way below those that are uses in rodent studies like the one by Indumathi et al., but don't you think that it is still remarkable that the same plastic poison aka BPA that leaches so readily into the acidic brown soup 50% of the US citizens guzzle on a daily basis, induces exactly the same nasty reductions in insulin receptor and GLUT-4 transporter expression, as well as glucose oxidation and the phosphorylation of Akt which are currently still ascribed exclusively to the soda itself (see figure 1).

  

  Figure 2: Effects of 20 or 200mg/kg body weight of BPA on insulin receptor and Akt phosphorylation, GLUT-4 expression in skeletal muscle and systemic insulin and testosterone levels (Indumathi. 2013)

  Now what's worst is that these pathological changes are not likely to be observed, because it happens "silently"; i.e. in the absence of elevated blood glucose levels.
  Did you know that the amount of BPA that leaches from plastics increases by x40, when you dishwash and reuse them (Brede. 2003)? And worst of all, these figures were observed in baby bottles and thus objects those of us get in contact for whom the otherwise probably harmless exposure could actually be dangerous (DiVall. 2013). Exposure to higher temperatures of liquids in plastic containers in the summer (>40°C) is another factor which contributes to an increased leakage of BPA from the container into the liquid (Makris.2013)
  With the latter being the only blood parameters that are evaluated on a regular basis within at least a reasonably large cross section of the population it's no wonder that many of us don't see how the diabetic beast and the BPA castrator are sneaking up on them before it's already too late. Obviously no reason for the FDA or any other governmental body to even bother. Aside from the U.S. Environmental Protection Agency which has published a reference dose of 0.05 mg/kg/day for BPA in 1993 (IRIS. 1993) an official acceptable daily reference intake for BPA is still lacking. Even if the current research does not suggest that our daily exposure is high enough to actually do any harm, I would expect the reference levels to reflect that - what about you?

• 

  In 1998 the Consumer Union wrote a letter to the FDA compaining about "endocrine disrupting chemicals" in cheese and dairy in plastics wrappings. I wonder if they knew about the masked phtalates in hygiene products, as well.

  More news for the"Plasti-Nations" (various): A couple of days ago Wu et el. published a paper on the TSH and estrogen suppressive effects of phtalates in Taiwanese children. With >40% lower TSH levels and estrogen levels the changes, in the 4-5 year olds with the highest (500ppm) phtalate exposure from food stuff is alarming. The only good news is that it these changes appear to be reversible, when further exposure is avoided (Wu.2013).
  
  Apropos good news, in December 2013, Fierens et al. investigated the effects of cooking at home on the phtalate content of foods and found that, except for veggies, the phtalate content of almost all foods decline after cooking (Fierens. 2013). I guess, I don't have to mention that this is not going to happen in a crock pot unless you pour away the brew.
  
  What you should also keep in mind is that your diet is by far not the only way you are exposed to phtalates, as a group of scientists working at a University right around my corner elucidated (Koch. 2013). The "pro-breast cancer" monoethyl carboxylpentyl phthalates (MEPs) for example usually come from personal hygiene products (it's the stuff thats called "fragrance"). The dosage, by the way, was high enough for the scientists to be able to actually measure rises in MEP concentrations after people (esp. men, by the way) took a shower. Ah, and not to forget a non-negligible amount of the low molecular weight phtalates is simply with ubiquitous sources including dust and indoor air. Up to now convincing evidence for the role of this constant assault in any of the ailments our society is suffering from is not conclusive.

• Don't like oats? Buckwheat has similar benefits (Stringer. 2013) -- In a recently published paper in the scientific journal Metabolism, a group of researchers from the University of Manitoba in Winnipeg, Canada, reports that the consumption of buckwheat cracker either instead of rice crackers or simply on their own could help both diabetics and non-diabetics maintain a healthy weight.
  
  

  

  4x more iron, 3x more calcium, >9 times more magnesium, ~6x more potassium and about twice as much zinc, copper and manganese that's what buckwheat flour has to offer compared to wheat (de Francischi. 1994). If you like those figures, what about havin' one of the pancakes you see above (recipe)

  Yet, despite an increased satiety effect and improvements (increases / decreases) in the corresponding hormones glucagon-like peptide-1 (GLP-1), glucose-dependent insulinotropic peptide (GIP) and pancreatic polypeptide (PPY) the glucose response to the buckwheat crackers was not significantly different from the one the scientists observed after the consumption of rice crackers.
  
  What's intriguing, though is that it appears as if these effects were not exclusively fiber-specific. After all, the rice crackers had almost as much fiber as the buckwheat. Moreover, a 2003 study Kawa et al. confirmed that even fiber-free buckwheat extracts exert potent anti-diabetic effects, the researchers ascribed to the presence of d-chiro-inositol in the extracts (Kawa. 2003).

• Anabolic vibes - Vibrate your way to higher testosterone levels (Couto.2013) -- If you still believe vibrators were for women only you got to check out the latest issue of the International Journal of Sports Medicine, in which a group of Brazilian scientists reports that the use of one of those fancy vibration devices (20-Hz and 12-mm) during the lat pulldown induced greater increases in testosterone and lactate concentrations. Dunno if that will also work if you just swipe your girlfriends vibrator and honestly, I don't even want to know that ;-)

• Does the testosterone  and overall hormonal response to workouts even count, or are we still chasing a hormonal ghost? (Schoenfeld. 2013) -- In his latest review of the literature, Brad Schoenfeld who has been busy writing reviews on everything muscle heads are interested in within the last couple of weeks, picks the role of the endocrine response to exercise apart. In that, Schoenfeld points out that it is important to look close before you can tell whether or not a certain "hormone" will effect or even drive skeletal muscle hypertrophy.
  
  

  

  Check out this previous analysis of post-workout anabolism here at the SuppVersity (read more)

  There is for example ample evidence for the involvement of the muscle specific IGF-1 isoform IGF-1Ec, or its locally expressed splice-variant MGF and the presence of high and low responders (cf. West. 2013). Studies using its parent growth hormone, which used injections of the artificially produced recombinant growth hormone are of questionable value, since they lack the natural diversity of "growth hormones" (different GH peptides). Schoenfeld also points out that the evidence that testosterone is anabolic "is inconvertible" (Schoenfeld. 2013) and that the debate would thus have to center around its influence in the vicinity of a workout, where - and this is interesting - we actually know that the effects should occur only after the initial repression of androgen receptors is reversed.
  
  In accordance with what I have pointed out in the Intermittent Thoughts on Building Muscle Series Schoenfeld comes to the conclusion that it would be inappropriate to totally discard the importance of the endocrine response to workouts (IGF-1 & Co, in particular), just because it does not promote the (imho totally overrated) short term protein synthetic response to exercise:

  "Based on limited cellular signaling data, it is conceivable that the primary effect of post-exercise hormonal elevations is to increase satellite cell activity as opposed to mediating acute increases in muscle protein synthesis. If so, this could favor greater long-term increases in muscle hypertrophy without significantly impacting short-term gains." (Schoenfeld. 2013)

  Obviously (and rightly so) Schoenfeld concludes this paragraph of the discussion of this excellent review with the sentence "This hypothesis requires further study." -- And you bet, I will keep an eye on the topic in order to let you know whether the 8% of which West and Phillips say that it's the upper limit of the contribution the transient increases in endocrine hormones have on skeletal muscle hypertrophy (West. 2013) is an over- or underestimation.

• Excess magnesium is good for your testosterone levels, bad for your prostate and could potentially become fatal for your heart (Chandra. 2013) -- According to the latest results from a rodent study, it appears as if an excess intake of magnesium, ingested not as supplement but in form of magnesium sulfate in the chow, can boost testosterone levels by almost 30% (figure 1):

  

  Figure 1: Testosterone  levels prostate weight, luteinizing hormone and serum magnesium levels (all data expressed relative to baseline) after 15 or 29 days on diets with different magnesium content.
  

  The increase in testosterone does yet not come without downsides in the form of slight, but significant increases in prostate size as well as a profound increase in magnesium levels, which would - if they were observed in human beings already mark the early stages of hypermagnesemia. So, as important an adequate amount of magnesium in your diet may be, it should be obvious that 1.5% of the diet or ~350mg/kg magnesium sulfate and thus 35mg elemental magnesium per kilogramm body weight (the HED of the dosage that was administered to the rodents; ) is simply too much - honestly, I am surprised that the rodents did not get chronic diarrhea, anyway ;-)

Since a wise man facebooked me earlier today to keep the SuppVersity posts short on this weekend, spending some time idling around, in order to avoid ending up totally burned out (I wonder if that really was an all altruistic advice of him ;-), I will now do just that - cut it short; yet not without pointing you towards the SuppVersity Facebook Wall, which does - as every day - hold 6-10 new short news for you to read up on.
 

+++ Have a nice weekend, everyone! +++

References:

• Brede C, Fjeldal P, Skjevrak I, Herikstad H. Increased migration levels of bisphenol A from polycarbonate baby bottles after dishwashing, boiling and brushing. Food Addit Contam. 2003 Jul;20(7):684-9.
• Chandra AK, Sengupta P, Goswami H, Sarkar M. Effects of dietary magnesium on testicular histology, steroidogenesis, spermatogenesis and oxidative stress markers in adult rats. Indian J Exp Biol. 2013 Jan;51(1):37-47.
• Couto BP, Silva HR, Filho AG, da Silveira Neves SR, Ramos MG, Szmuchrowski LA, Barbosa MP. Acute Effects of Resistance Training with Local Vibration. Int J Sports Med. 2013 Feb 26.
• de Francischi ML, Salgado JM, Leitão RF. Chemical, nutritional and technological characteristics of buckwheat and non-prolamine buckwheat flours in comparison of wheat flour. Plant Foods Hum Nutr. 1994 Dec;46(4):323-9.
• DiVall SA. The influence of endocrine disruptors on growth and development of children. Curr Opin Endocrinol Diabetes Obes. 2013 Feb;20(1):50-5.
• DWD. Press Release from February 27, 2013. < http://www.dwd.de/presse > 
• Fierens T, Vanermen G, Van Holderbeke M, De Henauw S, Sioen I. Effect of cooking at home on the levels of eight phthalates in foods. Food Chem Toxicol. 2013 Dec;50(12):4428-35.
• Indumathi D, Jayashree S, Selvaraj J, Sathish S, Mayilvanan C, Akilavalli N, Balasubramanian K. Effect of bisphenol-A on insulin signal transduction and glucose oxidation in skeletal muscle of adult male albino rat. Hum Exp Toxicol. 2013 Feb 19.
• Integrated Risk Information System (IRIS). Reference Dose (RfD): Description and use in health risk assessments. 1993 < http://www.epa.gov/ncea/iris/subst/0356.htm > 
• Kawa JM, Taylor CG, Przybylski R. Buckwheat concentrate reduces serum glucose in streptozotocin-diabetic rats. J Agric Food Chem. 2003 Dec 3;51(25):7287-91.
• Koch HM, Lorber M, Christensen KL, Pälmke C, Koslitz S, Brüning T. Identifying sources of phthalate exposure with human biomonitoring: Results of a 48h fasting study with urine collection and personal activity patterns. Int J Hyg Environ Health. 2013 Jan 17. 
• Makris Kc, Andra S, Jia A, Herrick L, Christophi C, Snyder Sa, Hauser R. The Association Between Water Consumption From Polycarbonate Containers And Bisphenol-A Intake During Harsh Environmental Conditions in Summer. Environ Sci Technol. 2013 Feb 28.
• Mendez, A M, Pera G, Agudo A, Bueno-de-Mesquita HB, Palli D, Boeing H, Carneiro F, Berrino F, Sacerdote C, Tumino R, Panico S, Berglund G, Manjer J, Johansson I, Stenling R, Martinez C, Dorronsoro M, Barricarte A, Tormo MJ, Quiros JR, Allen N, Key TJ, Bingham S, Linseisen J, Kaaks R, Overvad K, Jensen M, Olsen A, Tjønneland A, Peeters PH, Numans ME, Ocké MC, Clavel-Chapelon F, Boutron-Ruault MC, Trichopoulou A, Lund E, Slimani N, Jenab M, Ferrari P, Riboli E, González CA. Cereal fiber intake may reduce risk of gastric adenocarcinomas: the EPIC-EURGAST study. Int J Cancer. 2007 Oct 1;121(7):1618-23.
• Nagy-Szakal D, Hollister EB, Luna RA, Szigeti R, Tatevian N, Smith CW, Versalovic J, Kellermayer R. Cellulose supplementation early in life ameliorates colitis in adult mice. PLoS One. 2013;8(2):e56685. 
• Plante TG, Cage C, Clements S, Stover A. Psychological benefits of exercise paired with virtual reality: Outdoor exercise energizes whereas indoor virtual exercise relaxes. International Journal of Stress Management, Vol 13(1), Feb 2006, 108-117
• Roth J, Mobarhan S. Preventive role of dietary fiber in gastric cardia cancers. Nutr Rev. 2001 Nov;59(11):372-4.
• Schoenfeld B. Post-exercise hypertrophic adaptations: A re-examination of the hormone hypothesis and its applicability to resistance training program design. J Strength Cond Res. 2013 Feb 25. 
• Sleeges PJC, Moolenaar MN, Galetzka M, Pruyn A, Sarroukh BE, van der Zande B. Lighting affects students’ concentration positively: findings from three Dutch studies. Lighting Research and Technology. June 22, 2013.
• Stringer DM, Taylor CG, Appah P, Blewett H, Zahradka P. Consumption of buckwheat modulates the post-prandial response of selected gastrointestinal satiety hormones in individuals with type 2 diabetes mellitus. Metabolism. Available online 26 February 2013.
• Terry P, Lagergren J, Ye W, Wolk A, Nyrén O. Inverse association between intake of cereal fiber and risk of gastric cardia cancer. Gastroenterology. 2001 Feb;120(2):387-91
• 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.  
• Wu MT, Wu CF, Chen BH, Chen EK, Chen YL, Shiea J, Lee WT, Chao MC, Wu JR. Intake of phthalate-tainted foods alters thyroid functions in taiwanese children. PLoS One. 2013;8(1):e55005.