...INTENSITY...INSANITY...WATCH ME GROOW!!! - NaturalPursuit's Offseason Journey

[NaturalPursuit]

•••NEW BEAST FITNESS RADIO EPISODE•••
IFBB PRO Terrence Ruffin

Austin Stout and myself had the opportunity to sit down and chat with IFBB PRO and MPA sponsored athlete Terrence Ruffin! We covered everything from:

-his 2016 season
-his upcoming 2017 season
-what his training and nutrition looked like at that time
-what his training and nutrition currently look like
-what adjustments he's made to bring up lagging body parts
-how him and Matt approached peak week

And a TON more! Support Terrence by going to his website and following him at https://ruffinready.com



•••FIND THE EPISODES•••

https://itunes.apple.com/us/podcast/...t/id1065532968

www.youtube.com/user/NaturallyGreatBB

http://beastfitnessradio.libsyn.com

[NaturalPursuit]

A little bit I've written on Increasing Protein After a Deficit Part 1/3

"Coming out of a caloric deficit can be challenging for some. At this point, you’ve most likely dropped a significant amount of calories as well as increased cardiovascular work. Reverse dieting out is extremely important in my opinion as you’ll see time and time again that people will stop dieting, begin binging, and gain 20+ lbs of body fat back within a week. That pretty much ensures you’re going to be playing catch up the entire surplus/offseason and you will not have the most successful growing phase as you could. The goal would be to maintain a lean physique relative to the individual and slowly add back in calories to ensure fat gain is kept to a minimum. Obviously this amount to add back in over time varies drastically from person to person. Even more so, where those calories are coming from varies drastically from person to person. But one method I want to discuss today is beginning to add calories back in to someone’s diet, mainly from protein sources. Keep in mind this is merely one of hundreds of methods you can start a reverse diet. This is simply meant to educate and broaden your perspective on possible options and tools you can utilize during this period.

There are a number of reasons why increasing protein after a deficit may be more optimal for an individual than another way, so we’re going to go through some research to help you better understand why it holds merit. One study from Johnston et al in 2002 looked at postprandial thermogenesis in regards to a high protein/low fat diet compared with a high carbohydrate/low fat diet (1.) The recent literature suggests that high-protein, low-fat diets promote a greater degree of weight loss compared to high-carbohydrate, low-fat diets, but the mechanism of this enhanced weight loss is unclear. This study compared the acute, energy-cost of meal-induced thermogenesis on a high-protein, low-fat diet versus a high-carbohydrate, low-fat diet. The researchers had ten healthy, normal weight, non-smoking female volunteers aged 19-22 years were recruited from a campus population. Using a randomized, cross-over design, subjects consumed the high-protein and the high-carbohydrate diets for one day each, and testing was separated by a 28- or 56-day interval. Control diets were consumed for two days prior to each test day. On test day, the resting energy expenditure, the non-protein respiratory quotient and body temperature were measured following a 10-hour fast and at 2.5-hour post breakfast, lunch and dinner. Fasting blood samples were collected test day and the next morning, and complete 24-hour urine samples were collected the day of testing. The results showed postprandial thermogenesis at 2.5 hours post-meal averaged about twofold higher on the high protein diet versus the high carbohydrate diet, and differences were significant after the breakfast and the dinner meals (p < 0.05). Body temperature was slightly higher on the high protein diet (p = 0.08 after the dinner meal). Changes in the respiratory quotient post-meals did not differ by diet, and there was no difference in 24-hour glomerular filtration rates by diet. Nitrogen balance was significantly greater on the high-protein diet compared to the high-carbohydrate diet (7.6 +/- 0.9 and -0.4 +/- 0.5 gN/day, p < 0.05), and at 24-hour post-intervention, fasting plasma urea nitrogen concentrations were raised on the high protein diet versus the high-carbohydrate diet (13.9 +/- 0.9 and 11.2 +/- 1.0 mg/dL respectively, p < 0.05). These data indicate an added energy-cost associated with high-protein, low-fat diets and may help explain the efficacy of such diets for weight loss. We see that increasing dietary protein can increase the number of calories you burn for a given caloric intake. This means that coming out of a reverse diet, you can typically get away with adding in more calories to someone’s diet than if you were to begin adding in calories from other macronutrients (for a very simple example, say you can add 500 kcals from carbohydrates to someone’s reverse diet and they begin to reverse in a proper manner. If thats the case, you can typically get away with anywhere from 700 to possibly 900 kcals if you added those calories back in from protein. Again this is just an example and shouldnt be taken as hard specific numbers to stand by.)"


References

Postprandial thermogenesis is increased 100% on a high-protein, low-fat diet versus a high-carbohydrate, low-fat diet in healthy, young women. Carol S. Johnston, Carol S. Day, Pamela D. Swan. J Am Coll Nutr. 2002 (https://www.ncbi.nlm.nih.gov/pubmed/11838888)

Effects of variation in protein and carbohydrate intake on body mass and composition during energy restriction: a meta-regression. James W. Krieger, Harry S. Sitren, Michael J. Daniels, Bobbi Langkamp-Henken. Am J Clin Nutr. 2006 (https://www.ncbi.nlm.nih.gov/pubmed/16469983)

Protein, weight management, and satiety. Douglas Paddon-Jones, Eric Westman, Richard D. Mattes, Robert R. Wolfe, Arne Astrup, Margriet Westerterp-Plantenga. Am J Clin Nutr. 2008 (https://www.ncbi.nlm.nih.gov/pubmed/18469287)

Indicator Amino Acid-Derived Estimate of Dietary Protein Requirement for Male Bodybuilders on a Nontraining Day Is Several-Fold Greater than the Current Recommended Dietary Allowance. Bandegan A, Courtney-Martin G, Rafii M, Pencharz PB, Lemon PW. J Nutr. 2017. (https://www.ncbi.nlm.nih.gov/pubmed/28179492)

Effect of a high-protein breakfast on the postprandial ghrelin response. Wendy A. M. Blom, Anne Lluch, Annette Stafleu, Sophie Vinoy, Jens J. Holst, Gertjan Schaafsma, Henk F. J. Hendriks. Am J Clin Nutr. 2006 (https://www.ncbi.nlm.nih.gov/pubmed/16469977)

Ghrelin and glucagon-like peptide 1 concentrations, 24-h satiety, and energy and substrate metabolism during a high-protein diet and measured in a respiration chamber. Manuela P. G. M. Lejeune, Klaas R. Westerterp, Tanja C. M. Adam, Natalie D. Luscombe-Marsh, Margriet S. Westerterp-Plantenga. Am J Clin Nutr. 2006 (https://www.ncbi.nlm.nih.gov/pubmed/16400055)

Higher protein intake preserves lean mass and satiety with weight loss in pre-obese and obese women. Heather J. Leidy, Nadine S. Carnell, Richard D. Mattes, Wayne W. Campbell. Obesity (Silver Spring) 2007 (https://www.ncbi.nlm.nih.gov/pubmed/17299116)

The satiating effect of dietary protein is unrelated to postprandial ghrelin secretion. Lisa J. Moran, Natalie D. Luscombe-Marsh, Manny Noakes, Gary A. Wittert, Jennifer B. Keogh, Peter M. Clifton. J Clin Endocrinol Metab. 2005 (https://www.ncbi.nlm.nih.gov/pubmed/16014402)

Effects of Meals High in Carbohydrate, Protein, and Fat on Ghrelin and Peptide YY Secretion in Prepubertal Children. Lomenick, J. P., Melguizo, M. S., Mitchell, S. L., Summar, M. L., & Anderson, J. W. (2009). The Journal of Clinical Endocrinology and Metabolism. (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2775646/)

Ghrelin enhances appetite and increases food intake in humans. A. M. Wren, L. J. Seal, M. A. Cohen, A. E. Brynes, G. S. Frost, K. G. Murphy, W. S. Dhillo, M. A. Ghatei, S. R. Bloom. J Clin Endocrinol Metab. 2001 (https://www.ncbi.nlm.nih.gov/pubmed/11739476)

[NaturalPursuit]

"Magnesium may inhibit the inflammatory processes that plays a role in the hardening of arteries."


Magnesium intake and plasma concentrations of markers of systemic inflammation and endothelial dysfunction in women.

BACKGROUND:
Relations between magnesium intake and systemic inflammation and endothelial dysfunction are not well established.

OBJECTIVE:
The aim of the present study was to examine whether and to what extent magnesium intake is related to inflammatory and endothelial markers.

DESIGN:
We conducted a cross-sectional study of 657 women from the Nurses' Health Study cohort who were aged 43-69 y and free of cardiovascular disease, cancer, and diabetes mellitus when blood was drawn in 1989 and 1990. Plasma concentrations of C-reactive protein (CRP), interleukin 6 (IL-6), soluble tumor necrosis factor alpha receptor 2 (sTNF-R2), E-selectin, soluble intercellular adhesion molecule 1 (sICAM-1), and soluble vascular cell adhesion molecule 1 (sVCAM-1) were measured. Estimates from 2 semiquantitative food-frequency questionnaires, administered in 1986 and 1990, were averaged to assess dietary intakes.

RESULTS:
In age-adjusted linear regression analyses, magnesium intake was inversely associated with plasma concentrations of CRP (P for linear trend = 0.003), E-selectin (P = 0.001), and sICAM-1 (P = 0.03). After further adjustment for physical activity, smoking status, alcohol use, postmenopausal hormone use, and body mass index, dietary magnesium intake remained inversely associated with CRP and E-selectin. Multivariate-adjusted geometric means for women in the highest quintile of dietary magnesium intake were 24% lower for CRP (1.70 +/- 0.18 compared with 1.30 +/- 0.10 mg/dL; P for trend = 0.03) and 14% lower for E-selectin (48.5 +/- 1.84 compared with 41.9 +/- 1.58 ng/mL; P for trend = 0.01) than those for women in the lowest quintile.

CONCLUSION:
Magnesium intake from diet is modestly and inversely associated with some but not all markers of systematic inflammation and endothelial dysfunction in apparently healthy women.

https://www.ncbi.nlm.nih.gov/pubmed/17413107

[NaturalPursuit]

Safe to say the refeed yesterday didn't help one bit. On top of that, I woke up in the middle of the night with my throat almost swollen closed and could barely breathe. Looks like this sickness still isn't going away but at under 3 weeks out, I don't care if I break a bone, you can bet your ass I'm going to push through this. Might not be ideal but I'm obsessed with bringing a truly transformed version of myself to the stage this year.

Happy Easter everyone! And if your in prep over the holidays, make time for your family and don't hide away because you may or may not be able to enjoy a meal with them.

[NaturalPursuit]

I don't care if I make mistakes because I FREAKING LOVE EXPERIMENTING! Pushed my refeed from 24 to roughly 36 hours long and FINALLY filled out a little. Still retaining a ton of fluid from this sickness but that just means once I drop excess fluids, more body fat, and fill out completely, I'll be in a great position!

[NaturalPursuit]

About to have 3-Part Series Articles on just about every glucose disposal agent ingredient out there. Here's the current list of literature for Cinnamon as a GDA.

References
Relative bioavailability of coumarin from cinnamon and cinnamon-containing foods compared to isolated coumarin: a four-way crossover study in human volunteers. Klaus Abraham, Michael Pfister, Friederike Wöhrlin, Alfonso Lampen. Mol Nutr Food Res. 2011 (https://www.ncbi.nlm.nih.gov/pubmed/21462332)

Cinnamon extract inhibits α-glucosidase activity and dampens postprandial glucose excursion in diabetic rats. H Mohamed Sham Shihabudeen, D Hansi Priscilla, Kavitha Thirumurugan. Nutr Metab (Lond) 2011; 8: 46. Published online 2011 (https://www.ncbi.nlm.nih.gov/pubmed/21711570)

Inhibitory activity of cinnamon bark species and their combination effect with acarbose against intestinal α-glucosidase and pancreatic α-amylase. Sirichai Adisakwattana, Orathai Lerdsuwankij, Ubonwan Poputtachai, Aukkrapon Minipun, Chaturong Suparpprom. Plant Foods Hum Nutr. 2011 (https://www.ncbi.nlm.nih.gov/pubmed/21538147)

Regulation of PTP-1 and insulin receptor kinase by fractions from cinnamon: implications for cinnamon regulation of insulin signalling. J. Imparl-Radosevich, S. Deas, M. M. Polansky, D. A. Baedke, T. S. Ingebritsen, R. A. Anderson, D. J. Graves. Horm Res. 1998 (https://www.ncbi.nlm.nih.gov/pubmed/9762007)

The potential of cinnamon to reduce blood glucose levels in patients with type 2 diabetes and insulin resistance. S. Kirkham, R. Akilen, S. Sharma, A. Tsiami. Diabetes Obes Metab. 2009 (https://www.ncbi.nlm.nih.gov/pubmed/19930003)

Cinnamon improves glucose and lipids of people with type 2 diabetes. Alam Khan, Mahpara Safdar, Mohammad Muzaffar Ali Khan, Khan Nawaz Khattak, Richard A. Anderson. Diabetes Care. 2003 (https://www.ncbi.nlm.nih.gov/pubmed/14633804)

Effects of a cinnamon extract on plasma glucose, HbA, and serum lipids in diabetes mellitus type 2. B. Mang, M. Wolters, B. Schmitt, K. Kelb, R. Lichtinghagen, D. O. Stichtenoth, A. Hahn. Eur J Clin Invest. 2006 (https://www.ncbi.nlm.nih.gov/pubmed/16634838)

Cinnamon and health. Joerg Gruenwald, Janine Freder, Nicole Armbruester. Crit Rev Food Sci Nutr. 2010 (https://www.ncbi.nlm.nih.gov/pubmed/20924865)

Cinnamon Use in Type 2 Diabetes: An Updated Systematic Review and Meta-Analysis. Allen, R. W., Schwartzman, E., Baker, W. L., Coleman, C. I., & Phung, O. J. (2013). Annals of Family Medicine. (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3767714/)

Cinnamon extract lowers glucose, insulin and cholesterol in people with elevated serum glucose. Anderson, R. A., Zhan, Z., Luo, R., Guo, X., Guo, Q., Zhou, J. Stoecker, B. J. (2016). Journal of Traditional and Complementary Medicine (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5067830/)

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[NaturalPursuit]

GDAs (Chromium – Part 1 of 3)

GDAs or glucose disposal agents are growing in popularity within the supplement industry. Essentially what these are made for are to help manage glucose and insulin levels in an effort to increase partitioning into positive compartments. In this series, I want to go over my favorite glucose disposal agent ingredients including chromium, berberine, cinnamon, gymnema, banaba leaf, and alpha lipoic acid.

First, we’ll begin with chromium. Chromium regulates insulin levels and improves insulin actions within our bodies mainly from its main mechanism that is connected to chromodulin (a protein that changes the signaling of insulin receptors in the body.) Once chromodulin isn’t functioning properly, insulin functioning is drastically reduced. Luckily, chromium has a tremendous amount of literature I would like to go over to ensure you have a full understanding of its benefits and method of action. A study from Abdollahi et al looked at the effect of chromium on glucose and lipid profiles in patients with type 2 diabetes (a meta-analysis review of randomized trials.) The abstract is stated as follows: Chromium (Cr) as an essential trace element in metabolism of carbohydrate, lipid and protein is currently prescribed to control diabetes mellitus (DM). The objective of this meta-analysis was to compare the effect of Cr versus placebo (Pl) on glucose and lipid profiles in patients with type 2 DM. Literature searches in PubMed, Scopus, Scirus, Google Scholar and IranMedex was made by use of related terms during the period of 2000-2012. Eligible studies were randomized clinical trials (RCTs) with intake of Cr higher than 250 µg at least for three months in type 2 DM. Glycated hemoglobin (HbA1c), fasting blood sugar (FBS), total cholesterol (TC), high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C), very low-density lipoprotein cholesterol (VLDL-C), triglyceride (TG), and body mass index (BMI) were the main outcomes. Seven out of 13 relevant studies met the criteria and were included in the meta-analysis. HbA1c change in diabetic patients in Cr supplement therapy comparing to Pl was -0.33 with 95%CI= -0.72 to 0.06 (P= 0.1). Change of FBG in Cr therapy vs. Pl was -0.95 with 95%CI= -1.42 to -0.49 (P< 0.0001). TC change in Cr therapy vs. Pl was 0.07 with 95%CI= -0.16 to 0.31 (P= 0.54). TG change in diabetic patients in Cr supplement therapy comparing to Pl was -0.15 with 95%CI= -0.36 to 0.07 (P= 0.18). Cr lowers FBS but does not affect HbA1c, lipids and BMI (1.)

References

Effect of chromium on glucose and lipid profiles in patients with type 2 diabetes; a meta-analysis review of randomized trials. Mohammad Abdollahi, Amir Farshchi, Shekoufeh Nikfar, Meysam Seyedifar. J Pharm Pharm Sci. 2013 (https://www.ncbi.nlm.nih.gov/pubmed/23683609)

Characterization of the Metabolic and Physiologic Response from Chromium Supplementation in Subjects with Type 2 Diabetes. William T Cefalu, Jennifer Rood, Patricia Pinsonat, Jianhua Qin, Olga Sereda, Lilian Levitan, Richard Anderson, Xian H Zhang, Julie M Martin, Corby Martin, Zhong Q Wang, Bradley Newcomer. Metabolism. Author manuscript; available in PMC 2014 May 14. Published in final edited form as: Metabolism. 2010 (https://www.ncbi.nlm.nih.gov/pubmed/20022616)

Chromium pi****nate supplementation attenuates body weight gain and increases insulin sensitivity in subjects with type 2 diabetes. Julie Martin, Zhong Q. Wang, Xian H. Zhang, Deborah Wachtel, Julia Volaufova, Dwight E. Matthews, William T. Cefalu. Diabetes Care. 2006 (https://www.ncbi.nlm.nih.gov/pubmed/16873787)

Role of chromium supplementation in Indians with type 2 diabetes mellitus. Debjani Ghosh, Basudev Bhattacharya, Biswajit Mukherjee, Byomkesh Manna, Mitali Sinha, Jyothi Chowdhury, Subhankar Chowdhury. J Nutr Biochem. 2002 (https://www.ncbi.nlm.nih.gov/pubmed/12550067)

Chromium treatment has no effect in patients with type 2 diabetes in a Western population: a randomized, double-blind, placebo-controlled trial. Nanne Kleefstra, Sebastiaan T. Houweling, Stephan J. L. Bakker, Simon Verhoeven, Rijk O. B. Gans, Betty Meyboom-de Jong, Henk J. G. Bilo. Diabetes Care. 2007 (https://www.ncbi.nlm.nih.gov/pubmed/17303791)

Chromium as a supplement. H. C. Lukaski. Annu Rev Nutr. 1999 (https://www.ncbi.nlm.nih.gov/pubmed/10448525)

Purification and properties of biologically active chromium complex from bovine colostrum. A. Yamamoto, O. Wada, H. Suzuki. J Nutr. 1988 (https://www.ncbi.nlm.nih.gov/pubmed/3275760)

Age-related decreases in chromium levels in 51,665 hair, sweat, and serum samples from 40,872 patients–implications for the prevention of cardiovascular disease and type II diabetes mellitus. S. Davies, J. McLaren Howard, A. Hunnisett, M. Howard. Metabolism. 1997 (https://www.ncbi.nlm.nih.gov/pubmed/9160809)

Isolation and characterization of a biologically active chromium oligopeptide from bovine liver. C. M. Davis, J. B. Vincent. Arch Biochem Biophys. 1997 (https://www.ncbi.nlm.nih.gov/pubmed/9056266)

Chromium deficiency during total parenteral nutrition. H. Freund, S. Atamian, J. E. Fischer. JAMA. 1979 (https://www.ncbi.nlm.nih.gov/pmc/art...y/?tool=pubmed)

Effect of chromium nicotinic acid supplementation on selected cardiovascular disease risk factors. V. L. Thomas, S. S. Gropper. Biol Trace Elem Res. 1996 (https://www.ncbi.nlm.nih.gov/pubmed/9096856)

Glucose tolerance factor extracted from yeast: oral insulin-mimetic and insulin-potentiating agent: in vivo and in vitro studies. Sarah Weksler-Zangen, Tal Mizrahi, Itamar Raz, Nitsa Mirsky. Br J Nutr. 2012 (https://www.ncbi.nlm.nih.gov/pubmed/22172158)

Chromium in biological systems, I. Some observations on glucose tolerance factor in yeast. N. Mirsky, A. Weiss, Z. Dori. J Inorg Biochem. 1980 (https://www.ncbi.nlm.nih.gov/pubmed/6772742)

A glucose tolerance factor and its differentiation from factor 3. K. SCHWARZ, W. MERTZ. Arch Biochem Biophys. 1957 (https://www.ncbi.nlm.nih.gov/pubmed/13479136)

Effects of niacin-bound chromium and grape seed proanthocyanidin extract on the lipid profile of hypercholesterolemic subjects: a pilot study. H. G. Preuss, D. Wallerstedt, N. Talpur, S. O. Tutuncuoglu, B. Echard, A. Myers, M. Bui, D. Bagchi. J Med. 2000 (https://www.ncbi.nlm.nih.gov/pubmed/11508317)

Chromium: celebrating 50 years as an essential element? John B. Vincent. Dalton Trans. 2010 (https://www.ncbi.nlm.nih.gov/pubmed/20372701)

Chromium oligopeptide activates insulin receptor tyrosine kinase activity. C. M. Davis, J. B. Vincent. Biochemistry. 1997 (https://www.ncbi.nlm.nih.gov/pubmed/9109644)

The new elements of insulin signaling. Insulin receptor substrate-1 and proteins with SH2 domains. M. G. Myers, Jr, M. F. White. Diabetes. 1993 (https://www.ncbi.nlm.nih.gov/pubmed/8387037)

Molecular Mechanisms of Chromium in Alleviating Insulin Resistance. Yinan Hua, Suzanne Clark, Jun Ren, Nair Sreejayan. J Nutr Biochem. Author manuscript; available in PMC 2013 Apr 1. Published in final edited form as: J Nutr Biochem. 2012 (https://www.ncbi.nlm.nih.gov/pubmed/22423897)

Quest for the molecular mechanism of chromium action and its relationship to diabetes. J. B. Vincent. Nutr Rev. 2000 (https://www.ncbi.nlm.nih.gov/pubmed/10812920)

[NaturalPursuit]

GDAs (Chromium – Part 2 of 3) published at https://redcon1online.com/gdas-2/

"Cefalu et al looked at the characterization of the metabolic and physiologic response to chromium supplementation in subjects with type 2 diabetes mellitus in 2010 (2.) The objective of the study was to provide a comprehensive evaluation of chromium (Cr) supplementation on metabolic parameters in a cohort of type 2 diabetes mellitus subjects representing a wide phenotype range and to evaluate changes in “responders” and “nonresponders.” After preintervention testing to assess glycemia, insulin sensitivity (assessed by euglycemic clamps), Cr status, and body composition, subjects were randomized in a double-blind fashion to placebo or 1000 microg Cr. A substudy was performed to evaluate 24-hour energy balance/substrate oxidation and myocellular/intrahepatic lipid content. There was not a consistent effect of Cr supplementation to improve insulin action across all phenotypes. Insulin sensitivity was negatively correlated to soleus and tibialis muscle intramyocellular lipids and intrahepatic lipid content. Myocellular lipids were significantly lower in subjects randomized to Cr. At preintervention, responders, defined as insulin sensitivity change from baseline of at least 10% or greater, had significantly lower insulin sensitivity and higher fasting glucose and A(1c) when compared with placebo and nonresponders, that is, insulin sensitivity change from baseline of less than 10%. Clinical response was significantly correlated (P < .001) to the baseline insulin sensitivity, fasting glucose, and A(1c). There was no difference in Cr status between responder and nonresponders. Clinical response to Cr is more likely in insulin-resistant subjects who have more elevated fasting glucose and A(1c) levels. Chromium may reduce myocellular lipids and enhance insulin sensitivity in subjects with type 2 diabetes mellitus who do respond clinically independent of effects on weight or hepatic glucose production. Thus, modulation of lipid metabolism by Cr in peripheral tissues may represent a novel mechanism of action.

Moving forward to a more applicable study which looks at chromium supplementation in regards to body weight gain and insulin sensitivity (in…yep you guessed it…type 2 diabetics.) This study had thirty-seven subjects with type 2 diabetes were evaluated. After baseline, subjects were placed on a sulfonylurea (glipizide gastrointestinal therapeutic system 5 mg/day) with placebo for 3 months. Subjects were then randomized in a double-blind fashion to receive either the sulfonylurea plus placebo (n = 12) or the sulfonylurea plus 1,000 microg Cr as CrPic (n = 17) for 6 months. Body composition, insulin sensitivity, and glycemic control were determined at baseline, end of the 3-month single-blind placebo phase, and end of study. Subjects randomized to sulfonylurea/placebo, as opposed to those randomized to sulfonylurea/CrPic, had a significant increase in body weight (2.2 kg, P < 0.001 vs. 0.9 kg, P = 0.11), percent body fat (1.17%, P < 0.001 vs. 0.12%, P = 0.7), and total abdominal fat (32.5 cm(2), P < 0.05 vs. 12.2 cm(2), P < 0.10) from baseline. Subjects randomized to sulfonylurea/CrPic had significant improvements in insulin sensitivity corrected for fat-free mass (28.8, P < 0.05 vs. 15.9, P = 0.4), GHb (-1.16%, P < 0.005 vs. -0.4%, P = 0.3), and free fatty acids (-0.2 mmol/l, P < 0.001 vs. -0.12 mmol/l, P < 0.03) as opposed to sulfonylurea/placebo. This study demonstrates that CrPic supplementation in subjects with type 2 diabetes who are taking sulfonylurea agents significantly improves insulin sensitivity and glucose control. Further, CrPic supplementation significantly attenuated body weight gain and visceral fat accumulation compared with the placebo group (3.)"

References

Effect of chromium on glucose and lipid profiles in patients with type 2 diabetes; a meta-analysis review of randomized trials. Mohammad Abdollahi, Amir Farshchi, Shekoufeh Nikfar, Meysam Seyedifar. J Pharm Pharm Sci. 2013 (https://www.ncbi.nlm.nih.gov/pubmed/23683609)

Characterization of the Metabolic and Physiologic Response from Chromium Supplementation in Subjects with Type 2 Diabetes. William T Cefalu, Jennifer Rood, Patricia Pinsonat, Jianhua Qin, Olga Sereda, Lilian Levitan, Richard Anderson, Xian H Zhang, Julie M Martin, Corby Martin, Zhong Q Wang, Bradley Newcomer. Metabolism. Author manuscript; available in PMC 2014 May 14. Published in final edited form as: Metabolism. 2010 (https://www.ncbi.nlm.nih.gov/pubmed/20022616)

Chromium pi****nate supplementation attenuates body weight gain and increases insulin sensitivity in subjects with type 2 diabetes. Julie Martin, Zhong Q. Wang, Xian H. Zhang, Deborah Wachtel, Julia Volaufova, Dwight E. Matthews, William T. Cefalu. Diabetes Care. 2006 (https://www.ncbi.nlm.nih.gov/pubmed/16873787)

Role of chromium supplementation in Indians with type 2 diabetes mellitus. Debjani Ghosh, Basudev Bhattacharya, Biswajit Mukherjee, Byomkesh Manna, Mitali Sinha, Jyothi Chowdhury, Subhankar Chowdhury. J Nutr Biochem. 2002 (https://www.ncbi.nlm.nih.gov/pubmed/12550067)

Chromium treatment has no effect in patients with type 2 diabetes in a Western population: a randomized, double-blind, placebo-controlled trial. Nanne Kleefstra, Sebastiaan T. Houweling, Stephan J. L. Bakker, Simon Verhoeven, Rijk O. B. Gans, Betty Meyboom-de Jong, Henk J. G. Bilo. Diabetes Care. 2007 (https://www.ncbi.nlm.nih.gov/pubmed/17303791)

Chromium as a supplement. H. C. Lukaski. Annu Rev Nutr. 1999 (https://www.ncbi.nlm.nih.gov/pubmed/10448525)

Purification and properties of biologically active chromium complex from bovine colostrum. A. Yamamoto, O. Wada, H. Suzuki. J Nutr. 1988 (https://www.ncbi.nlm.nih.gov/pubmed/3275760)

Age-related decreases in chromium levels in 51,665 hair, sweat, and serum samples from 40,872 patients–implications for the prevention of cardiovascular disease and type II diabetes mellitus. S. Davies, J. McLaren Howard, A. Hunnisett, M. Howard. Metabolism. 1997 (https://www.ncbi.nlm.nih.gov/pubmed/9160809)

Isolation and characterization of a biologically active chromium oligopeptide from bovine liver. C. M. Davis, J. B. Vincent. Arch Biochem Biophys. 1997 (https://www.ncbi.nlm.nih.gov/pubmed/9056266)

Chromium deficiency during total parenteral nutrition. H. Freund, S. Atamian, J. E. Fischer. JAMA. 1979 (https://www.ncbi.nlm.nih.gov/pmc/art...y/?tool=pubmed)

Effect of chromium nicotinic acid supplementation on selected cardiovascular disease risk factors. V. L. Thomas, S. S. Gropper. Biol Trace Elem Res. 1996 (https://www.ncbi.nlm.nih.gov/pubmed/9096856)

Glucose tolerance factor extracted from yeast: oral insulin-mimetic and insulin-potentiating agent: in vivo and in vitro studies. Sarah Weksler-Zangen, Tal Mizrahi, Itamar Raz, Nitsa Mirsky. Br J Nutr. 2012 (https://www.ncbi.nlm.nih.gov/pubmed/22172158)

Chromium in biological systems, I. Some observations on glucose tolerance factor in yeast. N. Mirsky, A. Weiss, Z. Dori. J Inorg Biochem. 1980 (https://www.ncbi.nlm.nih.gov/pubmed/6772742)

A glucose tolerance factor and its differentiation from factor 3. K. SCHWARZ, W. MERTZ. Arch Biochem Biophys. 1957 (https://www.ncbi.nlm.nih.gov/pubmed/13479136)

Effects of niacin-bound chromium and grape seed proanthocyanidin extract on the lipid profile of hypercholesterolemic subjects: a pilot study. H. G. Preuss, D. Wallerstedt, N. Talpur, S. O. Tutuncuoglu, B. Echard, A. Myers, M. Bui, D. Bagchi. J Med. 2000 (https://www.ncbi.nlm.nih.gov/pubmed/11508317)

Chromium: celebrating 50 years as an essential element? John B. Vincent. Dalton Trans. 2010 (https://www.ncbi.nlm.nih.gov/pubmed/20372701)

Chromium oligopeptide activates insulin receptor tyrosine kinase activity. C. M. Davis, J. B. Vincent. Biochemistry. 1997 (https://www.ncbi.nlm.nih.gov/pubmed/9109644)

The new elements of insulin signaling. Insulin receptor substrate-1 and proteins with SH2 domains. M. G. Myers, Jr, M. F. White. Diabetes. 1993 (https://www.ncbi.nlm.nih.gov/pubmed/8387037)

Molecular Mechanisms of Chromium in Alleviating Insulin Resistance. Yinan Hua, Suzanne Clark, Jun Ren, Nair Sreejayan. J Nutr Biochem. Author manuscript; available in PMC 2013 Apr 1. Published in final edited form as: J Nutr Biochem. 2012 (https://www.ncbi.nlm.nih.gov/pubmed/22423897)

Quest for the molecular mechanism of chromium action and its relationship to diabetes. J. B. Vincent. Nutr Rev. 2000 (https://www.ncbi.nlm.nih.gov/pubmed/10812920)

[NaturalPursuit]

16 DAYS OUT. In a good spot considering I can see my glutes and hamstrings while I'm transitioning into my rear and side poses.

[NaturalPursuit]

GDAs (Cinnamon Part 1 of 3)

There was a tremendous amount of requests for me to continue on with my articles focusing on glucose disposal agents and I thought the next best one to chose would be cinnamon (as its typically the most common BUT can be toxic very easily. Cinnamon works as a glucose disposal agent (GDA) by slowing down the rate at which glucose actually enters our bodies. This means that you have a two-fold effect of lowering spikes in blood sugar as well as improving glucose utilization within the cell itself. Now, before we continue on with the research and see just how effective cinnamon can be, we need to cover the “warning” precaution. The type of cinnamon CAN CAUSE TOXICITY ISSUES. If you look, the typical cinnamon you purchase at Wal-Mart will have a liver toxin called coumarin which can be very toxin when taken in the high dosages needed for it to aid in glucose metabolism. This is why we want ceylon cinnamon as it possesses lower levels of that liver toxin. Being that the basic dosage can be upwards of 5-10 grams of cinammon, ensuring you have ceylon cinnamon is in your best interest. Abraham et al actually conducted a study looking at the relative bioavailability of coumarin from cinnamon and cinnamon-containing foods compared to isolated coumarin (1.) Their abstract states the following: Cassia cinnamon contains high levels (up to 1 %) of coumarin. Heavy consumption of this spice may result in a dose exceeding the tolerable daily intake (TDI). In this context, the question was raised whether coumarin in the plant matrix of cinnamon has the same bioavailability as isolated coumarin. A four-way crossover study was performed, in which the same dose of 12 mg coumarin was administered in different formulations to 24 healthy volunteers. The relative extent of absorption measured as urinary excretion of the main metabolite 7-hydroxycoumarin (7OHC) was found to be 62.8% for isolated coumarin in a capsule (reference), 56.0% for cinnamon in capsules, 66.1% for cinnamon tea, and 54.7% for cinnamon in rice pudding (means, n=23, observation period 8 hours). Additionally, 7OHC plasma levels were measured for 105 minutes after administration and revealed a fast absorption of coumarin from cinnamon tea leading to the highest peak concentrations. The relative extent of absorption of coumarin from powder of cassia cinnamon is only slightly lower than that of isolated coumarin. Therefore, the TDI of coumarin can be used for risk assessment of coumarin exposure from cinnamon-containing meals.

Now, onto my favorite part of writing these articles! Digging through the literature to find proper sources that support the claims made! Our first bit of research comes to us from Shihabudeen et al and looks at Cinnamon extract inhibiting α-glucosidase activity and dampening postprandial glucose excursion in diabetic rats (2.) α-glucosidase inhibitors regulate postprandial hyperglycemia (PPHG) by impeding the rate of carbohydrate digestion in the small intestine and thereby hampering the diet associated acute glucose excursion. PPHG is a major risk factor for diabetic vascular complications leading to disabilities and mortality in diabetics. Cinnamomum zeylanicum, a spice, has been used in traditional medicine for treating diabetes. In this study we have evaluated the α-glucosidase inhibitory potential of cinnamon extract to control postprandial blood glucose level in maltose, sucrose loaded STZ induced diabetic rats. The methanol extract of cinnamon bark was prepared by Soxhlet extraction. Phytochemical analysis was performed to find the major class of compounds present in the extract. The inhibitory effect of cinnamon extract on yeast α-glucosidase and rat-intestinal α-glucosidase was determined in vitro and the kinetics of enzyme inhibition was studied. Dialysis experiment was performed to find the nature of the inhibition. Normal male Albino wistar rats and STZ induced diabetic rats were treated with cinnamon extract to find the effect of cinnamon on postprandial hyperglycemia after carbohydrate loading. Phytochemical analysis of the methanol extract displayed the presence of tannins, flavonoids, glycosides, terpenoids, coumarins and anthraquinones. In vitro studies had indicated dose-dependent inhibitory activity of cinnamon extract against yeast α-glucosidase with the IC 50 value of 5.83 μg/ml and mammalian α-glucosidase with IC 50 value of 670 μg/ml. Enzyme kinetics data fit to LB plot pointed out competitive mode of inhibition and the membrane dialysis experiment revealed reversible nature of inhibition.

References

Relative bioavailability of coumarin from cinnamon and cinnamon-containing foods compared to isolated coumarin: a four-way crossover study in human volunteers. Klaus Abraham, Michael Pfister, Friederike Wöhrlin, Alfonso Lampen. Mol Nutr Food Res. 2011 (https://www.ncbi.nlm.nih.gov/pubmed/21462332)

Cinnamon extract inhibits α-glucosidase activity and dampens postprandial glucose excursion in diabetic rats. H Mohamed Sham Shihabudeen, D Hansi Priscilla, Kavitha Thirumurugan. Nutr Metab (Lond) 2011; 8: 46. Published online 2011 (https://www.ncbi.nlm.nih.gov/pubmed/21711570)

Inhibitory activity of cinnamon bark species and their combination effect with acarbose against intestinal α-glucosidase and pancreatic α-amylase. Sirichai Adisakwattana, Orathai Lerdsuwankij, Ubonwan Poputtachai, Aukkrapon Minipun, Chaturong Suparpprom. Plant Foods Hum Nutr. 2011 (https://www.ncbi.nlm.nih.gov/pubmed/21538147)

Regulation of PTP-1 and insulin receptor kinase by fractions from cinnamon: implications for cinnamon regulation of insulin signalling. J. Imparl-Radosevich, S. Deas, M. M. Polansky, D. A. Baedke, T. S. Ingebritsen, R. A. Anderson, D. J. Graves. Horm Res. 1998 (https://www.ncbi.nlm.nih.gov/pubmed/9762007)

The potential of cinnamon to reduce blood glucose levels in patients with type 2 diabetes and insulin resistance. S. Kirkham, R. Akilen, S. Sharma, A. Tsiami. Diabetes Obes Metab. 2009 (https://www.ncbi.nlm.nih.gov/pubmed/19930003)

Cinnamon improves glucose and lipids of people with type 2 diabetes. Alam Khan, Mahpara Safdar, Mohammad Muzaffar Ali Khan, Khan Nawaz Khattak, Richard A. Anderson. Diabetes Care. 2003 (https://www.ncbi.nlm.nih.gov/pubmed/14633804)

Effects of a cinnamon extract on plasma glucose, HbA, and serum lipids in diabetes mellitus type 2. B. Mang, M. Wolters, B. Schmitt, K. Kelb, R. Lichtinghagen, D. O. Stichtenoth, A. Hahn. Eur J Clin Invest. 2006 (https://www.ncbi.nlm.nih.gov/pubmed/16634838)

Cinnamon and health. Joerg Gruenwald, Janine Freder, Nicole Armbruester. Crit Rev Food Sci Nutr. 2010 (https://www.ncbi.nlm.nih.gov/pubmed/20924865)

Cinnamon Use in Type 2 Diabetes: An Updated Systematic Review and Meta-Analysis. Allen, R. W., Schwartzman, E., Baker, W. L., Coleman, C. I., & Phung, O. J. (2013). Annals of Family Medicine. (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3767714/)

Cinnamon extract lowers glucose, insulin and cholesterol in people with elevated serum glucose. Anderson, R. A., Zhan, Z., Luo, R., Guo, X., Guo, Q., Zhou, J. Stoecker, B. J. (2016). Journal of Traditional and Complementary Medicine (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5067830/)

[NaturalPursuit]

13 days out and looking back through some comparison pictures I put together throughout prep. Here was a cool one from not too long ago that I never posted.

145 lbs at my last show VS 200ish lbs taken sometime in prep (probably around 2 months ago or so.) This is the product of progressive overload, progressive eating, and being willing to experiment and learn from my mistakes.

Jordan Peters would appreciate the difference in strength between these pictures:
Squat: low 200's to low 600's
Bench: low 100's to mid 400
Deadlift: mid 200's to 700

Get stronger. Eat intelligently. And give yourself time to grow just like Stan Efferding Austin Stout and myself talked about on our last podcast episode.

[NaturalPursuit]

GDAs (Cinnamon Part 2 of 3)

"In vitro studies had indicated dose-dependent inhibitory activity of cinnamon extract against yeast α-glucosidase with the IC 50 value of 5.83 μg/ml and mammalian α-glucosidase with IC 50 value of 670 μg/ml. Enzyme kinetics data fit to LB plot pointed out competitive mode of inhibition and the membrane dialysis experiment revealed reversible nature of inhibition. In vivo animal experiments are indicative of ameliorated postprandial hyperglycemia as the oral intake of the cinnamon extract (300 mg/kg body wt.) significantly dampened the postprandial hyperglycemia by 78.2% and 52.0% in maltose and sucrose loaded STZ induced diabetic rats respectively, compared to the control. On the other hand, in rats that received glucose and cinnamon extract, postprandial hyperglycemia was not effectively suppressed, which indicates that the observed postprandial glycemic amelioration is majorly due to α-glucosidase inhibition. The current study demonstrates one of the mechanisms in which cinnamon bark extract effectively inhibits α-glucosidase leading to suppression of postprandial hyperglycemia in STZ induced diabetic rats loaded with maltose, sucrose. This bark extract shows competitive, reversible inhibition on α-glucosidase enzyme. Cinnamon extract could be used as a potential nutraceutical agent for treating postprandial hyperglycemia. In future, specific inhibitor has to be isolated from the crude extract, characterized and therapeutically exploited.

As we are looking at some of the inhibitory aspects of cinammon, Adisakwattana and colleagues had a fairly interesting paper on the inhibitory activity of cinnamon bark species and their combination effect with acarbose against intestinal α-glucosidase and pancreatic α-amylase. They state within the abstract “Inhibition of α-glucosidase and pancreatic α-amylase is one of the therapeutic approaches for delaying carbohydrate digestion, resulting in reduced postprandial glucose. The aim of this study was to evaluate the phytochemical analysis and the inhibitory effect of various cinnamon bark species against intestinal α-glucosidase and pancreatic α-amylase. The results showed that the content of total phenolic, flavonoid, and condensed tannin ranged from 0.17 to 0.21 g gallic acid equivalent/g extract, from 48.85 to 65.52 mg quercetin equivalent/g extract, and from 0.12 to 0.15 g catechin equivalent/g extract, respectively. The HPLC fingerprints of each cinnamon species were established. Among cinnamon species, Thai cinnamon extract was the most potent inhibitor against the intestinal maltase with the IC(50) values of 0.58 ± 0.01 mg/ml. The findings also showed that Ceylon cinnamon was the most effective intestinal sucrase and pancreatic α-amylase inhibitor with the IC(50) values of 0.42 ± 0.02 and 1.23 ± 0.02 mg/ml, respectively. In addition, cinnamon extracts produced additive inhibition against intestinal α-glucosidase and pancreatic α-amylase when combined with acarbose. These results suggest that cinnamon bark extracts may be potentially useful for the control of postprandial glucose in diabetic patients through inhibition of intestinal α-glucosidase and pancreatic α-amylase” (3.) Even further more is the regulation of PTP-1 and insulin receptor kinase by fractions from cinammon. Bioactive compound(s) extracted from cinnamon potentiate insulin activity, as measured by glucose oxidation in the rat epididymal fat cell assay. Wortmannin, a potent PI 3′-kinase inhibitor, decreases the biological response to insulin and bioactive compound(s) from cinnamon similarly, indicating that cinnamon is affecting an element(s) upstream of PI 3′-kinase. Enzyme studies done in vitro show that the bioactive compound(s) can stimulate autophosphorylation of a truncated form of the insulin receptor and can inhibit PTP-1, a rat homolog of a tyrosine phosphatase (PTP-1B) that inactivates the insulin receptor. No inhibition was found with alkaline phosphate or calcineurin suggesting that the active material is not a general phosphatase inhibitor. It is suggested, then, that a cinnamon compound(s), like insulin, affects protein phosphorylation-dephosphorylation reactions in the intact adipocyte. Bioactive cinnamon compounds may find further use in studies of insulin resistance in adult-onset diabetes (4.)"

References

Relative bioavailability of coumarin from cinnamon and cinnamon-containing foods compared to isolated coumarin: a four-way crossover study in human volunteers. Klaus Abraham, Michael Pfister, Friederike Wöhrlin, Alfonso Lampen. Mol Nutr Food Res. 2011 (https://www.ncbi.nlm.nih.gov/pubmed/21462332)

Cinnamon extract inhibits α-glucosidase activity and dampens postprandial glucose excursion in diabetic rats. H Mohamed Sham Shihabudeen, D Hansi Priscilla, Kavitha Thirumurugan. Nutr Metab (Lond) 2011; 8: 46. Published online 2011 (https://www.ncbi.nlm.nih.gov/pubmed/21711570)

Inhibitory activity of cinnamon bark species and their combination effect with acarbose against intestinal α-glucosidase and pancreatic α-amylase. Sirichai Adisakwattana, Orathai Lerdsuwankij, Ubonwan Poputtachai, Aukkrapon Minipun, Chaturong Suparpprom. Plant Foods Hum Nutr. 2011 (https://www.ncbi.nlm.nih.gov/pubmed/21538147)

Regulation of PTP-1 and insulin receptor kinase by fractions from cinnamon: implications for cinnamon regulation of insulin signalling. J. Imparl-Radosevich, S. Deas, M. M. Polansky, D. A. Baedke, T. S. Ingebritsen, R. A. Anderson, D. J. Graves. Horm Res. 1998 (https://www.ncbi.nlm.nih.gov/pubmed/9762007)

The potential of cinnamon to reduce blood glucose levels in patients with type 2 diabetes and insulin resistance. S. Kirkham, R. Akilen, S. Sharma, A. Tsiami. Diabetes Obes Metab. 2009 (https://www.ncbi.nlm.nih.gov/pubmed/19930003)

Cinnamon improves glucose and lipids of people with type 2 diabetes. Alam Khan, Mahpara Safdar, Mohammad Muzaffar Ali Khan, Khan Nawaz Khattak, Richard A. Anderson. Diabetes Care. 2003 (https://www.ncbi.nlm.nih.gov/pubmed/14633804)

Effects of a cinnamon extract on plasma glucose, HbA, and serum lipids in diabetes mellitus type 2. B. Mang, M. Wolters, B. Schmitt, K. Kelb, R. Lichtinghagen, D. O. Stichtenoth, A. Hahn. Eur J Clin Invest. 2006 (https://www.ncbi.nlm.nih.gov/pubmed/16634838)

Cinnamon and health. Joerg Gruenwald, Janine Freder, Nicole Armbruester. Crit Rev Food Sci Nutr. 2010 (https://www.ncbi.nlm.nih.gov/pubmed/20924865)

Cinnamon Use in Type 2 Diabetes: An Updated Systematic Review and Meta-Analysis. Allen, R. W., Schwartzman, E., Baker, W. L., Coleman, C. I., & Phung, O. J. (2013). Annals of Family Medicine. (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3767714/)

Cinnamon extract lowers glucose, insulin and cholesterol in people with elevated serum glucose. Anderson, R. A., Zhan, Z., Luo, R., Guo, X., Guo, Q., Zhou, J. Stoecker, B. J. (2016). Journal of Traditional and Complementary Medicine (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5067830/)

[Kewbrah]

Bump

How did the contest go?

[eyeguy]

Hey man been following along. How did you do in the contest

[furiana]

In for the research. Good stuff!

[DiamondMaker]

lol 191 pages of bull****. Half of it defending being natural, then clearly not being natural.
Then the final ultimate nail in the coffin, posting progress for an entire prep and not posting results.

[Devils]

lol there it is