Full Moon…Time to Feast…I'm a Monster…IM A BEAST!!!

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I personally havent see rose-hip make any difference in practical application with 99% of clients


A powder made from seeds and shells of a rose‐hip subspecies (Rosa canina) reduces symptoms of knee and hip osteoarthritis: a randomized, double‐blind, placebo‐controlled clinical trial

Objective: The aim of this study was to determine whether a herbal remedy made from a subspecies of rose‐hip (Rosa canina) might reduce symptoms of osteoarthritis and consumption of rescue medication in patients suffering from osteoarthritis.

Methods: Ninety‐four patients with osteoarthritis of the hip or knee were enrolled in a randomized, placebo‐controlled, double‐blind crossover trial. Forty‐seven patients were given 5 g of the herbal remedy daily for a period of 3 months and the remaining patients were given a similar amount of placebo. The group initially treated with placebo was then changed to rose‐hip and vice versa for another 3‐month period. Upon inclusion and after 3 weeks and 3 months of each treatment period, pain, stiffness, disability, and global severity of the disease were scored on a Western Ontario and McMaster Universities (WOMAC) questionnaire. After 3 weeks of treatment, patients, if possible, were allowed to reduce their consumption of ‘rescue medication’. Data were analysed on the basis of intention to treat.

Results: Rose‐hip resulted in a significant reduction in WOMAC pain (p<0.014) as compared to placebo, when testing after 3 weeks of treatment. The consumption of ‘rescue medication’ significantly declined as a result of active treatment (p<0.027). WOMAC disability, stiffness, and global assessment of severity of the disease were not altered by 3 weeks but decreased significantly (p<0.018, p<0.038, and p<0.035, respectively) after 3 months of treatment.

Conclusion: The data suggest that the present herbal remedy can alleviate symptoms of osteoarthritis and reduce the consumption of ‘rescue medication’.

http://www.tandfonline.com/doi/abs/1...nalCode=irhe20

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One of the reasons why I'm usually in favor of keeping blood sugar levels stable is due to the impact it can have on hunger.


The glucostatic theory of appetite control and the risk of obesity and diabetes.

More than 50 years ago, Jean Mayer proposed that changes in blood glucose concentrations or arteriovenous glucose differences are detected by glucoreceptors that affect energy intake. According to this theory, an increase in blood glucose concentrations results in increased feelings of satiety whereas a drop in blood glucose concentrations has the opposite effect. The pioneering work of Mayer has recently received support from our group as low glycemia has been shown to be linked with body weight gain prospectively and has been considered as a strong predictor of the amount of weight regained after weight loss. This state of mild hypoglycemia also predicts the increase in depressive symptoms with weight loss and a greater propensity to glucose intolerance and type 2 diabetes, particularly for individuals having short sleep durations. Furthermore, knowledge-based work has been shown to induce a significant increase in spontaneous energy intake being related to changes in glycemic control. In accordance with the glucostatic theory, this oriented review suggests that factors favoring a trend toward hypoglycemia and/or glucose instability might induce excess energy intake, overweight and impaired glucose tolerance. Data also raise the possibility that fat gain might be protective against mild hypoglycemia by providing compensation to the stimuli promoted by a modern environment.

https://www.ncbi.nlm.nih.gov/pubmed/19002144

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Part 2 of my article on Boswellia Serrata.

"Continuing on with the research, we see multiple studies looking further in depth into its anti-inflammatory properties (that seem to have possible cardioprotective benefits as well.) Roy et al looked into the regulation of vascular responses to inflammation (inducible matrix metalloproteinase-3 expression in human microvascular endothelial cells is sensitive to anti-inflammatory boswellia.) They stated that endothelial cells are critical elements in the pathophysiology of inflammation. Tumor necrosis factor (TNF) alpha potently induces inflammatory responses in endothelial cells. Recently we have examined the genetic basis of the antiinflammatory effects of Boswellia extract (BE) in a system of TNF alpha-induced gene expression in human microvascular endothelial cells (HMECs). Of the 522 genes induced by TNFalpha in HMECs, 113 genes were sensitive to BE. BE prevented the TNFalpha-induced expression of matrix metalloproteinases (MMPs). In the current work, we sought to test the effects of BE on TNFalpha-inducible MMP expression in HMECs. Acetyl-11-ketobeta- boswellic acid (AKBA) is known to be an active principle in BE. To evaluate the significance of AKBA in the antiinflammatory properties of BE, effects of BE containing either 3% (BE3%) or 30% (BE30%, 5- Loxin) were compared. Pretreatment of HMECs for 2 days with BE potently prevented TNFalpha-induced expression and activity of MMP-3, MMP-10, and MMP-12. In vivo, BE protected against experimental arthritis. In all experiments, both in vitro and in vivo, BE30% was more effective than BE3%. In sum, this work lends support to our previous report that BE has potent anti inflammatory properties both in vitro as well as in vivo (4.)

Moving forward, we look more closely into its anti-cancer properties (which should be a major concern for all.) Boswellia is more anti-proliferative rather than apoptotic. Referring back to one of the main bioactvies (3-O-Acetyl-11-keto-β-Boswellic Acid) AKBA, actually inhibits Hypoxia Inducible Factor 1 (HIF-1), which has been marked as a main target for chemotherapy, when hypoxia is induced. In fact, many of the initial studies had rodents that were injected with tumors that showed boswellia suppressing their growth as well as lowering overall inflammatory markers and used as a phytopharmaceutical for brain edema (5, 6, 7.) All of this literature doesnt even scratch the surface of the potential benefits of boswellia. You can look into its interactions within the kidneys and lungs or its potential effects on testosterone and cortisol and find some promising results. In conclusion, lets discuss practical application and dosages. As with every supplement, the form it is taken in will usually dictate the dosage. Based on the literature I’ve read, it seems the following is a good guideline to follow as a proper dosing strategy for boswellia’s health benefits.

Boswellia Serrata Resin seems to be potent within the 2-3 gram range (split up throughout the day in 1 gram dosages)
If using a more potent form that contains more AKBA like the 5-Loxin I previously mentioned, then 200mgs taken once per day seems to be sufficient
No matter what supplement you take and any study you read, you will have a unique biological response that may differ drastically than another person’s. This is why I always recommend beginning with the lowest effective dosage possible and increasing that dosage over time IF the increase is warranted. With a substance like boswellia, I would hazard to say that more may be slightly more beneficial than less."


References

Determination of major boswellic acids in plasma by high-pressure liquid chromatography/mass spectrometry. Kathleen Gerbeth, Juergen Meins, Simon Kirste, Felix Momm, Manfred Schubert-Zsilavecz, Mona Abdel-Tawab. J Pharm Biomed Anal. 2011 (https://www.ncbi.nlm.nih.gov/pubmed/21855244)

Regulation of vascular responses to inflammation: inducible matrix metalloproteinase-3 expression in human microvascular endothelial cells is sensitive to antiinflammatory Boswellia. Sashwati Roy, Savita Khanna, Alluri V. Krishnaraju, Gottumukkala V. Subbaraju, Taharat Yasmin, Debasis Bagchi, Chandan K. Sen. 2006 (https://www.ncbi.nlm.nih.gov/pubmed/16677108)

A lipoxygenase inhibitor in breast cancer brain metastases. D. F. Flavin. J Neurooncol. 2007 (https://www.ncbi.nlm.nih.gov/pubmed/17001517)

Regulation of vascular responses to inflammation: inducible matrix metalloproteinase-3 expression in human microvascular endothelial cells is sensitive to antiinflammatory Boswellia. Sashwati Roy, Savita Khanna, Alluri V. Krishnaraju, Gottumukkala V. Subbaraju, Taharat Yasmin, Debasis Bagchi, Chandan K. Sen. Antioxid Redox Signal. 2006 (https://www.ncbi.nlm.nih.gov/pubmed/16677108)

Isolation of hypoxia-inducible factor 1 (HIF-1) inhibitors from frankincense using a molecularly imprinted polymer. Achillia Lakka, Ilias Mylonis, Sophia Bonanou, George Simos, Andreas Tsakalof. Invest New Drugs. 2011 (https://www.ncbi.nlm.nih.gov/pubmed/20437079)

Hypoxia inducible factor-1: a novel target for cancer therapy. Vladimir E. Belozerov, Erwin G. Van Meir. Anticancer Drugs. 2005 (https://www.ncbi.nlm.nih.gov/pubmed/16162966)

Response of radiochemotherapy-associated cerebral edema to a phytotherapeutic agent, H15. J. R. Streffer, M. Bitzer, M. Schabet, J. Dichgans, M. Weller. Neurology. 2001 (https://www.ncbi.nlm.nih.gov/pubmed/11342692)

Evaluation of the efficacy of ginger, Arabic gum, and Boswellia in acute and chronic renal failure. Mona Fouad Mahmoud, Abdalla Ahmed Diaai, Fahmy Ahmed. Ren Fail. 2012 (https://www.ncbi.nlm.nih.gov/pubmed/22017619)

11beta-Hydroxysteroid dehydrogenase 1 inhibiting constituents from Eriobotrya japonica revealed by bioactivity-guided isolation and computational approaches. Judith M. Rollinger, Denise V. Kratschmar, Daniela Schuster, Petra H. Pfisterer, Christel Gumy, Evelyne M. Aubry, Sarah Brandstötter, Hermann Stuppner, Gerhard Wolber, Alex Odermatt. Bioorg Med Chem. 2010 (https://www.ncbi.nlm.nih.gov/pubmed/20100662)

Effects of Boswellia serrata gum resin in patients with bronchial asthma: results of a double-blind, placebo-controlled, 6-week clinical study. I. Gupta, V. Gupta, A. Parihar, S. Gupta, R. Lüdtke, H. Safayhi, H. P. Ammon. Eur J Med Res. 1998 (https://www.ncbi.nlm.nih.gov/pubmed/9810030)

Herbal interventions for chronic asthma in adults and children: a systematic review and meta-analysis. Christopher E. Clark, Elizabeth Arnold, Toby J. Lasserson, Taixiang Wu. Prim Care Respir J. 2010 (https://www.ncbi.nlm.nih.gov/pubmed/20640388)

TRPV3 and TRPV4 mediate warmth-evoked currents in primary mouse keratinocytes. Man-Kyo Chung, Hyosang Lee, Atsuko Mizuno, Makoto Suzuki, Michael J. Caterina. J Biol Chem. 2004 (https://www.ncbi.nlm.nih.gov/pubmed/15004014)

TRPV3 is a temperature-sensitive vanilloid receptor-like protein. G. D. Smith, M. J. Gunthorpe, R. E. Kelsell, P. D. Hayes, P. Reilly, P. Facer, J. E. Wright, J. C. Jerman, J-P Walhin, L. Ooi, et al. Nature. 2002 (https://www.ncbi.nlm.nih.gov/pubmed/12077606)

A double blind, randomized, placebo controlled study of the efficacy and safety of 5-Loxin® for treatment of osteoarthritis of the knee. Krishanu Sengupta, Krishnaraju V Alluri, Andey Rama Satish, Simanchala Mishra, Trimurtulu Golakoti, Kadainti VS Sarma, Dipak Dey, Siba P Raychaudhuri. Arthritis Res Ther. 2008 (https://www.ncbi.nlm.nih.gov/pubmed/18667054)

The 5-lipoxygenase/leukotriene pathway in obesity, insulin resistance, and fatty liver disease. Marcos Martínez-Clemente, Joan Clària, Esther Titos. Curr Opin Clin Nutr Metab Care. 2011 (https://www.ncbi.nlm.nih.gov/pubmed/21587068)

Mechanism of 5-lipoxygenase inhibition by acetyl-11-keto-beta-boswellic acid. H. Safayhi, E. R. Sailer, H. P. Ammon. Mol Pharmacol. 1995 (https://www.ncbi.nlm.nih.gov/pubmed/7603462)

[NaturalPursuit]

Working on putting together some research in regards to leptin!

Central nervous system control of food intake and body weight. G. J. Morton, D. E. Cummings, D. G. Baskin, G. S. Barsh, M. W. Schwartz. Nature. 2006 (https://www.ncbi.nlm.nih.gov/pubmed/16988703)

Leptin reverses weight loss–induced changes in regional neural activity responses to visual food stimuli. Rosenbaum, M., Sy, M., Pavlovich, K., Leibel, R. L., & Hirsch, J. (2008). The Journal of Clinical Investigation. (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2430499/)

Role of leptin in the neuroendocrine response to fasting. R. S. Ahima, D. Prabakaran, C. Mantzoros, D. Qu, B. Lowell, E. Maratos-Flier, J. S. Flier. Nature. 1996 (https://www.ncbi.nlm.nih.gov/pubmed/8717038)

Clinical review 94: What's in a name? In search of leptin's physiologic role. J. S. Flier. J Clin Endocrinol Metab. 1998 (https://www.ncbi.nlm.nih.gov/pubmed/9589630)

The role of falling leptin levels in the neuroendocrine and metabolic adaptation to short-term starvation in healthy men. Chan, J. L., Heist, K., DePaoli, A. M., Veldhuis, J. D., & Mantzoros, C. S. (2003). Journal of Clinical Investigation. (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC154448/)

Beneficial effects of leptin on obesity, T cell hyporesponsiveness, and neuroendocrine/metabolic dysfunction of human congenital leptin deficiency. I. Sadaf Farooqi, Giuseppe Matarese, Graham M. Lord, Julia M. Keogh, Elizabeth Lawrence, Chizo Agwu, Veronica Sanna, Susan A. Jebb, Francesco Perna, Silvia Fontana, Robert I. Lechler, Alex M. DePaoli, Stephen O’Rahilly. J Clin Invest. 2002 (https://www.ncbi.nlm.nih.gov/pubmed/12393845)

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As always...IT DEPENDS. Fasted cardio works amazing for some and is horrible for others (and vice versa.)

"Concluding some research from one of my favorite researchers (Dr. Brad Schoenfeld), we find a study conducted overviewing the body composition changes associated with fasted versus non-fasted aerobic exercise. The purpose of this study was to investigate changes in fat mass and fat-free mass following four weeks of volume-equated fasted versus fed aerobic exercise in young women adhering to a hypocaloric diet. Twenty healthy young female volunteers were randomly assigned to 1 of 2 experimental groups: a fasted training (FASTED) group that performed exercise after an overnight fast (n = 10) or a post-prandial training (FED) group that consumed a meal prior to exercise (n = 10). Training consisted of 1 hour of steady-state aerobic exercise performed 3 days per week. Subjects were provided with customized dietary plans designed to induce a caloric deficit. Nutritional counseling was provided throughout the study period to help ensure dietary adherence and self-reported food intake was monitored on a regular basis. A meal replacement shake was provided either immediately prior to exercise for the FED group or immediately following exercise for the FASTED group, with this nutritional provision carried out under the supervision of a research assistant. Both groups showed a significant loss of weight (P = 0.0005) and fat mass (P = 0.02) from baseline, but no significant between-group differences were noted in any outcome measure. These findings indicate that body composition changes associated with aerobic exercise in conjunction with a hypocaloric diet are similar regardless whether or not an individual is fasted prior to training (3.)

Now that we understand the basics, we can put it all together as long as we remember to keep biological inter-individuality at the forefront of our minds. I personally have coached hundreds of athletes. There are dozens upon dozens of prep coaches and researchers out there that have utilized fed and/or fasted cardio and gotten extreme fat loss. This means that as always, there is no right answer. Fasted cardio seems to enhance fat loss for some while it may be detrimental to others. Fasted cardio seems to decrease appetite for some while for others, it actually increases their hunger levels. The fact of the matter is there is no right answer simply because of biological inter-individuality. The best course of action to finding out what works for you is to experiment with yourself (and/or your clients), be unbiased, take notes, and adjust accordingly."


References

Effects of post-absorptive and postprandial exercise on 24 h fat oxidation. Kenshiro Shimada, Yuki Yamamoto, Kaito Iwayama, Kazuteru Nakamura, Sachiko Yamaguchi, Masanobu Hibi, Yoshiharu Nabekura, Kumpei Tokuyama. Metabolism. 2013 (https://www.ncbi.nlm.nih.gov/pubmed/23313101)

Appetite, energy intake and resting metabolic responses to 60 min treadmill running performed in a fasted versus a postprandial state. Kevin Deighton, Jessica C. Zahra, David J. Stensel. Appetite. 2012 (https://www.ncbi.nlm.nih.gov/pubmed/22366285)

Body composition changes associated with fasted versus non-fasted aerobic exercise. Brad Jon Schoenfeld, Alan Albert Aragon, ****n D Wilborn, James W Krieger, Gul T Sonmez. J Int Soc Sports Nutr. 2014 (https://www.ncbi.nlm.nih.gov/pubmed/25429252)

Training in the fasted state improves glucose tolerance during fat-rich diet. Karen Van Proeyen, Karolina Szlufcik, Henri Nielens, Koen Pelgrim, Louise Deldicque, Matthijs Hesselink, Paul P Van Veldhoven, Peter Hespel. J Physiol. 2010 (https://www.ncbi.nlm.nih.gov/pubmed/20837645)

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True thickness comes from busting your ass on the compound movements. When I get check ins from clients and I see this, it makes me damn happy because I KNOW THEYRE PUTTING IN THE WORK!

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Fu et al looking at the Interaction between leucine and phosphodiesterase 5 inhibition in modulating insulin sensitivity and lipid metabolism. They concluded "VO2 in severe-intensity exercise was significantly lowered by the ingestion of 6 mmol beetroot juice compared with placebo and compared with 6 mmil nitrate. Overall, beetroot juice seems to be more effective in terms of lowering VO2 compared with nitrate. These differences may originate from the facilitated nitrite conversion to NO, which may have been catalyzed by polyphenols, vitamin C, and other antioxidants present in the beetroot juice, in combination with nitrate."



https://www.dovepress.com/interactio...d-article-DMSO

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People need to stop blaming a high carbohydrate diet and its effects on insulin for why they are fat. Nearly everything you ingest WILL have some effect on insulin and glucose levels. Obviously that number changes from source to source and macronutrient to macronutrient...but you're not at 30% body fat because you ate bread instead of peanut butter.


The acute effects of four protein meals on insulin, glucose, appetite and energy intake in lean men.

Different dietary proteins vary in their ability to influence satiety and reduce food intake. The present study compared the effects of four protein meals, whey, tuna, turkey and egg albumin, on postprandial glucose and insulin concentrations as well as on appetite measures and energy intake in twenty-two lean, healthy men. This was a randomised, cross-over design study where participants consumed four liquid test meals on separate occasions followed by the collection of regular blood samples (fasting, +30, 60, 90, 120, 180 and 240 min). They were then offered a buffet meal 4 h later. The blood glucose response after the consumption of the test meal, as an incremental area under the curve (AUC), was significantly lower with the whey meal than with the turkey (P < 0.023) and egg (P < 0.001) meals, but it was not lower than with the tuna meal (P < 0.34). The AUC blood insulin after the consumption of the test meal was significantly higher with the whey meal than with the tuna, turkey and egg meals (all P < 0.001). The AUC rating of hunger was significantly lower with the whey meal than with the tuna (P < 0.033), turkey (P < 0.001) and egg (P < 0.001) meals. Mean energy intake at the ad libitum meal was significantly lower (P < 0.001) with the whey meal than with the tuna, egg and turkey meals. There was a strong relationship between self-rated appetite, postprandial insulin response and energy intake at lunch. Whey protein meal produced a greater insulin response, reduced appetite and decreased ad libitum energy intake at a subsequent meal compared with the other protein meals, indicating a potential for appetite suppression and weight loss in overweight or obese individuals.

https://www.ncbi.nlm.nih.gov/pubmed/20456814

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Part of an article I wrote on Gelatine and Bodybuilding

"One of the major dipeptides we will be referring to during this article is hydroxyprolylglycine which consists of a hydroxylproline and a glycine part. This is essentially the most important metabolite that appears withinin your blood after eating gelatin/collagen (1.) It seems to not only exhibit anabolic effects within skeletal muscle tissue but also improve collagen resynthesis, skin health, bone health, and a number of other beneficial aids for bodybuilders.

First, lets look at a study from Kitakaze et al that observed the collagen derived dipeptide hydroxyprolyl-glycine and how it promotes C2C12 myoblast differentiation and myotube hypertrophy. They state: “The majority of studies on possible roles for collagen hydrolysates in human health have focused on their effects on bone and skin. Hydroxyprolyl-glycine (Hyp-Gly) was recently identified as a novel collagen hydrolysate-derived dipeptide in human blood. However, any possible health benefits of Hyp-Gly remain unclear. Here, we report the effects of Hyp-Gly on differentiation and hypertrophy of murine skeletal muscle C2C12 cells. Hyp-Gly increased the fusion index, the myotube size, and the expression of the myotube-specific myosin heavy chain (MyHC) and tropomyosin structural proteins. Hyp-Gly increased the phosphorylation of Akt, mTOR, and p70S6K in myoblasts, whereas the phosphatidylinositol 3-kinase (PI3K) inhibitor LY294002 inhibited their phosphorylation by Hyp-Gly. LY294002 and the mammalian target of rapamycin (mTOR) inhibitor rapamycin repressed the enhancing effects of Hyp-Gly on MyHC and tropomyosin expression. The peptide/histidine transporter 1 (PHT1) was highly expressed in both myoblasts and myotubes, and co-administration of histidine inhibited Hyp-Gly-induced phosphorylation of p70S6K in myoblasts and myotubes. These results indicate that Hyp-Gly can induce myogenic differentiation and myotube hypertrophy and suggest that Hyp-Gly promotes myogenic differentiation by activating the PI3K/Akt/mTOR signaling pathway, perhaps depending on PHT1 for entry into cells” (2.) Suggesting to a bodybuilder that hydroxyprolylglycine may actually increase hypertrophy might have them scratching their heads confused. If hydroxyprolylglycine can promote hypertrophy, obviously it seems like a simple decision to add it into your diet. But what if it does more? In fact and as previously stated, it does a tremendous amount more. Kimira et al saw it promoting differentiation of MC3T3-E1 osteoblastic cells. They found that cells treated with prolyl-hydroxyproline (Pro-Hyp) significantly upregulated gene expression of Runx2, Osterix, and Col1α1. These results indicate that Pro-Hyp promotes osteoblast differentiation. This demonstrates that Pro-Hyp has a positive effect on osteoblast differentiation with upregulation of Runx2, Osterix, and Collα1 gene expression (3.)

As if increased skeletal muscle tissue and increased bone health was not enough, it also promotes cartilage resynthesis and overall healthy joints. In vivo, collagen hydrolysate (CH) and prolyl-hydroxyproline (Pro-Hyp) inhibited the loss of chondrocytes and thinning of the articular cartilage layer caused by phosphorus-induced degradation. In the in vitro study, CH and Pro-Hyp did not affect chondrocyte proliferation but inhibited their differentiation into mineralized chondrocytes. A combination of amino acids such as proline, hydroxyproline and prolyl-hydroxyprolyl-glycine did not affect chondrocyte proliferation or differentiation. Moreover, CH and Pro-Hyp caused two and threefold increases, respectively, in the staining area of glycosaminoglycan in the extracellular matrix of ATDC5 cells. RT-PCR indicated that Pro-Hyp increased the aggrecan mRNA level approximately twofold and decreased the Runx1 and osteocalcin mRNA levels by two-thirds and one-tenth, respectively (4.) Even more so, Shaw et al actually looked at vitamin c enriched gelatin supplementation before intermittent activity and how it augments collagen synthesis. Their study had eight healthy male subjects who completed a randomized, double-blinded, crossover-design study in which they consumed either 5 or 15 g of vitamin C-enriched gelatin or a placebo control. After the initial drink, blood was taken every 30 min to determine amino acid content in the blood. A larger blood sample was taken before and 1 h after consumption of gelatin for treatment of engineered ligaments. One hour after the initial supplement, the subjects completed 6 min of rope-skipping to stimulate collagen synthesis. This pattern of supplementation was repeated 3 times/d with ≥6 h between exercise bouts for 3 d. Blood was drawn before and 4, 24, 48, and 72 h after the first exercise bout for determination of amino-terminal propeptide of collagen I content. The results showed that supplementation with increasing amounts of gelatin increased circulating glycine, proline, hydroxyproline, and hydroxylysine, peaking 1 h after the supplement was given. Engineered ligaments treated for 6 d with serum from samples collected before or 1 h after subjects consumed a placebo or 5 or 15 g gelatin showed increased collagen content and improved mechanics. Subjects who took 15 g gelatin 1 h before exercise showed double the amino-terminal propeptide of collagen I in their blood, indicating increased collagen synthesis. They could conclude from this data that adding gelatin to an exercise program improves collagen synthesis and could play a beneficial role in injury prevention and tissue repair (5.)"


References

Identification of food-derived collagen peptides in human blood after oral ingestion of gelatin hydrolysates. Iwai K, Hasegawa T, Taguchi Y, Morimatsu F, Sato K, Nakamura Y, Higashi A, Kido Y, Nakabo Y, Ohtsuki K. J Agric Food Chem. 2005 (https://www.ncbi.nlm.nih.gov/pubmed/16076145)

The collagen derived dipeptide hydroxyprolyl-glycine promotes C2C12 myoblast differentiation and myotube hypertrophy. Kitakaze T, Sakamoto T, Kitano T, Inoue N, Sugihara F, Harada N, Yamaji R. Biochem Biophys Res Commun. 2016 (https://www.ncbi.nlm.nih.gov/pubmed/27553280)

Collagen-derived dipeptide prolyl-hydroxyproline promotes differentiation of MC3T3-E1 osteoblastic cells. Yoshifumi Kimira, Kana Ogura, Yuri Taniuchi, Aya Kataoka, Naoki Inoue, Fumihito Sugihara, Sachie Nakatani, Jun Shimizu, Masahiro Wada, Hiroshi Mano. Biochem Biophys Res Commun. 2014 (https://www.ncbi.nlm.nih.gov/pubmed/25285626)

Chondroprotective effect of the bioactive peptide prolyl-hydroxyproline in mouse articular cartilage in vitro and in vivo. Nakatani S, Mano H, Sampei C, Shimizu J, Wada M. Osteoarthritis Cartilage. 2009 (https://www.ncbi.nlm.nih.gov/pubmed/19615963)

Vitamin C–enriched gelatin supplementation before intermittent activity augments collagen synthesis. Gregory Shaw, Ann Lee-Barthel, Megan LR Ross, Bing Wang, Keith Baar. Am J Clin Nutr. 2017 (https://www.ncbi.nlm.nih.gov/pubmed/27852613)

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Stimulatory effect of lactate on testosterone production by rat Leydig cells

Previously we found that the increased plasma testosterone levels in male rats during exercise partially resulted from a direct and luteinizing hormone (LH)-independent stimulatory effect of lactate on the secretion of testosterone. In the present study, the acute and direct effects of lactate on testosterone production by rat Leydig cells were investigated. Leydig cells from rats were purified by Percoll density gradient centrifugation subsequent to enzymatic isolation of testicular interstitial cells. Purified rat Leydig cells (1 x 10(5) cells/ml) were in vitro incubated with human chorionic gonadotropin (hCG, 0.05 IU/ml), forskolin (an adenylyl cyclase activator, 10(-5) M), or 8-bromo-adenosine-3':5'-cyclic monophosphate (8-Br-cAMP, 10(-4) M), SQ22536 (an adenylyl cyclase inhibitor, 10(-6)-10(-5) M), steroidogenic precursors (25-hydroxy-cholesterol, pregnenolone, progesterone, and androstenedione, 10(-5) M each), nifedipine (a L-type Ca(2+) channel blocker, 10(-5)-10(-4) M), or nimodipine (a potent L-type Ca(2+) channel antagonist, 10(-5)-10(-4) M) in the presence or absence of lactate at 34 degrees C for 1 h. The concentration of medium testosterone was measured by radioimmunoassay. Administration of lactate at 5-20 mM dose-dependently increased the basal testosterone production by 63-187% but did not alter forskolin- and 8-Br-cAMP-stimulated testosterone release in rat Leydig cells. Lactate at 10 mM enhanced the stimulation of testosterone production induced by 25-hydroxy-cholesterol in rat Leydig cells but not other steroidogenic precursors. Lactate (10 mM) affected neither 30- nor 60-min expressions of cytochrome P450 side chain cleavage enzyme (P450scc) and steroidogenic acute regulatory (StAR) protein. The lactate-stimulated testosterone production was decreased by administration of nifedipine or nimodipine. These results suggested that the physiological level of lactate stimulated testosterone production in rat Leydig.

https://www.ncbi.nlm.nih.gov/pubmed/11500963

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Busted out a 3 part article series on Krill Oil supplementation which should be out within the next week or so

References
1. Lipid composition of two species of Antarctic krill: Euphausia superba and E. crystallorophias. N. R. Bottino. Comp Biochem Physiol B. 1975 (https://www.ncbi.nlm.nih.gov/pubmed/1116352)

2. Metabolic Effects of Krill Oil are Essentially Similar to Those of Fish Oil but at Lower Dose of EPA and DHA, in Healthy Volunteers. Stine M. Ulven, Bente Kirkhus, Amandine Lamglait, Samar Basu, Elisabeth Elind, Trond Haider, Kjetil Berge, Hogne Vik, Jan I. Pedersen. Lipids. 2011 (https://www.ncbi.nlm.nih.gov/pubmed/21042875)

3. Evaluation of the effects of Neptune Krill Oil on the clinical course of hyperlipidemia. Ruxandra Bunea, Khassan El Farrah, Luisa Deutsch. Altern Med Rev. 2004 (https://www.ncbi.nlm.nih.gov/pubmed/15656713)

4. Metabolic Effects of Krill Oil are Essentially Similar to Those of Fish Oil but at Lower Dose of EPA and DHA, in Healthy Volunteers. Stine M. Ulven, Bente Kirkhus, Amandine Lamglait, Samar Basu, Elisabeth Elind, Trond Haider, Kjetil Berge, Hogne Vik, Jan I. Pedersen. Lipids. 2011 (https://www.ncbi.nlm.nih.gov/pubmed/21042875)

5. Enhanced cognitive function and antidepressant-like effects after krill oil supplementation in rats. Karin Wibrand, Kjetil Berge, Michaël Messaoudi, Anaïs Duffaud, Debabrata Panja, Clive R Bramham, Lena Burri. Lipids Health Dis. 2013 (https://www.ncbi.nlm.nih.gov/pubmed/23351783)

6. Supplementation with omega3 polyunsaturated fatty acids and all-rac alpha-tocopherol alone and in combination failed to exert an anti-inflammatory effect in human volunteers. Sonia Vega-López, Nalini Kaul, Sridevi Devaraj, Ru Ya Cai, Bruce German, Ishwarlal Jialal. Metabolism. 2004 (https://www.ncbi.nlm.nih.gov/pubmed/14767877)

7. Influence of very long-chain n-3 fatty acids on plasma markers of inflammation in middle-aged men. Hayati M. Yusof, Elizabeth A. Miles, Philip Calder. Prostaglandins Leukot Essent Fatty Acids. 2008 (https://www.ncbi.nlm.nih.gov/pubmed/18403189)

8. The effects of eicosapentaenoic acid-fortified food on inflammatory markers in healthy subjects--A randomized, placebo-controlled, double-blind study. Shuntaro Fujioka, Kei Hamazaki, Miho Itomura, Mingming Huan, Hiroto Nishizawa, Shigeki Sawazaki, Isao Kitajima, Tomohito Hamazaki. J Nutr Sci Vitaminol (Tokyo) 2006 (https://www.ncbi.nlm.nih.gov/pubmed/17087052)

9. Supplementation of diet with krill oil protects against experimental rheumatoid arthritis. Michelle Ierna, Alison Kerr, Hannah Scales, Kjetil Berge, Mikko Griinari. BMC Musculoskelet Disord. 2010 (https://www.ncbi.nlm.nih.gov/pubmed/20587038)

10. Evaluation of the effect of Neptune Krill Oil on chronic inflammation and arthritic symptoms. Luisa Deutsch. J Am Coll Nutr. 2007 (https://www.ncbi.nlm.nih.gov/pubmed/17353582)

[NaturalPursuit]

•••NEW BEAST FITNESS RADIO EPISODE•••
Clinically Researched List of Health and Ergogenic Bodybuilding Supplements

Getting back to the beginning of how we started this podcast, it was just Austin and myself covering our entire supplement intake that consists of clinically backed and research health and ergogenic bodybuilding supplements. We could have gone on and on but covered just about everything in this one! Below is some of the literature referenced within the episode (for those that enjoy to take the education process one step forward.)



•••FIND THE EPISODES•••

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

www.youtube.com/user/NaturallyGreatBB

http://beastfitnessradio.libsyn.com

[NaturalPursuit]

"The researchers suspect that humans react to beta-cryptoxanthin in approximately the same way as mice do. In 2008 the Japanese researchers published a study in which obese men lost abdominal fat when given beta-cryptoxanthin."

http://journal.frontiersin.org/artic...011.00067/full

[NaturalPursuit]

Part 1/3 on Krill Oil

"Krill Oil is an oil that is derived from krill and has the same fatty acids as fish oil (those being EPA and DHA or Eicosapentaenoic Acid and Docosahexaenoic Acid) but their form is varied from fish oil (that form being a phospholipid, with a phosphate group on the end of the fatty acid making its bioavailability much greater than that of fish oil.) If you look at its composition it also contains myristic acid, palmitic acid, stearic acid, arachidonic acid, behanic acid, and a few others (with EPA making up roughly 19% while DHA constitutes around 11%.) Around 30-60% of these acids are phospholipids (1, 2.) There is much more to krill oil’s composition and pharmacokinetics but given the amount of literature we have to cover on its benefits, we will leave it with those basic facts for now. I’d like to first introduce one of the more popular places (as its a good place to begin being that it compares krill oil to fish oil.) Bunea et al (3) wanted to assess the effects of krill oil on blood lipids, specifically total cholesterol, triglycerides, low-density lipoprotein (LDL), and high-density lipoprotein (HDL). This was a multi-center, three-month, prospective, randomized study followed by a three-month, controlled follow-up of patients treated with 1 g and 1.5 g krill oil daily. Patients with hyperlipidemia able to maintain a healthy diet and with blood cholesterol levels between 194 and 348 mg per dL were eligible for enrollment in the trial. A sample size of 120 patients (30 patients per group) was randomly assigned to one of four groups. Group A received krill oil at a body mass index (BMI)-dependent daily dosage of 2-3 g daily. Patients in Group B were given 1-1.5 g krill oil daily, and Group C was given fish oil containing 180 mg eicosapentaenoic acid (EPA) and 120 mg docosahexaenoic acid (DHA) per gram of oil at a dose of 3 g daily. Group D was given a placebo containing microcrystalline cellulose. The krill oil used in this study was Neptune Krill Oil, provided by Neptune Technologies and Bioresources, Laval, Quebec, Canada. The primary parameters tested (baseline and 90-day visit) were total blood cholesterol, triglycerides, LDL, HDL, and glucose. They found that krill oil 1-3 g per day (BMI-dependent) was found to be effective for the reduction of glucose, total cholesterol, triglycerides, LDL, and HDL, compared to both fish oil and placebo. The results of the present study demonstrate within high levels of confidence that krill oil is effective for the management of hyperlipidemia by significantly reducing total cholesterol, LDL, and triglycerides, and increasing HDL levels. At lower and equal doses, krill oil was significantly more effective than fish oil for the reduction of glucose, triglycerides, and LDL levels."

References

Lipid composition of two species of Antarctic krill: Euphausia superba and E. crystallorophias. N. R. Bottino. Comp Biochem Physiol B. 1975 (https://www.ncbi.nlm.nih.gov/pubmed/1116352)

Metabolic Effects of Krill Oil are Essentially Similar to Those of Fish Oil but at Lower Dose of EPA and DHA, in Healthy Volunteers. Stine M. Ulven, Bente Kirkhus, Amandine Lamglait, Samar Basu, Elisabeth Elind, Trond Haider, Kjetil Berge, Hogne Vik, Jan I. Pedersen. Lipids. 2011 (https://www.ncbi.nlm.nih.gov/pubmed/21042875)

Evaluation of the effects of Neptune Krill Oil on the clinical course of hyperlipidemia. Ruxandra Bunea, Khassan El Farrah, Luisa Deutsch. Altern Med Rev. 2004 (https://www.ncbi.nlm.nih.gov/pubmed/15656713)

Metabolic Effects of Krill Oil are Essentially Similar to Those of Fish Oil but at Lower Dose of EPA and DHA, in Healthy Volunteers. Stine M. Ulven, Bente Kirkhus, Amandine Lamglait, Samar Basu, Elisabeth Elind, Trond Haider, Kjetil Berge, Hogne Vik, Jan I. Pedersen. Lipids. 2011 (https://www.ncbi.nlm.nih.gov/pubmed/21042875)

Enhanced cognitive function and antidepressant-like effects after krill oil supplementation in rats. Karin Wibrand, Kjetil Berge, Michaël Messaoudi, Anaïs Duffaud, Debabrata Panja, Clive R Bramham, Lena Burri. Lipids Health Dis. 2013 (https://www.ncbi.nlm.nih.gov/pubmed/23351783)

Supplementation with omega3 polyunsaturated fatty acids and all-rac alpha-tocopherol alone and in combination failed to exert an anti-inflammatory effect in human volunteers. Sonia Vega-López, Nalini Kaul, Sridevi Devaraj, Ru Ya Cai, Bruce German, Ishwarlal Jialal. Metabolism. 2004 (https://www.ncbi.nlm.nih.gov/pubmed/14767877)

Influence of very long-chain n-3 fatty acids on plasma markers of inflammation in middle-aged men. Hayati M. Yusof, Elizabeth A. Miles, Philip Calder. Prostaglandins Leukot Essent Fatty Acids. 2008 (https://www.ncbi.nlm.nih.gov/pubmed/18403189)

The effects of eicosapentaenoic acid-fortified food on inflammatory markers in healthy subjects–A randomized, placebo-controlled, double-blind study. Shuntaro Fujioka, Kei Hamazaki, Miho Itomura, Mingming Huan, Hiroto Nishizawa, Shigeki Sawazaki, Isao Kitajima, Tomohito Hamazaki. J Nutr Sci Vitaminol (Tokyo) 2006 (https://www.ncbi.nlm.nih.gov/pubmed/17087052)

Supplementation of diet with krill oil protects against experimental rheumatoid arthritis. Michelle Ierna, Alison Kerr, Hannah Scales, Kjetil Berge, Mikko Griinari. BMC Musculoskelet Disord. 2010 (https://www.ncbi.nlm.nih.gov/pubmed/20587038)

Evaluation of the effect of Neptune Krill Oil on chronic inflammation and arthritic symptoms. Luisa Deutsch. J Am Coll Nutr. 2007 (https://www.ncbi.nlm.nih.gov/pubmed/17353582)

[NaturalPursuit]

"Postexercise high-fat feeding does not augment the mRNA expression of genes associated with regulatory roles in mitochondrial biogenesis, although it does increase lipid gene expression. However, postexercise ribo****l protein S6 kinase 1 activity is reduced under conditions of high-fat feeding, thus potentially impairing skeletal muscle remodeling processes."

http://insights.ovid.com/crossref?an...01611000-00005

[NaturalPursuit]

Krill Oil Part 2/3

"Lets compare that to a study from Stine et al where the purpose of their study was to investigate the effects of krill oil and fish oil on serum lipids and markers of oxidative stress and inflammation and to evaluate if different molecular forms, triacylglycerol and phospholipids, of omega-3 polyunsaturated fatty acids (PUFAs) influence the plasma level of EPA and DHA differently. They had one hundred thirteen subjects with normal or slightly elevated total blood cholesterol and/or triglyceride levels were randomized into three groups and given either six capsules of krill oil (N = 36; 3.0 g/day, EPA + DHA = 543 mg) or three capsules of fish oil (N = 40; 1.8 g/day, EPA + DHA = 864 mg) daily for 7 weeks. A third group did not receive any supplementation and served as controls (N = 37). There was a significant increase in plasma EPA, DHA, and DPA was observed in the subjects supplemented with n-3 PUFAs as compared with the controls, but there were no significant differences in the changes in any of the n-3 PUFAs between the fish oil and the krill oil groups. There was no statistically significant differences in changes in any of the serum lipids or the markers of oxidative stress and inflammation between the study groups were observed. Krill oil and fish oil thus represent comparable dietary sources of n-3 PUFAs, even if the EPA + DHA dose in the krill oil was 62.8% of that in the fish oil (4.)

Those pieces of literature confirm what we previously knew given its composition of higher bioavailable EPA/DHA as well as other contributing acids. This clearly makes krill oil fairly superior to fish oil when it comes to correcting a poor lipid profile. But like I mentioned, it does a lot more than simply improve your lipid panel. Wibrand et al looked at the enhanced cognitive function and antidepressant-like effects after krill oil supplementation in rats (5.) Cognition was assessed using the Aversive Light Stimulus Avoidance Test (ALSAT). The Unavoidable Aversive Light Stimulus (UALST) and the Forced Swimming Test (FST) were used to evaluate the antidepressant-like effects of KO. Imipramine (IMIP) was used as the antidepressant reference substance. After 7 weeks of KO intake, both males and females treated with KO were significantly better in discriminating between the active and the inactive levers in the ALSAT from day 1 of training (p<0.01). Both KO and IMIP prevented resignation/depression on the third day in the UALST. Similarly, a shorter immobility time was observed for the KO and IMIP groups compared to the control in the FST (p<0.001). These data support a robust antidepressant-like potential and beneficial cognitive effect of KO. Changes in expression of synaptic plasticity-related genes in the prefrontal cortex and hippocampus were also investigated. mRNA for brain-derived neurotrophic factor (Bdnf) was specifically upregulated in the hippocampus of female rats receiving 7 weeks of KO supplementation (p=0.04) and a similar trend was observed in males (p=0.08). Males also exhibited an increase in prefrontal cortex expression of Arc mRNA, a key protein in long-term synaptic plasticity (p=0.05). IMIP induced clear effects on several plasticity related genes including Bdnf and Arc. These results indicate that active components (eicosapentaenoic acid, docosahexaenoic acid and astaxanthin) in KO facilitate learning processes and provide antidepressant-like effects. Our findings also suggest that KO might work through different physiological mechanisms than IMIP."

References

Lipid composition of two species of Antarctic krill: Euphausia superba and E. crystallorophias. N. R. Bottino. Comp Biochem Physiol B. 1975 (https://www.ncbi.nlm.nih.gov/pubmed/1116352)

Metabolic Effects of Krill Oil are Essentially Similar to Those of Fish Oil but at Lower Dose of EPA and DHA, in Healthy Volunteers. Stine M. Ulven, Bente Kirkhus, Amandine Lamglait, Samar Basu, Elisabeth Elind, Trond Haider, Kjetil Berge, Hogne Vik, Jan I. Pedersen. Lipids. 2011 (https://www.ncbi.nlm.nih.gov/pubmed/21042875)

Evaluation of the effects of Neptune Krill Oil on the clinical course of hyperlipidemia. Ruxandra Bunea, Khassan El Farrah, Luisa Deutsch. Altern Med Rev. 2004 (https://www.ncbi.nlm.nih.gov/pubmed/15656713)

Metabolic Effects of Krill Oil are Essentially Similar to Those of Fish Oil but at Lower Dose of EPA and DHA, in Healthy Volunteers. Stine M. Ulven, Bente Kirkhus, Amandine Lamglait, Samar Basu, Elisabeth Elind, Trond Haider, Kjetil Berge, Hogne Vik, Jan I. Pedersen. Lipids. 2011 (https://www.ncbi.nlm.nih.gov/pubmed/21042875)

Enhanced cognitive function and antidepressant-like effects after krill oil supplementation in rats. Karin Wibrand, Kjetil Berge, Michaël Messaoudi, Anaïs Duffaud, Debabrata Panja, Clive R Bramham, Lena Burri. Lipids Health Dis. 2013 (https://www.ncbi.nlm.nih.gov/pubmed/23351783)

Supplementation with omega3 polyunsaturated fatty acids and all-rac alpha-tocopherol alone and in combination failed to exert an anti-inflammatory effect in human volunteers. Sonia Vega-López, Nalini Kaul, Sridevi Devaraj, Ru Ya Cai, Bruce German, Ishwarlal Jialal. Metabolism. 2004 (https://www.ncbi.nlm.nih.gov/pubmed/14767877)

Influence of very long-chain n-3 fatty acids on plasma markers of inflammation in middle-aged men. Hayati M. Yusof, Elizabeth A. Miles, Philip Calder. Prostaglandins Leukot Essent Fatty Acids. 2008 (https://www.ncbi.nlm.nih.gov/pubmed/18403189)

The effects of eicosapentaenoic acid-fortified food on inflammatory markers in healthy subjects–A randomized, placebo-controlled, double-blind study. Shuntaro Fujioka, Kei Hamazaki, Miho Itomura, Mingming Huan, Hiroto Nishizawa, Shigeki Sawazaki, Isao Kitajima, Tomohito Hamazaki. J Nutr Sci Vitaminol (Tokyo) 2006 (https://www.ncbi.nlm.nih.gov/pubmed/17087052)

Supplementation of diet with krill oil protects against experimental rheumatoid arthritis. Michelle Ierna, Alison Kerr, Hannah Scales, Kjetil Berge, Mikko Griinari. BMC Musculoskelet Disord. 2010 (https://www.ncbi.nlm.nih.gov/pubmed/20587038)

Evaluation of the effect of Neptune Krill Oil on chronic inflammation and arthritic symptoms. Luisa Deutsch. J Am Coll Nutr. 2007 (https://www.ncbi.nlm.nih.gov/pubmed/17353582)

[NaturalPursuit]

Part 3/3 on Krill Oil

"Thus far, we have krill oil aiding in a healthy lipid profile as well as having some cognitive improvements. Obviously, we’re not even scratching the surface of its benefits! Its very common knowledge that fish oil aids in reduction of overall inflammation (6, 7, 8) but does krill oil offer the same (or possibly better) benefits in inflammation reduction? We can answer this study by looking at two studies as well as applying some common sense. Our first study comes again from Lerna et al looking at supplementation of diet with krill oil and how it protects against experimental rheumatoid arthritis. Researchers had collagen-induced arthritis susceptible DBA/1 mice were provided ad libitum access to a control diet or diets supplemented with either krill oil or fish oil throughout the study. There were 14 mice in each of the 3 treatment groups. The level of EPA + DHA was 0.44 g/100 g in the krill oil diet and 0.47 g/100 g in the fish oil diet. Severity of arthritis was determined using a clinical scoring system. Arthritis joints were analysed by histopathology and graded. Serum samples were obtained at the end of the study and the levels of IL-1alpha, IL-1beta, IL-7, IL-10, IL-12p70, IL-13, IL-15, IL-17 and TGF-beta were determined by a Luminex assay system. They found that the consumption of krill oil and supplemented diet significantly reduced the arthritis scores and hind paw swelling when compared to a control diet not supplemented with EPA and DHA. However, the arthritis score during the late phase of the study was only significantly reduced after krill oil administration. Furthermore, mice fed the krill oil diet demonstrated lower infiltration of inflammatory cells into the joint and synovial layer hyperplasia, when compared to control. Inclusion of fish oil and krill oil in the diets led to a significant reduction in hyperplasia and total histology score. Krill oil did not modulate the levels of serum cytokines whereas consumption of fish oil increased the levels of IL-1alpha and IL-13. They concluding saying this study suggests that krill oil may be a useful intervention strategy against the clinical and histopathological signs of inflammatory arthritis (9.) The second study comes from Luisa Deutsch in 2007 on the evaluation of the effect of Neptune Krill Oil on chronic inflammation and arthritic symptoms (10.) Luisa had a randomized, double blind, placebo controlled study. Ninety patients were recruited with confirmed diagnosis of cardiovascular disease and/or rheumatoid arthritis and/or osteoarthritis and with increased levels of CRP (>1.0 mg/dl) upon three consecutive weekly blood analysis. Group A received NKO (300 mg daily) and Group B received a placebo. CRP and Western Ontario and McMaster Universities (WOMAC) osteoarthritis score were measured at baseline and days 7, 14 and 30. After 7 days of treatment NKO reduced CRP by 19.3% compared to an increase by 15.7% observed in the placebo group (p = 0.049). After 14 and 30 days of treatment NKO further decreased CRP by 29.7% and 30.9% respectively (p < 0.001). The CRP levels of the placebo group increased to 32.1% after 14 days and then decreased to 25.1% at day 30. The between group difference was statistically significant; p = 0.004 at day 14 and p = 0.008 at day 30. NKO showed a significant reduction in all three WOMAC scores. After 7 days of treatment, NKO reduced pain scores by 28.9% (p = 0.050), reduced stiffness by 20.3% (p = 0.001) and reduced functional impairment by 22.8% (p = 0.008). The results of the present study clearly indicate that NKO at a daily dose of 300 mg significantly inhibits inflammation and reduces arthritic symptoms within a short treatment period of 7 and 14 days. Given that research we must apply our common sense and problem solving skills. These studies clearly indicate it has benefits for those suffering from rheumatoid arthritis as that was the population tested. But how does that apply to healthy exercising individuals? Well, we can conclude that it will have the same anti-inflammatory properties if not better because of their mechanism of action as well as the knowledge that krill oil has a higher bioavailability.

That concludes this three pieces article on krill oil in bodybuilding and we still have just barely scratched the surface of its benefits. It truly is a supplement I would recommend to any serious athlete that cares about keeping their performance maximal and their health markers in check. Krill oil was, as I stated in the opening of part 1 of this series, introduced to me by Dante Trudel (who had bloodwork done on himself utilizing krill oil with tremendous success.) I have since replicated the study’s as well as Dante’s design with my own clients and have seen clear improvements across the board. Whether someone had a poor lipid panel or a good one, improvements were seen regardless (the only difference was obviously the degree of increase.)"

References

Metabolic Effects of Krill Oil are Essentially Similar to Those of Fish Oil but at Lower Dose of EPA and DHA, in Healthy Volunteers. Stine M. Ulven, Bente Kirkhus, Amandine Lamglait, Samar Basu, Elisabeth Elind, Trond Haider, Kjetil Berge, Hogne Vik, Jan I. Pedersen. Lipids. 2011 (https://www.ncbi.nlm.nih.gov/pubmed/21042875)

Evaluation of the effects of Neptune Krill Oil on the clinical course of hyperlipidemia. Ruxandra Bunea, Khassan El Farrah, Luisa Deutsch. Altern Med Rev. 2004 (https://www.ncbi.nlm.nih.gov/pubmed/15656713)

Metabolic Effects of Krill Oil are Essentially Similar to Those of Fish Oil but at Lower Dose of EPA and DHA, in Healthy Volunteers. Stine M. Ulven, Bente Kirkhus, Amandine Lamglait, Samar Basu, Elisabeth Elind, Trond Haider, Kjetil Berge, Hogne Vik, Jan I. Pedersen. Lipids. 2011 (https://www.ncbi.nlm.nih.gov/pubmed/21042875)

Enhanced cognitive function and antidepressant-like effects after krill oil supplementation in rats. Karin Wibrand, Kjetil Berge, Michaël Messaoudi, Anaïs Duffaud, Debabrata Panja, Clive R Bramham, Lena Burri. Lipids Health Dis. 2013 (https://www.ncbi.nlm.nih.gov/pubmed/23351783)

Supplementation with omega3 polyunsaturated fatty acids and all-rac alpha-tocopherol alone and in combination failed to exert an anti-inflammatory effect in human volunteers. Sonia Vega-López, Nalini Kaul, Sridevi Devaraj, Ru Ya Cai, Bruce German, Ishwarlal Jialal. Metabolism. 2004 (https://www.ncbi.nlm.nih.gov/pubmed/14767877)

Influence of very long-chain n-3 fatty acids on plasma markers of inflammation in middle-aged men. Hayati M. Yusof, Elizabeth A. Miles, Philip Calder. Prostaglandins Leukot Essent Fatty Acids. 2008 (https://www.ncbi.nlm.nih.gov/pubmed/18403189)

The effects of eicosapentaenoic acid-fortified food on inflammatory markers in healthy subjects–A randomized, placebo-controlled, double-blind study. Shuntaro Fujioka, Kei Hamazaki, Miho Itomura, Mingming Huan, Hiroto Nishizawa, Shigeki Sawazaki, Isao Kitajima, Tomohito Hamazaki. J Nutr Sci Vitaminol (Tokyo) 2006 (https://www.ncbi.nlm.nih.gov/pubmed/17087052)

Supplementation of diet with krill oil protects against experimental rheumatoid arthritis. Michelle Ierna, Alison Kerr, Hannah Scales, Kjetil Berge, Mikko Griinari. BMC Musculoskelet Disord. 2010 (https://www.ncbi.nlm.nih.gov/pubmed/20587038)

Evaluation of the effect of Neptune Krill Oil on chronic inflammation and arthritic symptoms. Luisa Deutsch. J Am Coll Nutr. 2007 (https://www.ncbi.nlm.nih.gov/pubmed/17353582)

[NaturalPursuit]

•••NEW BEAST FITNESS RADIO EPISODE•••
Kala Duncan - Prepping Female Competitors

Another fun time sitting down and recording with Austin Stout! This episode we had the opportunity to have a very knowledgeable female prep coach on to discuss the differences between working with male and female competitors as well as specifics on female dieting and training strategies! As always its full of information so be sure to get your notepads and pencils out! Check out Kala and support her at http://theomnifit.com



•••FIND THE EPISODES•••

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

www.youtube.com/user/NaturallyGreatBB

http://beastfitnessradio.libsyn.com

[NaturalPursuit]

Big 3 part article coming on "Increasing Protein After a Deficit." Some references I'll be utilizing below.

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]

Vinegar Improves Insulin Sensitivity to a High-Carbohydrate Meal in Subjects With Insulin Resistance or Type 2 Diabetes

The number of Americans with type 2 diabetes is expected to increase by 50% in the next 25 years; hence, the prevention of type 2 diabetes is an important objective. Recent large-scale trials (the Diabetes Prevention Program and STOP-NIDDM) have demonstrated that therapeutic agents used to improve insulin sensitivity in diabetes, metformin and acarbose, may also delay or prevent the onset of type 2 diabetes in high-risk populations. Interestingly, an early report showed that vinegar attenuated the glucose and insulin responses to a sucrose or starch load (1). In the present report, we assessed the effectiveness of vinegar in reducing postprandial glycemia and insulinemia in subjects with varying degrees of insulin sensitivity.

Our study included nondiabetic subjects who were either insulin sensitive (control subjects, n = 8) or insulin resistant (n = 11) and 10 subjects with type 2 diabetes. Subjects provided written informed consent and were not taking diabetes medications. Fasting subjects were randomly assigned to consume the vinegar (20 g apple cider vinegar, 40 g water, and 1 tsp saccharine) or placebo drink and, after a 2-min delay, the test meal, which was composed of a white bagel, butter, and orange juice (87 g total carbohydrates). The cross-over trial was conducted 1 week later. Blood samples were collected at fasting and 30 and 60 min postmeal for glucose and insulin analyses. Whole-body insulin sensitivity during the 60-min postmeal interval was estimated using a composite score (2).

Fasting glucose concentrations were elevated ∼55% in subjects with diabetes compared with the other subject groups (P < 0.01, Tukey’s post hoc test), and fasting insulin concentrations were elevated 95–115% in subjects with insulin resistance or type 2 diabetes compared with control subjects (P < 0.01). Compared with placebo, vinegar ingestion raised whole-body insulin sensitivity during the 60-min postmeal interval in insulin-resistant subjects (34%, P = 0.01, paired t test) and slightly improved this parameter in subjects with type 2 diabetes (19%, P = 0.07). Postprandial fluxes in insulin were significantly reduced by vinegar in control subjects, and postprandial fluxes in both glucose and insulin were significantly reduced in insulin-resistant subjects (Fig. 1).

These data indicate that vinegar can significantly improve postprandial insulin sensitivity in insulin-resistant subjects. Acetic acid has been shown to suppress disaccharidase activity (3) and to raise glucose-6-phosphate concentrations in skeletal muscle (4); thus, vinegar may possess physiological effects similar to acarbose or metformin. Further investigations to examine the efficacy of vinegar as an antidiabetic therapy are warranted.

http://care.diabetesjournals.org/content/27/1/281

[NaturalPursuit]

Effect of vanadium on insulin sensitivity in patients with impaired glucose tolerance.


https://www.ncbi.nlm.nih.gov/pubmed/19033682

[NaturalPursuit]

Part of an article I wrote on Higenamine

"Higenamine (also known as Norcoclaurine, 1-[(4- hydroxyphenyl)methyl]-1, 2, 3, 4-tetrahydroisoquinoline-6, 7-diol), is found within ethanol extracts of plants. A very well known mechanism of higenamine is its ability to increase acetylcholine release from motor neurons with the action being mediated via the beta 2 adrenergic agonism. As you can guess, higenamine has similar mechanisms as other beta adrenergic agonists (1, 2.) One of those being its ability to increase heart rate, which is evident by work from Kimura et al on the positive chronotropic and inotropic effects of higenamine and its enhancing action on the aconitine-induced tachyarrhythmia in isolated murine atria. Kimura investigated the cardiac effects of these compounds on murine right and left atria and the interaction of higenamine with aconitine on the rate of spontaneously beating right atria. Higenamine increased the rate and the force of contraction, the maximal responses being comparable with those of isoproterenol. The positive chronotropic effect of higenamine was antagonized by propranolol and practolol, but not by butoxamine, indicating that it was a beta 1-adrenoceptor- mediated action. The positive chronotropic effect of higenamine was not changed by pretreatment with reserpine. Aconitine induced tachyarrhythmia in right atria was attenuated by quinidine , atropine and AF-DX 116, suggesting that aconitine activates sodium channels and muscarinic receptors. Higenamine and dobutamine did not cause chronotropic effects by themselves, but enhanced the aconitine-induced tachyarrhythmia. These results indicate that higenamine is a beta 1-adrenoceptor full agonist in murine atria and that the aconitine-induced tachyarrhythmia is augmented by the beta 1-adrenergic action of higenamine (3.)

A very similar mechanism of action can be seen in regards to its ability to actually increase lipolysis. This, obviously is the main reason why many chose to supplement with higenamine in the first place and it has enough literature to back up its fat loss claims. As previously stated, since its mechanism of action is very similar to other beta adrenergic agonists (ephedrine being one of them), it will effect a vast array of tissues during its process of action. One tremendous study from Lee and colleagues observed the acute oral intake of a higenamine-based dietary supplement increases circulating free fatty acids and energy expenditure in human subjects. This is one of my more favored studies in regards to higenamine as it is slightly easier to draw conclusions when an ingredient is tested in a similar setting that we would apply it in. The researchers had sixteen healthy subjects ingested a dietary supplement containing a combination of higenamine, caffeine (270 mg), and yohimbe bark extract or a placebo, on two separate occasions in a double-blind, randomized, cross-over design, separated by 6–8 days. Blood samples were collected immediately before ingestion, and at 30, 60, 120, and 180 minutes post ingestion, and analyzed for plasma free fatty acids (FFA) and glycerol. Breath samples were collected at the same times for a measure of kilocalorie expenditure and respiratory exchange ratio (RER) using indirect calorimetry. Heart rate and blood pressure were recorded at all times. Data collection occurred in the morning following a 10 hour overnight fast. A condition effect was noted for both FFA and kilocalorie expenditure, with values higher for supplement compared to placebo at 60, 120, and 180 minutes post ingestion. No statistically significant effects were noted for glycerol or RER. A condition effect was noted for heart rate and systolic blood pressure, with values higher for supplement compared to placebo.They concluded that the ingestion of a higenamine-based dietary supplement stimulates lipolysis and energy expenditure, as evidenced by a significant increase in circulating FFA and kilocalorie expenditure. The same supplement results in a moderate increase in heart rate and systolic blood pressure, which is consistent with previous studies evaluating moderate doses of caffeine and yohimbine, suggesting that higenamine contributes little to the increase in these hemodynamic variables (4.)

As the study above only shows an increase in heart rate of 3 BPM, we must take into consideration the supplement as a whole. If you are in a deficit with a properly periodized training and nutritional program (with additional cardiovascular work as needed), adding in little goodies like higenamine, like yohimbine, like caffeine, and like all of these other fat loss aimed supplements, you are going to be making the process more efficient. In the competition world, that 5% difference can be the difference between 1st and 5th place if you’re in a tough line up and these many small changes add up over the course of a deficit."

References

Beta2-adrenoceptor- mediated tracheal relaxation induced by higenamine from Nandina domestica Thunberg. Muneo Tsukiyama, Takuro Ueki, Yoichi Yasuda, Hiroko Kikuchi, Tatsuhiro Akaishi, Hidenobu Okumura, Kazuho Abe. Planta Med. 2009 (https://www.ncbi.nlm.nih.gov/pubmed/19468973)

1. β2-adrenoceptor agonists: current and future direction. Cazzola, M., Calzetta, L., &amp; Matera, M. G. British Journal of Pharmacology. 2011 (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3085864/)

2. Positive chronotropic and inotropic effects of higenamine and its enhancing action on the aconitine-induced tachyarrhythmia in isolated murine atria. I. Kimura, M. Makino, Y. Takamura, M. A. Islam, M. Kimura. Jpn J Pharmacol. 1999 (https://www.ncbi.nlm.nih.gov/pubmed/7861670)

3. Acute oral intake of a higenamine-based dietary supplement increases circulating free fatty acids and energy expenditure in human subjects. Lee, S.-R., Schriefer, J. M., Gunnels, T. A., Harvey, I. C., &amp; Bloomer, R. J. Lipids in Health and Disease. 2013.(https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4016229/)

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Effect of Extended Release Gymnema Sylvestre Leaf Extract (Beta Fast GXR) Alone or In Combination With Oral Hypoglycemics or Insulin Regimens for Type 1 and Type 2 Diabetes

OBJECTIVE: The prevalence of diabetes has increased dramatically in recent years1. Gymnema sylvestre is an Indian herb used in Ayurveda, the ancient Hindi medicine system of India. Its primary application was for adult-onset diabetes (NIDDM), a condition for which it continues to be recommended today in India. The gradual hypoglycemic action of Gymnema leaves, first documented in the 1930, differs from the rapid effect of many prescription hypoglycemic drugs.2 Gymnema leaves raise insulin levels, according to research in healthy volunteers2 possibly due to regeneration of the b-cells in the pancreas.3 The leaves are also noted for lowering serum cholesterol and triglycerides.4 A water-soluble acidic fraction of the leaves provides hypoglycemic actions, possibly gymnemic acid.5 Its action in the reduction of intestinal glucose uptake has also been noted.6 The purpose of this work was to investigate the acute effects of supplementing the diet with Gymnema sylvestre (Beta Fast GXR®) in regards to it’s glucose lowering thereby reducing the HbA1c and therefore the complications from diabetes.

By reducing the HbA1c (Average Blood Glucose) 1%, the DCCT7 study showed Type 1 diabetics could reduce the complications of Retinopathy by 38%, Nephropathy by 28% Neuropathy by 35%. The UKPDS8 showed that reducing the HbA1c in Type 2 diabetics by 0.9% could reduce any diabetic end point by 12%, reduce any microvascular end point by 25%, reduce MI by 16%, reduce retinopathy by 21% and reduce microalbuminurea at 12 years by 34%. The UKPDS also showed that Postprandial (1-2 hours after eating) glucose is a better indicator of glycemic control than fasting glucose levels9. Treatment of postprandial hyperglycemia is critical to achieving optimal outcomes in type 2 diabetes10.

METHODS: Sixty-five (65) patients (37male/28 female) completed the study. Their pre-study average fasting glucose (163 mg/dl) and postprandial blood glucose (212 mg/dl), and a base HbA1c (8.8) were taken. Patients were instructed to take two (2) tablets per day, one in AM, one in PM for 90 days. They continued to monitor fasting and postprandial blood glucose through the study period. At the conclusion of the 90-day period, their levels were measured.

RESULTS: Sixty-five participants completed the study. After the 90 days of the Gymnema sylvestre (Beta Fast GXR®) supplementation, mean daily preprandial plasma glucose concentrations were 11% lower (161 vs 144 mg/dl). The Gymnema sylvestre (Beta Fast GXR®) supplementation also lowered the 2-hour post prandial plasma glucose concentrations, by 13% (207 vs 180mg/dl). The Gymnema sylvestre (Beta Fast GXR®) supplementation lowered HbA1c from 8.8% to 8.2% (0.6% decrease).

In the sub set of participants whose pre-study HbA1c was 9% or above the results were more profound. Mean daily preprandial plasma glucose concentrations were 15 percent lower (191 vs 161 mg/dl). The Gymnema sylvestre (Beta Fast GXR®) supplementation also lowered the 2-hour postprandial plasma glucose concentrations, by 21 percent (250 vs. 199 mg/dl). The Gymnema sylvestre (Beta Fast GXR®) supplementation lowered HbA1c from 10.1% to 9.3% (0.8% decrease).

In the poorest controlled patients, those with a starting HbA1c of 10% or greater, mean daily preprandial plasma glucose concentrations were 18 percent lower (216 vs 178 mg/dl). The Gymnema sylvestre (Beta Fast GXR®) supplementation also lowered the 2-hour postprandial plasma glucose concentrations by 28 percent (295 vs 212 mg/dl). The Gymnema sylvestre (Beta Fast GXR®) supplementation lowered HbA1c from 11.1% to 9.9% (1.1% decrease). In addition 11 patients (16%) had a decrease in prescription medicine intake.

CONCLUSIONS: As can be seen from the data above, the use of Gymnema sylvestre (Beta Fast GXR®) supplementation in all patients with diabetes has a positive result. In addition the use of Gymnema sylvestre (Beta Fast GXR®) supplementation in patients with the poorest control is even more critical. It appears that the largest effect occurs from decrease of post-prandial glucose levels, which is consistent with the mechanisms of action stated. Gymnema sylvestre (Beta Fast GXR®) supplementation appears to improve glycemic control in patients with type 2 diabetes. Reducing postprandial blood glucose significantly caused a decrease of HbA1c, therefore reducing the complications from diabetes.7,8,9,10

Beckles GLA et al. Diabetes Care. 1998;21:1432-1438.American Diabetes Association. Diabetes Care. 1998;21(Suppl 2).Colwell JA. Ann Intern Med. 1996;124(1pt2):131- 135.Abraira C et al. Diabetes Care. 1992;15:1560-1571.Klein R et al. Am J Epidemiol. 1987;126:415-428.Cowie CC et al. Diabetes in America. 2nd ed.vol. 44, November 2001.
Mhasker KS, Caius JF. A study of Indian medicinal plants. II. Gymnema sylvestre R.Br. Indian J Med Res Memoirs 1930;16:2–75.
Shanmugasundaram KR, Panneerselvam C, Sumudram P, Shanmugasundaram ERB. Insulinotropic activity of G. sylvestre, R.Br. and Indian medicinal herb used in controlling diabetes mellitus. Pharmacol Res Commun 1981;13:475–86.
Shanmugasundaram ERB, Leela Gopinath K, Radha Shanmugasundaram K, Rajendran VM. Possible regeneration of the islets of Langerhans in streptozotocin diabetic rats given Gymnema sylvestre leaf extracts. J Ethnopharmacol 1990;30:265–79.
Bishayee A, Chatterjee M. Hypolipidemic and antiatherosclerotic effects of oral Gymnema sylvestre R.Br. leaf extract in albino rats fed on high fat diet. Phytother Res 1994;8:118–20.
Gymnema. Lawrence Review of Natural Products Aug 1993 (monograph). Fushiki T, Kojima A, Imoto T, et al. An extract of Gymnema sylvestre leaves and purified gymnemic acid inhibits glucose-stimulated gastric inhibitory peptide secretion in rats. J Nutr 1992;122:2367–73. 1995.
The New England Journal of Medicine — September 30, 1993 — Vol. 329, No. 14-DCCT research group, Diabetes 95;44:969-983;
Hawaii Med J 2000 Jul;59(7):295-8, 313; BMJ. 2000 Aug 12;321(7258):405-12.
Harris et al. Diabetes Care. 1994.
De Veciana et al. N Engl J Med. 1995;333:1239

http://www.diabetesincontrol.com/eff...beta-fast-gxr/

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Glycemic and oxidative status of patients with type 2 diabetes mellitus following oral administration of alpha-lipoic acid: a randomized double-blinded placebo-controlled study.


https://www.ncbi.nlm.nih.gov/pubmed/22374556

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Highly Branched Cyclic Dextrin literature from an older article I wrote

References
1. Enhancement of swimming endurance in mice by highly branched cyclic dextrin. H. Takii, K. Ishihara, T. Kometani, S. Okada, T. Fushiki. Biosci Biotechnol Biochem. 1999 Dec (https://www.ncbi.nlm.nih.gov/pubmed/10664836)

2. A sports drink based on highly branched cyclic dextrin generates few gastrointestinal disorders in untrained men during bicycle exercise. Takii, H., Kometani, T., Nishimura, T., Kuriki, T., and Fushiki, T. Food Sci. Technol. Res. 2004 (https://www.jstage.jst.go.jp/article...4_428/_article)

3. Fluids containing a highly branched cyclic dextrin influence
the gastric emptying rate. Takii, H., Takii Nagao, Y., Kometani, T., Nishimura, T., Nakae, T., Kuriki, T., and Fushiki, T. Int. J. Sports Med. 2005 (https://www.ncbi.nlm.nih.gov/pubmed/15900642)

4. Factors limiting gastric emptying during rest and exercise. Costill, D.L. and Saltin, B. J. Appl. Physiol. 1974 (http://jap.physiology.org/content/37/5/679)

5. The pattern of emptying of the human stomach. J. N. Hunt, W. R. Spurrell. J Physiol. 1951 (https://www.ncbi.nlm.nih.gov/pubmed/14832765)

6. Evaluation of Exercise Performance with the Intake of Highly Branched Cyclic Dextrin in Athletes. Shiraki, T., Kometani T., Yo****ani, K., Takata H., Nomura T. Food Science and Technology Research. 2015 (https://www.jstage.jst.go.jp/article...499/_html#bib3)

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5 years and 53 lbs later



Left: 145 lbs on stage at my last show
Right: 198 lbs roughly 4 weeks out

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[boxteross]

Crazy man. Great work.

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Well...second time in the past two weeks I picked up some virus/bug which is really a pain in this ass being this far into prep. Oh well! Could be worse! Here's another comparison I posted up from my last show VS a week or so ago.

145 lbs VS 198 lbs (yes I know...not the exact same pose but you get the idea)

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•••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