Deprecated: Function create_function() is deprecated in /var/www/wp-content/themes/Newspaper/includes/widgets/td_page_builder_widgets.php on line 7

Deprecated: Function create_function() is deprecated in /var/www/wp-content/themes/Newspaper/includes/widgets/td_page_builder_widgets.php on line 14

Deprecated: Function create_function() is deprecated in /var/www/wp-content/themes/Newspaper/includes/widgets/td_page_builder_widgets.php on line 21

Deprecated: Function create_function() is deprecated in /var/www/wp-content/themes/Newspaper/includes/widgets/td_page_builder_widgets.php on line 28

Deprecated: Function create_function() is deprecated in /var/www/wp-content/themes/Newspaper/includes/widgets/td_page_builder_widgets.php on line 35

Deprecated: Function create_function() is deprecated in /var/www/wp-content/themes/Newspaper/includes/widgets/td_page_builder_widgets.php on line 42

Deprecated: Function create_function() is deprecated in /var/www/wp-content/themes/Newspaper/includes/widgets/td_page_builder_widgets.php on line 49

Deprecated: Function create_function() is deprecated in /var/www/wp-content/themes/Newspaper/includes/widgets/td_page_builder_widgets.php on line 56

Deprecated: Function create_function() is deprecated in /var/www/wp-content/themes/Newspaper/includes/widgets/td_page_builder_widgets.php on line 63

Deprecated: Function create_function() is deprecated in /var/www/wp-content/themes/Newspaper/includes/widgets/td_page_builder_widgets.php on line 70

Deprecated: Function create_function() is deprecated in /var/www/wp-content/themes/Newspaper/includes/widgets/td_page_builder_widgets.php on line 77

Deprecated: Function create_function() is deprecated in /var/www/wp-content/themes/Newspaper/includes/widgets/td_page_builder_widgets.php on line 84

Deprecated: Function create_function() is deprecated in /var/www/wp-content/themes/Newspaper/includes/widgets/td_page_builder_widgets.php on line 91

Deprecated: Function create_function() is deprecated in /var/www/wp-content/themes/Newspaper/includes/widgets/td_page_builder_widgets.php on line 98

Deprecated: Function create_function() is deprecated in /var/www/wp-content/themes/Newspaper/includes/widgets/td_page_builder_widgets.php on line 105

Deprecated: Function create_function() is deprecated in /var/www/wp-content/themes/Newspaper/includes/widgets/td_page_builder_widgets.php on line 112

Deprecated: Function create_function() is deprecated in /var/www/wp-content/themes/Newspaper/includes/widgets/td_page_builder_widgets.php on line 119

Deprecated: Function create_function() is deprecated in /var/www/wp-content/themes/Newspaper/includes/widgets/td_page_builder_widgets.php on line 126

Deprecated: Function create_function() is deprecated in /var/www/wp-content/themes/Newspaper/includes/widgets/td_page_builder_widgets.php on line 133

Deprecated: Function create_function() is deprecated in /var/www/wp-content/themes/Newspaper/includes/widgets/td_page_builder_widgets.php on line 140

Deprecated: Function create_function() is deprecated in /var/www/wp-content/themes/Newspaper/includes/widgets/td_page_builder_widgets.php on line 147

Deprecated: Function create_function() is deprecated in /var/www/wp-content/themes/Newspaper/includes/widgets/td_page_builder_widgets.php on line 154

Deprecated: Function create_function() is deprecated in /var/www/wp-content/themes/Newspaper/includes/widgets/td_page_builder_widgets.php on line 161

Deprecated: Function create_function() is deprecated in /var/www/wp-content/themes/Newspaper/includes/widgets/td_page_builder_widgets.php on line 168

Deprecated: Function create_function() is deprecated in /var/www/wp-content/themes/Newspaper/includes/widgets/td_page_builder_widgets.php on line 175

Deprecated: Function create_function() is deprecated in /var/www/wp-content/themes/Newspaper/includes/widgets/td_page_builder_widgets.php on line 182

Deprecated: Function create_function() is deprecated in /var/www/wp-content/themes/Newspaper/includes/widgets/td_page_builder_widgets.php on line 189

Deprecated: Function create_function() is deprecated in /var/www/wp-content/themes/Newspaper/includes/widgets/td_page_builder_widgets.php on line 196

Deprecated: Function create_function() is deprecated in /var/www/wp-content/themes/Newspaper/includes/widgets/td_page_builder_widgets.php on line 203

Deprecated: Function create_function() is deprecated in /var/www/wp-content/themes/Newspaper/includes/widgets/td_page_builder_widgets.php on line 210

Deprecated: Function create_function() is deprecated in /var/www/wp-content/themes/Newspaper/includes/widgets/td_page_builder_widgets.php on line 217

Deprecated: Function create_function() is deprecated in /var/www/wp-content/themes/Newspaper/includes/widgets/td_page_builder_widgets.php on line 223

Deprecated: Function create_function() is deprecated in /var/www/wp-content/themes/Newspaper/includes/widgets/td_page_builder_widgets.php on line 228

Deprecated: Function create_function() is deprecated in /var/www/wp-content/themes/Newspaper/functions.php on line 68

Warning: Cannot modify header information - headers already sent by (output started at /var/www/wp-content/themes/Newspaper/includes/widgets/td_page_builder_widgets.php:161) in /var/www/wp-includes/feed-rss2.php on line 8
best creatine supplement – Redcon1 Online Official https://redcon1online.com The Highest State of Readiness Wed, 02 Aug 2017 15:44:26 +0000 en-US hourly 1 https://wordpress.org/?v=6.5.2 Benefits of Boosting Your Testosterone Level https://redcon1online.com/boosting-testosterone/ Sat, 05 Aug 2017 04:00:49 +0000 https://redcon1online.com/?p=4381 Clinical studies estimate that as much as 5.6% of America’s male population in their 20’s and younger may suffer from low endogenous testosterone levels. This number sharply rises after men reach their 30’s. The symptoms and effects of a low testosterone level are varied and diverse, with many not manifesting externally. This makes it particularly difficult for one to assess one’s own level accurately without getting bloodwork done. With that said, lets delve into some of the more common signs of low levels and some reasons that boosting testosterone benefits men.

The most well-known indication of low testosterone is sexual difficulties. These can range widely. Men with low levels commonly experience reduced or subpar sex drives. A reduced number of spontaneous erections, difficulty gaining an erection, and lower duration of an erection are all commonly seen as well. This is particularly common in men aged 30 or older, due to their naturally declining androgen levels as well as a higher amount of their remaining testosterone being bound to SHBG (sexual hormone binding globulin) which renders it unavailable for use. Infertility is less commonly seen than other more typical indicators, but is by no means unheard of.

Sleep problems and/or difficulty in remaining asleep for long periods of time may also be experienced. The role that testosterone plays in this issue has not been clearly defined yet, despite extensive research. What is known however, is that a definitive and strong relationship exists between having low levels of free testosterone in the male body and difficulty in getting a full night’s sleep. Science may have been unsuccessful in isolating the mechanism by which this relationship stands, but it clearly exists.

One of the other known functions of testosterone is that of emotional regulation. It has been established that mood swings and depression in men are more common among those suffering from low levels of testosterone. There is even a term for this condition, known as “irritable male syndrome.” It is typically defined as a state of constant frustration, hypersensitivity, and sometimes even anger. Men who have successfully raised their levels commonly describe an improved sense of wellbeing, as well as higher self-confidence and motivation. Better memory recall and concentration are reported as well. Less susceptibility to stress and irritation are also reported. 

For those who seek to enhance their performance at the gym, a healthy testosterone level is a must. Testosterone promotes increased protein synthesis in lean muscle tissue. This is accomplished by stimulation of a growth hormone response in the pituitary gland, which in turn promotes amino acid uptake. It can also serve to escalate the number of neurotransmitters at the uptake site in muscle fibers and encourage faster tissue growth. It is also theorized that testosterone may have a relationship with satellite cells. Increased strength and endurance will be noted by the athlete who ensures healthy androgen levels in his body. The obvious and immediate effects of this will be the ability to move more weight in the gym, the inclination to train harder utilizing heavier lifts, and a quicker post-workout recovery time. Decreased soreness after training sessions is also a common benefit.

One common way of approaching this issue is to seek testosterone replacement therapy (known as TRT). This medical process is rapidly attracting more adherents, with some estimates stating that the number of men who seek TRT has more than tripled in the past ten years. The established means of procuring TRT begins by requesting one’s personal doctor to order bloodwork done utilizing a sample taken from the patient. After low testosterone levels have been established, a pharmaceutical prescription (commonly aiming for shots of around 100-200 mg. of testosterone per week) will be given, and the patient can begin injections.

Many athletes seek to elevate their testosterone levels through non-medical means. Some men turn to over the counter testosterone booster products. In recent years there has been an increase in use of plant based products. The plant hormone laxogenin in particular has seen elevated use among supplement companies. The metalloid boron is also a common ingredient in many booster products. Saponin compounds such as fenugreek extract have also been tried.

The health and fitness craze of today’s world leaves many seeking to acquire an edge over their competition when it comes to physical performance. Due in part to this, the use of natural testosterone boosters has skyrocketed. Whatever method that you ultimately choose to boost your testosterone level, the many health benefits will be worth it.

]]>
Sulforaphane to Inhibit Myostatin? 3 https://redcon1online.com/sulforaphane-inhibit-myostatin-3/ Sat, 24 Jun 2017 16:29:22 +0000 https://redcon1online.com/?p=4055 In closing, lets bring in its ability to act as a significant anti-inflammatory and anti-cancer agent. I would like to look at three pieces of literature. The first is on the inhibition of histone deacetylase 6 acetylates and disrupts the chaperone function of heat shock protein 90: a novel basis for antileukemia activity of histone deacetylase inhibitors by Bali et al. The second is on  histone deacetylase inhibitors: signalling towards p21cip1/waf1 from Matthias Ocker. The third and final is entitled “A novel mechanism of chemoprotection by sulforaphane: inhibition of histone deacetylase” from Myzak et al. The hydroxamic acid (HAA) analogue pan-histone deacetylase (HDAC) inhibitors (HDIs) LAQ824 and LBH589 have been shown to induce acetylation and inhibit the ATP binding and chaperone function of heat shock protein (HSP) 90. This promotes the polyubiquitylation and degradation of the pro-growth and pro-survival client proteins Bcr-Abl, mutant FLT-3, c-Raf, and AKT in human leukemia cells. HDAC6 is a member of the class IIB HDACs. It is predominantly cytosolic, microtubule-associated alpha-tubulin deacetylase that is also known to promote aggresome inclusion of the misfolded polyubiquitylated proteins. Here we demonstrate that in the Bcr-abl oncogene expressing human leukemia K562 cells, HDAC6 can be co-immunoprecipitated with HSP90, and the knock-down of HDAC6 by its siRNA induced the acetylation of HSP90 and alpha-tubulin. Depletion of HDAC6 levels also inhibited the binding of HSP90 to ATP, reduced the chaperone association of HSP90 with its client proteins, e.g. Bcr-Abl, and induced polyubiquitylation and partial depletion of Bcr-Abl. Conversely, the ectopic overexpression of HDAC6 inhibited LAQ824-induced acetylation of HSP90 and alpha-tubulin and reduced LAQ824-mediated depletion of Bcr-Abl, AKT, and c-Raf. Collectively, these findings indicate that HDAC6 is also an HSP90 deacetylase. Targeted inhibition of HDAC6 leads to acetylation of HSP90 and disruption of its chaperone function, resulting in polyubiquitylation and depletion of pro-growth and pro-survival HSP90 client proteins including Bcr-Abl. Depletion of HDAC6 sensitized human leukemia cells to HAA-HDIs and proteasome inhibitors (9.) Chromatin-modifying enzymes such as histone deacetylases (HDAC) facilitate a closed chromatin structure and hence transcriptional repression. HDAC are commonly affected in human cancer diseases. Thus, inhibition of HDAC represents a novel therapeutic approach. Several studies have shown that HDAC inhibitors strongly activate the expression of the cyclin-dependent kinase inhibitor p21(cip1/waf1) through (i) enhanced histone acetylation around the p21(cip1/waf1) promoter and (ii) the Sp1 sites on the p21(cip1/waf1) promoter releasing the repressor HDAC1 from its binding. p21(cip1/waf1) expression is regulated in a p53-dependent and p53-independent manner. The decision if p21(cip1/waf1) up-regulation results in cell cycle arrest or apoptosis, decides about the therapeutic efficacy of an anti-cancer treatment with HDAC inhibitors (10.) Sulforaphane (SFN), a compound found at high levels in broccoli and broccoli sprouts, is a potent inducer of phase 2 detoxification enzymes and inhibits tumorigenesis in animal models. SFN also has a marked effect on cell cycle checkpoint controls and cell survival and/or apoptosis in various cancer cells, through mechanisms that are poorly understood. We tested the hypothesis that SFN acts as an inhibitor of histone deacetylase (HDAC). In human embryonic kidney 293 cells, SFN dose-dependently increased the activity of a beta-catenin-responsive reporter (TOPflash), without altering beta-catenin or HDAC protein levels. Cytoplasmic and nuclear extracts from these cells had diminished HDAC activity, and both global and localized histone acetylation was increased, compared with untreated controls. Studies with SFN and with media from SFN-treated cells indicated that the parent compound was not responsible for the inhibition of HDAC, and this was confirmed using an inhibitor of glutathione S-transferase, which blocked the first step in the metabolism of SFN, via the mercapturic acid pathway. Whereas SFN and its glutathione conjugate (SFN-GSH) had little or no effect, the two major metabolites SFN-cysteine and SFN-N-acetylcysteine were effective HDAC inhibitors in vitro. Finally, several of these findings were recapitulated in HCT116 human colorectal cancer cells: SFN dose-dependently increased TOPflash reporter activity and inhibited HDAC activity, there was an increase in acetylated histones and in p21(Cip1/Waf1), and chromatin immunoprecipitation assays revealed an increase in acetylated histones bound to the P21 promoter. Collectively, these findings suggest that SFN may be effective as a tumor-suppressing agent and as a chemotherapeutic agent, alone or in combination with other HDAC inhibitors currently undergoing clinical trials (11.)

Sulforaphane’s ability to do everything we just discussed should make you want to start eating your broccoli as well as possibly supplementing with a good sulforaphane product (which is very few and fair between.) In terms of an applicable dosage, it seems that right around the 30mg per day mark is proven in literature to be beneficial (with some even dosing it up to double based on their body weight being higher.) Sulforaphane’s benefits are endless and is a must have health AND ergogenic aid supplement for any serious competitor (or at least it is in my eyes.)

References

  1. Protein oxidation and aging. E. R. Stadtman. Science. 1992 (https://www.ncbi.nlm.nih.gov/pubmed/1355616)
  2. Sulforaphane Activates Heat Shock Response and Enhances Proteasome Activity through Up-regulation of Hsp27. Nanqin Gan, Yu-Chieh Wu, Mathilde Brunet, Carmen Garrido, Fung-Lung Chung, Chengkai Dai, Lixin Mi. J Biol Chem. 2010 (https://www.ncbi.nlm.nih.gov/pubmed/20833711)
  3. Role of increased expression of the proteasome in the protective effects of sulforaphane against hydrogen peroxide-mediated cytotoxicity in murine neuroblastoma cells. Mi-Kyoung Kwak, Jeong-Min Cho, Bo Huang, Soona Shin, Thomas W. Kensler. Free Radic Biol Med. 2007 (https://www.ncbi.nlm.nih.gov/pubmed/17664144)
  4. Sulforaphane induced adipolysis via hormone sensitive lipase activation, regulated by AMPK signaling pathway. Ju-Hee Lee, Myung-Hee Moon, Jae-Kyo Jeong, Yang-Gyu Park, You-Jin Lee, Jae-Won Seol, Sang-Youel Park. Biochem Biophys Res Commun. 2012 (https://www.ncbi.nlm.nih.gov/pubmed/22982310)
  5. Identification and role of the basal phosphorylation site on hormone-sensitive lipase. A. J. Garton, S. J. Yeaman. Eur J Biochem. 1990 (https://www.ncbi.nlm.nih.gov/pubmed/2165906)
  6. 5-Aminoimidazole-4-carboxamide-1-beta-D-ribofuranoside-induced AMP-activated protein kinase phosphorylation inhibits basal and insulin-stimulated glucose uptake, lipid synthesis, and fatty acid oxidation in isolated rat adipocytes. Mandeep Pinky Gaidhu, Sergiu Fediuc, Rolando Bacis Ceddia. J Biol Chem. 2006 (https://www.ncbi.nlm.nih.gov/pubmed/16816404)
  7. Sulforaphane causes a major epigenetic repression of myostatin in porcine satellite cells. Huitao Fan, Rui Zhang, Dawit Tesfaye, Ernst Tholen, Christian Looft, Michael Hölker, Karl Schellander, Mehmet Ulas Cinar. Epigenetics. 2012 (https://www.ncbi.nlm.nih.gov/pubmed/23092945)
  8. Sulforaphane attenuates hepatic fibrosis via NF-E2-related factor 2-mediated inhibition of transforming growth factor-β/Smad signaling. Chang Joo Oh, Joon-Young Kim, Ae-Kyung Min, Keun-Gyu Park, Robert A. Harris, Han-Jong Kim, In-Kyu Lee. Free Radic Biol Med. 2012 (https://www.ncbi.nlm.nih.gov/pubmed/22155056)
  9. Inhibition of histone deacetylase 6 acetylates and disrupts the chaperone function of heat shock protein 90: a novel basis for antileukemia activity of histone deacetylase inhibitors. Purva Bali, Michael Pranpat, James Bradner, Maria Balasis, Warren Fiskus, Fei Guo, Kathy Rocha, Sandhya Kumaraswamy, Sandhya Boyapalle, Peter Atadja, et al. J Biol Chem. 2005 (https://www.ncbi.nlm.nih.gov/pubmed/15937340)
  10. Histone deacetylase inhibitors: signalling towards p21cip1/waf1. Matthias Ocker, Regine Schneider-Stock. Int J Biochem Cell Biol. 2007 (https://www.ncbi.nlm.nih.gov/pubmed/17412634)
  11. A novel mechanism of chemoprotection by sulforaphane: inhibition of histone deacetylase. Melinda C. Myzak, P. Andrew Karplus, Fung-Lung Chung, Roderick H. Dashwood. Cancer Res. 2004 (https://www.ncbi.nlm.nih.gov/pubmed/15313918)
]]>
Why You Might Not Be Growing Part 2 https://redcon1online.com/not-growing-2/ Wed, 21 Jun 2017 04:00:58 +0000 https://redcon1online.com/?p=3995 Participants completed the visual analog scales for global vigor and global affect at 2-hour intervals each day. Comparisons between conditions were performed using 2-sided nonparametric Wilcoxon tests with a significance level of .05. The 10 healthy men had a mean (SD) age of 24.3 (4.3) years and a mean (SD) body mass index of 23.5 (2.4) (calculated as weight in kilograms divided by height in meters squared). Total (SD) sleep time decreased from 8 hours 55 minutes (35 min) to 4 hours 48 minutes (6 min) with sleep restriction (P = .002). Relative to the rested condition, during each restricted night, participants lost a total (SD) of 2 hours 45 minutes (29 min) of stage-2 sleep (P = .002) and 1 hour 3 minutes (18 min) of REM sleep (P = .002) and gained 9 minutes (8 min) of sleep in stages 3 + 4 (P = .01). During waking hours common to both conditions (8 AM-10 PM), testosterone levels were lower after sleep restriction than in the rested condition (16.5 [2.8] nmol/L vs 18.4 [3.8] nmol/L; P = .049). The effect of restricted sleep was especially apparent between 2 PM and 10 PM (15.5 [3.1] nmol/L vs 17.9 [4.0] nmol/L; P = .02). Daytime cortisol profiles were similar under both conditions. Daily sleep restriction was associated with a progressive decrease in mean (SD) vigor scores from 28 (5) after the first night to 19 (7) after the seventh night (P = .002).  Shown are mean values. In the rested condition, bedtimes were from 10 PM to 8 AM. Values for partial sleep restriction were taken after 1 week of restriction, for which bedtimes were from 12:30 AM to 5:30 AM. On average over the 68 time points, the SD of testosterone levels at each time point was 5.01 nmol/L (range, 2.98-7.53 nmol/L) in the rested condition and 4.26 nmol/L (range, 2.82-6.92 nmol/L) in the restricted condition. On average over the 68 time points, the SD of cortisol levels at each time point was 67.1 nmol/L (range, 15.2-142.7 nmol/L) in the rested condition and 54.0 nmol/L (range, 7.7-162.3 nmol/L) in the restricted condition (2.)

In close relation is a study on sleep deprivation and how it reduces circulating androgens in healthy men. “The acute effect of sleep deprivation on the pituitary-testis axis was evaluated in 13 healthy men. To study such association, the circulating levels of follicle-stimulating hormone (FSH), luteinizing hormone (LH), prolactin (PRL), Androstenedione (A), Testosterone (T), Dihydro-testosterone (DHT) and Estradiol (E2) were measured along with Cortisol (C) before and after sleep deprivation. Morning (8:00 AM) venous blood samples were obtained prior and after a continuous restless period of 24 hr and the values were analyzed by the paired Student’s t test. There was a significant and parallel decrease of each androgen and E2 but not of FSH, L.H. PRL, or C, associated with the acute sleep deprivation” (3.) The issues that we are seeing tie directly into cortisol. The issue that arises is that coristol usually pulsates in pattern (meaning its higher in the morning and lower at night) BUT when sleep is deprived, it essentially disrupts this pattern and there by increases serum cortisol levels. Leproult shows this very well in a study from 1997. Sleep curtailment constitutes an increasingly common condition in industrialized societies and is thought to affect mood and performance rather than physiological functions. There is no evidence for prolonged or delayed effects of sleep loss on the hypothalamo-pituitary-adrenal (HPA) axis. We evaluated the effects of acute partial or total sleep deprivation on the nighttime and daytime profile of cortisol levels. Plasma cortisol profiles were determined during a 32-hour period (from 1800 hours on day 1 until 0200 hours on day 3) in normal young men submitted to three different protocols: normal sleep schedule (2300-0700 hours), partial sleep deprivation (0400-0800 hours), and total sleep deprivation. Alterations in cortisol levels could only be demonstrated in the evening following the night of sleep deprivation. After normal sleep, plasma cortisol levels over the 1800-2300-hour period were similar on days 1 and 2. After partial and total sleep deprivation, plasma cortisol levels over the 1800-2300-hour period were higher on day 2 than on day 1 (37 and 45% increases, p = 0.03 and 0.003, respectively), and the onset of the quiescent period of cortisol secretion was delayed by at least 1 hour. We conclude that even partial acute sleep loss delays the recovery of the HPA from early morning circadian stimulation and is thus likely to involve an alteration in negative glucocorticoid feedback regulation. Sleep loss could thus affect the resiliency of the stress response and may accelerate the development of metabolic and cognitive consequences of glucocorticoid excess (4.)

References

  1. Acute partial sleep deprivation increases food intake in healthy men. Laurent Brondel, Michael A. Romer, Pauline M. Nougues, Peio Touyarou, Damien Davenne. Am J Clin Nutr. 2010 (https://www.ncbi.nlm.nih.gov/pubmed/20357041)
  2. Effect of 1 Week of Sleep Restriction on Testosterone Levels in Young Healthy Men. Leproult, R., & Van Cauter, E. (2011). (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4445839/)
  3. Sleep deprivation reduces circulating androgens in healthy men. V. Cortés-Gallegos, G. Castañeda, R. Alonso, I. Sojo, A. Carranco, C. Cervantes, A. Parra. Arch Androl. 1983 (https://www.ncbi.nlm.nih.gov/pubmed/6405703)
  4. Sleep loss results in an elevation of cortisol levels the next evening. R. Leproult, G. Copinschi, O. Buxton, E. Van Cauter. Sleep. 1997 (https://www.ncbi.nlm.nih.gov/pubmed/9415946)
  5. Sleep disturbances are correlated with decreased morning awakening salivary cortisol. Jutta Backhaus, Klaus Junghanns, Fritz Hohagen. Psychoneuroendocrinology. 2004 (https://www.ncbi.nlm.nih.gov/pubmed/15219642)
  6. Growth hormone secretion during sleep. Y. Takahashi, D. M. Kipnis, W. H. Daughaday. J Clin Invest. 1968 (https://www.ncbi.nlm.nih.gov/pubmed/5675428)
  7. Effect of sleep deprivation on overall 24 h growth-hormone secretion. G. Brandenberger, C. Gronfier, F. Chapotot, C. Simon, F. Piquard. Lancet. 2000 (https://www.ncbi.nlm.nih.gov/pubmed/11052586)
  8. Influence of partial sleep deprivation on energy balance and insulin sensitivity in healthy women. Anja Bosy-Westphal, Silvia Hinrichs, Kamila Jauch-Chara, Britta Hitze, Wiebke Later, Britta Wilms, Uta Settler, Achim Peters, Dieter Kiosz, Manfred James Muller. Obes Facts. 2008 (https://www.ncbi.nlm.nih.gov/pubmed/20054188)
  9. Optimism and self-esteem are related to sleep. Results from a large community-based sample. Sakari Lemola, Katri Räikkönen, Veronica Gomez, Mathias Allemand. Int J Behav Med. 2013 (https://www.ncbi.nlm.nih.gov/pubmed/23055029)
  10. Sleep duration and cardiometabolic risk: a review of the epidemiologic evidence. Kristen L. Knutson. Best Pract Res Clin Endocrinol Metab. (https://www.ncbi.nlm.nih.gov/pubmed/21112022)
]]>
Protein Requirements for Bodybuilders- Part 2 https://redcon1online.com/protein-requirements-bodybuilders-part-2/ Wed, 24 May 2017 04:00:47 +0000 https://redcon1online.com/?p=3735 We must once again look to the works from Dr. Antonio (2) on the effects of a high protein diet on indices of health and body composition (a crossover trial in resistance-trained men.) The study was eight weeks of a high protein diet (>3 g/kg/day) coupled with a periodized heavy resistance training program has been shown to positively affect body composition with no deleterious effects on health. Using a randomized, crossover design, resistance-trained male subjects underwent a 16-week intervention (i.e., two 8-week periods) in which they consumed either their normal (i.e., habitual) or a higher protein diet (>3 g/kg/day). Thus, the purpose of this study was to ascertain if significantly increasing protein intake would affect clinical markers of health (i.e., lipids, kidney function, etc.) as well as performance and body composition in young males with extensive resistance training experience. Twelve healthy resistance-trained men volunteered for this study (mean ± SD: age 25.9 ± 3.7 years; height 178.0 ± 8.5 cm; years of resistance training experience 7.6 ± 3.6) with 11 subjects completing most of the assessments. In a randomized crossover trial, subjects were tested at baseline and after two 8-week treatment periods (i.e., habitual [normal] diet and high protein diet) for body composition, measures of health (i.e., blood lipids, comprehensive metabolic panel) and performance. Each subject maintained a food diary for the 16-week treatment period (i.e., 8 weeks on their normal or habitual diet and 8 weeks on a high protein diet). Each subject provided a food diary of two weekdays and one weekend day per week. In addition, subjects kept a diary of their training regimen that was used to calculate total work performed. During the normal and high protein phase of the treatment period, subjects consumed 2.6 ± 0.8 and 3.3 ± 0.8 g/kg/day of dietary protein, respectively. The mean protein intake over the 4-month period was 2.9 ± 0.9 g/kg/day. The high protein group consumed significantly more calories and protein (p < 0.05) than the normal protein group. There were no differences in dietary intake between the groups for any other measure. Moreover, there were no significant changes in body composition or markers of health in either group. There were no side effects (i.e., blood lipids, glucose, renal, kidney function etc.) regarding high protein consumption. In resistance-trained young men who do not significantly alter their training regimen, consuming a high protein diet (2.6 to 3.3 g/kg/day) over a 4-month period has no effect on blood lipids or markers of renal and hepatic function. Nor were there any changes in performance or body composition. This is the first crossover trial using resistance-trained subjects in which the elevation of protein intake to over four times the recommended dietary allowance has shown no harmful effects.

Dr. Jose Antonio’s research continues. This study (3) looked at the consumption of a high protein diet (>4 g/kg/d) in trained men and women who did not alter their exercise program. Thus, the purpose of this investigation was to determine if a high protein diet in conjunction with a periodized heavy resistance training program would affect indices of body composition, performance and health. Forty-eight healthy resistance-trained men and women completed this study (mean ± SD; Normal Protein group [NP n = 17, four female and 13 male]: 24.8 ± 6.9 yr; 174.0 ± 9.5 cm height; 74.7 ± 9.6 kg body weight; 2.4 ± 1.7 yr of training; High Protein group [HP n = 31, seven female and 24 male]: 22.9 ± 3.1 yr; 172.3 ± 7.7 cm; 74.3 ± 12.4 kg; 4.9 ± 4.1 yr of training). Moreover, all subjects participated in a split-routine, periodized heavy resistance-training program. Training and daily diet logs were kept by each subject. Subjects in the NP and HP groups were instructed to consume their baseline (~2 g/kg/d) and >3 g/kg/d of dietary protein, respectively. Subjects in the NP and HP groups consumed 2.3 and 3.4 g/kg/day of dietary protein during the treatment period. The NP group consumed significantly (p < 0.05) more protein during the treatment period compared to their baseline intake. The HP group consumed more (p < 0.05) total energy and protein during the treatment period compared to their baseline intake. Furthermore, the HP group consumed significantly more (p < 0.05) total calories and protein compared to the NP group. There were significant time by group (p ≤ 0.05) changes in body weight (change: +1.3 ± 1.3 kg NP, −0.1 ± 2.5 HP), fat mass (change: −0.3 ± 2.2 kg NP, −1.7 ± 2.3 HP), and % body fat (change: −0.7 ± 2.8 NP, −2.4 ± 2.9 HP). The NP group gained significantly more body weight than the HP group; however, the HP group experienced a greater decrease in fat mass and % body fat. There was a significant time effect for FFM; however, there was a non-significant time by group effect for FFM (change: +1.5 ± 1.8 NP, +1.5 ± 2.2 HP). Furthermore, a significant time effect (p ≤ 0.05) was seen in both groups vis a vis improvements in maximal strength (i.e., 1-RM squat and bench) vertical jump and pull-ups; however, there were no significant time by group effects (p ≥ 0.05) for all exercise performance measures. Additionally, there were no changes in any of the blood parameters (i.e., basic metabolic panel). They concluded by stating “consuming a high protein diet (3.4 g/kg/d) in conjunction with a heavy resistance-training program may confer benefits with regards to body composition. Furthermore, there is no evidence that consuming a high protein diet has any deleterious effects.”

References

  1. A High Protein Diet Has No Harmful Effects: A One-Year Crossover Study in Resistance-Trained Males. Jose AntonioAnya EllerbroekTobin SilverLeonel VargasArmando TamayoRichard Buehn, and Corey A. Peacock. Exercise and Sport Science Laboratory, Nova Southeastern University, Davie, FL, USA. 2016. (https://www.hindawi.com/journals/jnme/2016/9104792/)
  2. The effects of a high protein diet on indices of health and body composition – a crossover trial in resistance-trained men. Jose Antonio, Anya Ellerbroek, Tobin Silver, Leonel Vargas and Corey Peacock. Journal of the International Society of Sports Nutrition. 2016 (https://jissn.biomedcentral.com/articles/10.1186/s12970-016-0114-2)
  3. A high protein diet (3.4 g/kg/d) combined with a heavy resistance training program improves body composition in healthy trained men and women – a follow-up investigation. Jose Antonio, Anya Ellerbroek, Tobin Silver, Steve Orris, Max Scheiner, Adriana Gonzalez and Corey A Peacock. Journal of the International Society of Sports Nutrition. 2015 (https://jissn.biomedcentral.com/articles/10.1186/s12970-015-0100-0)
  4. International Society of Sports Nutrition position stand: protein and exercise. Bill Campbell, Richard B Kreider, Tim Ziegenfuss, Paul La Bounty, Mike Roberts, Darren Burke, Jamie Landis, Hector Lopez and Jose Antonio. Journal of the International Society of Sports Nutrition. 2007 (https://jissn.biomedcentral.com/articles/10.1186/1550-2783-4-8)
  5. Protein requirements and muscle mass/strength changes during intensive training in novice bodybuilders. P. W. Lemon, M. A. Tarnopolsky, J. D. MacDougall, S. A. Atkinson. J Appl Physiol (1985) (https://www.ncbi.nlm.nih.gov/pubmed/1400008)
  6. Protein requirements and muscle mass/strength changes during intensive training in novice bodybuilders. P. W. Lemon, M. A. Tarnopolsky, J. D. MacDougall, S. A. Atkinson. J Appl Physiol (1985) (https://www.ncbi.nlm.nih.gov/pubmed/1400008)
  7. Exercise-induced changes in protein metabolism. K. D. Tipton, R. R. Wolfe. Acta Physiol Scand. 1998 (https://www.ncbi.nlm.nih.gov/pubmed/9578384)
  8. Muscle protein synthesis in response to nutrition and exercise. P. J. Atherton, K. Smith. The Journal of Physiology. 2012 (http://onlinelibrary.wiley.com/doi/10.1113/jphysiol.2011.225003/abstract)
  9. Beyond the zone: protein needs of active individuals. P. W. Lemon. J Am Coll Nutr. 2000 (https://www.ncbi.nlm.nih.gov/pubmed/11023001)
  10. Meta-analysis of nitrogen balance studies for estimating protein requirements in healthy adults. William M. Rand, Peter L. Pellett, Vernon R. Young. Am J Clin Nutr. 2003 (https://www.ncbi.nlm.nih.gov/pubmed/12499330)
]]>
Why Every Athlete SHOULD Use TUDCA Part 2 https://redcon1online.com/tudca-part-2/ Sun, 21 May 2017 04:00:46 +0000 https://redcon1online.com/?p=3700 Normally, athletes ingest TUDCA simply for those liver benefits it possesses, but little credit is ever given to its interactions with skeletal muscle, adipose tissue, and glucose metabolism. One of my more favorite TUDCA studies actually comes from Kars et al and looks directly at how it improves liver and muscle insulin sensitivity but does not improve adipose tissue insulin sensitivity (which is a good thing!) Insulin resistance is commonly associated with obesity. Studies conducted in obese mouse models found that endoplasmic reticulum (ER) stress contributes to insulin resistance, and treatment with tauroursodeoxycholic acid (TUDCA), a bile acid derivative that acts as a chemical chaperone to enhance protein folding and ameliorate ER stress, increases insulin sensitivity. The purpose of this study was to determine the effect of TUDCA therapy on multiorgan insulin action and metabolic factors associated with insulin resistance in obese men and women. In this study, twenty obese subjects ([means +/- SD] aged 48 +/- 11 years, BMI 37 +/- 4 kg/m2) were randomized to 4 weeks of treatment with TUDCA (1,750 mg/day) or placebo. A two-stage hyperinsulinemic-euglycemic clamp procedure in conjunction with stable isotopically labeled tracer infusions and muscle and adipose tissue biopsies were used to evaluate in vivo insulin sensitivity, cellular factors involved in insulin signaling, and cellular markers of ER stress. RESULTS Hepatic and muscle insulin sensitivity increased by approximately 30% (P < 0.05) after treatment with TUDCA but did not change after placebo therapy. In addition, therapy with TUDCA, but not placebo, increased muscle insulin signaling (phosphorylated insulin receptor substrate(Tyr) and Akt(Ser473) levels) (P < 0.05). Markers of ER stress in muscle or adipose tissue did not change after treatment with either TUDCA or placebo. This data demonstrate that TUDCA might be an effective pharmacological approach for treating insulin resistance. Additional studies are needed to evaluate the target cells and mechanisms responsible for this effect (4.)

Although that is the only credible study I can attribute positive results on those fronts, we can play “connect the dots” with some other pieces of literature such as the ones done on TUDCA supplementation in correlation to glucose metabolism. A study done in 2006 (5) linked endoplasmic reticulum stress to obesity, insulin resistance, and diabetes. They state” here, we provide evidence that this mechanistic link can be exploited for therapeutic purposes with orally active chemical chaperones. 4-Phenyl butyric acid and taurine-conjugated ursodeoxycholic acid alleviated ER stress in cells and whole animals. Treatment of obese and diabetic mice with these compounds resulted in normalization of hyperglycemia, restoration of systemic insulin sensitivity, resolution of fatty liver disease, and enhancement of insulin action in liver, muscle, and adipose tissues. Our results demonstrate that chemical chaperones enhance the adaptive capacity of the ER and act as potent antidiabetic modalities with potential application in the treatment of type 2 diabetes.” Another study along similar lines of endoplasmic reticulum stress and its correlation to insulin resistance looked at glucose-induced beta cell dysfunction in vivo in rats which showed a link between oxidative stress and endoplasmic reticulum stress. Healthy Wistar rats were infused i.v. with glucose for 48 h to achieve 20 mmol/l hyperglycaemia with or without the co-infusion of the superoxide dismutase mimetic tempol (TPO), or the chemical chaperones 4-phenylbutyrate (PBA) or tauroursodeoxycholic acid (TUDCA). This was followed by assessment of beta cell function and measurement of ER stress markers and superoxide in islets. Glucose infusion for 48 h increased mitochondrial superoxide and ER stress markers and impaired beta cell function. Co-infusion of TPO, which we previously found to reduce mitochondrial superoxide and prevent glucose-induced beta cell dysfunction, reduced ER stress markers. Similar to findings with TPO, co-infusion of PBA, which decreases mitochondrial superoxide, prevented glucose-induced beta cell dysfunction in isolated islets. TUDCA was also effective. Also similar to findings with TPO, PBA prevented beta cell dysfunction during hyperglycaemic clamps in vivo and after hyperglycaemia (15 mmol/l) for 96 h. Here, we causally implicate ER stress in hyperglycaemia-induced beta cell dysfunction in vivo. We show that: (1) there is a positive feedback cycle between oxidative stress and ER stress in glucose-induced beta cell dysfunction, which involves mitochondrial superoxide; and (2) this cycle can be interrupted by superoxide dismutase mimetics as well as chemical chaperones, which are of potential interest to preserve beta cell function in type 2 diabetes (6.)

I could continue on and on about the benefits of TUDCA! Heck, we didn’t even cover the fact that bile acids have the ability to induce energy expenditure by promoting intracellular thyroid hormone activation (7.) But, I do feel I’ve presented enough pertinent information to prove TUDCA has its place in everyone’s supplement regimen given the fact that it is a potent health and ergogenic aid that is more than affordable. In terms of practical application, there have been studies done showing improvements of liver regenesis rates at a dosage as low as 10mgs and other studies showing benefits for muscle tissue insulin sensitivity and for the treatment of liver disease as high as almost 2000mgs. In actual application I personally recommend my clients (that are competitive athletes) to supplement with 250mgs of TUDCA per day year round. Then, during periods of high stress such as a contest prep or anytime you’re truly pushing your “supplements”, upwards of 1000mgs per day. You will obviously need to get bloodwork done to see where your liver enzyme levels are and how they change at what specific dosage to know for sure (once again, thank you biological inter-individuality!) I have also included four more studies linked below in the reference section for your academic pleasure (8, 9, 10, 11.) Please read more and make the decision for yourself if TUDCA is something that could be beneficial in your everyday supplement stack.

References

  1. Metabolism of orally administered tauroursodeoxycholic acid in patients with primary biliary cirrhosis. K D Setchell, C M Rodrigues, M Podda, A Crosignani. Gut. 1996 (https://www.ncbi.nlm.nih.gov/pubmed/8675100)
  2. Ursodeoxycholic and tauro-ursodeoxycholic acids for the treatment of primary biliary cirrhosis: a pilot crossover study. A. Larghi, A. Crosignani, P. M. Battezzati, G. De Valle, M. Allocca, P. Invernizzi, M. Zuin, M. Podda. Aliment Pharmacol Ther. 1997 (https://www.ncbi.nlm.nih.gov/pubmed/9146783)
  3. Tauroursodeoxycholic acid for treatment of primary biliary cirrhosis. A dose-response study. A. Crosignani, P. M. Battezzati, K. D. Setchell, P. Invernizzi, G. Covini, M. Zuin, M. Podda. Dig Dis Sci. 1996 (https://www.ncbi.nlm.nih.gov/pubmed/8674405)
  4. Tauroursodeoxycholic Acid May Improve Liver and Muscle but Not Adipose Tissue Insulin Sensitivity in Obese Men and Women. Marleen Kars, Ling Yang, Margaret F. Gregor, B. Selma Mohammed, Terri A. Pietka, Brian N. Finck, Bruce W. Patterson, Jay D. Horton, Bettina Mittendorfer, Gökhan S. Hotamisligil, Samuel Klein. Diabetes. 2010 (https://www.ncbi.nlm.nih.gov/pubmed/20522594)
  5. Chemical Chaperones Reduce ER Stress and Restore Glucose Homeostasis in a Mouse Model of Type 2 Diabetes. Umut Özcan, Erkan Yilmaz, Lale Özcan, Masato Furuhashi, Eric Vaillancourt, Ross O. Smith, Cem Z. Görgün, Gökhan S. Hotamisligil. Science. Author manuscript; available in PMC 2016 Feb 4.. Published in final edited form as: Science. 2006 (https://www.ncbi.nlm.nih.gov/pubmed/16931765)
  6. Glucose-induced beta cell dysfunction in vivo in rats: link between oxidative stress and endoplasmic reticulum stress. C. Tang, K. Koulajian, I. Schuiki, L. Zhang, T. Desai, A. Ivovic, P. Wang, C. Robson-Doucette, M. B. Wheeler, B. Minassian, et al. Diabetologia. 2012 (https://www.ncbi.nlm.nih.gov/pubmed/22396011)
  7. Bile acids induce energy expenditure by promoting intracellular thyroid hormone activation. Mitsuhiro Watanabe, Sander M. Houten, Chikage Mataki, Marcelo A. Christoffolete, Brian W. Kim, Hiroyuki Sato, Nadia Messaddeq, John W. Harney, Osamu Ezaki, Tatsuhiko Kodama, et al. Nature. 2006 (https://www.ncbi.nlm.nih.gov/pubmed/16400329)
  8. Differences in the metabolism and disposition of ursodeoxycholic acid and of its taurine-conjugated species in patients with primary biliary cirrhosis. P. Invernizzi, K. D. Setchell, A. Crosignani, P. M. Battezzati, A. Larghi, N. C. O’Connell, M. Podda. Hepatology. 1999 (https://www.ncbi.nlm.nih.gov/pubmed/9918905)
  9. Does tauroursodeoxycholic acid (TUDCA) treatment increase hepatocyte proliferation in patients with chronic liver disease? C. Panella, E. Ierardi, M. F. De Marco, M. Barone, F. W. Guglielmi, L. Polimeno, A. Francavilla. Ital J Gastroenterol. 1995 (https://www.ncbi.nlm.nih.gov/pubmed/8541578)
  10. TUDCA and UDCA are incorporated into hepatocyte membranes: different sites, but similar effects. U. Leuschner, S. Guldutuna, S. Bhatti, A. Elze, M. Imhof, T. You, G. Zimmer. Ital J Gastroenterol. 1995 (https://www.ncbi.nlm.nih.gov/pubmed/8563010)
  11. Effects of prolonged glucose infusion on insulin secretion, clearance, and action in normal subjects. G. Boden, J. Ruiz, C. J. Kim, X. Chen. Am J Physiol. 1996 (https://www.ncbi.nlm.nih.gov/pubmed/8779946)
]]>
Why Every Athlete SHOULD Use TUDCA Part 1 https://redcon1online.com/tudca-1/ Sat, 20 May 2017 04:00:06 +0000 https://redcon1online.com/?p=3697 You guys have heard me talk and briefly touch on TUDCA in previous articles but after a high amount of demand for more information on this ingredient, I felt compelled to give it a full amount of my time and efforts because it seems people are still somewhat undecided as to whether this supplement would benefit them. In reality, I believe EVERYONE, especially if your an athlete, SHOULD BE SUPPLEMENTING WITH TUDCA YEAR ROUND. The only thing I feel needs to be undulated is the dosage…but we’ll get more into that later. Lets start off with the basics to make sure we’re all understanding of this molecule, its pharmacokinetics and dynamics, its benefits, as well as practical application. TUDCA (AKA Tauroursodeoxycholic Acid) is a water soluble bile acid that is very well known for having the ability to counteract the toxicity of normal bile acids that can cause a host of damaging effects to your body (especially on the liver.) Normal bile salts will reach our intestines -> become metabolized into UDCA -> then are bound to a taurine molecule (forming TUDCA.) TUDCA seems much more effective at raising bile concentrations of UDCA than UDCA alone because that taurine molecule which enhances overall bioavailability (1.)

Now that we all have that understanding of the basics of what TUDCA is, lets move into the portion that you actually care about…what does TUDCA possess thats so beneficial to athletes. TUDCA has been shown to help with overall healthy functioning of the liver and has numerous beneficial interactions with glucose metabolism, fat mass, and skeletal muscle. Larghi et al states “results from animal studies and preliminary data from pilot studies in patients with primary biliary cirrhosis suggest that tauroursodeoxycholic acid has metabolic properties that may favour its long-term use as an alternative to ursodeoxycholic acid for patients with chronic cholestatic liver diseases. No direct comparison of tauroursodeoxycholic and ursodeoxycholic acids have yet been carried out in primary biliary cirrhosis. The effects of ursodeoxycholic and tauroursodeoxycholic acids were compared in 23 patients with primary biliary cirrhosis according to a crossover design. Both drugs were administered at the daily dose of 500 mg. in a randomly assigned sequence for two 6-month periods separated by a 3-month wash-out period. Serum liver enzymes related to cholestasis and cytolysis consistently improved, as compared to baseline values, during the administration of both ursodeoxycholic and tauro-ursodeoxycholic acids, but no significant difference between these two bile acids was found. Both treatments were well tolerated and no patient complained of side effects. In the short-term, tauro-ursodeoxycholic acid appears to be safe and at least as effective as ursodeoxycholic acid for the treatment of primary biliary cirrhosis” (2.) An even more interesting study entitled “Tauroursodeoxycholic acid for treatment of primary biliary cirrhosis. A dose-response study” (3) actually looked at dosages of 500, 1000, and 1500 mugs of TUDCA over a 6 month period. They performed a dose-response study on 24 patients with primary biliary cirrhosis who were randomly assigned to receive 500, 1000, or 1500 mg daily of tauroursodeoxycholic acid for six months. Biliary enrichment with ursodeoxycholic acid ranged from 15% to 48% and was not related with the dose. Serum liver enzyme levels decreased significantly after the first month of treatment with all the three doses. No significant difference among the three doses was found, although further reduction over time occurred with 1000 and 1500mg daily. Plasma total and HDL cholesterol significantly decreased in patients administered the two higher doses. Diarrhea was the only side effect. In conclusion, a dose of about 10mg/kg body wt/day of tauroursodeoxycholic acid should be used for long-term studies in patients with primary biliary cirrhosis. It is very clear that TUDCA supplementation aids in overall healthy liver functioning by lowering cholesterol levels, lowering liver enzymes, and improving/restoring normal function.

References

  1. Metabolism of orally administered tauroursodeoxycholic acid in patients with primary biliary cirrhosis. K D Setchell, C M Rodrigues, M Podda, A Crosignani. Gut. 1996 (https://www.ncbi.nlm.nih.gov/pubmed/8675100)
  2. Ursodeoxycholic and tauro-ursodeoxycholic acids for the treatment of primary biliary cirrhosis: a pilot crossover study. A. Larghi, A. Crosignani, P. M. Battezzati, G. De Valle, M. Allocca, P. Invernizzi, M. Zuin, M. Podda. Aliment Pharmacol Ther. 1997 (https://www.ncbi.nlm.nih.gov/pubmed/9146783)
  3. Tauroursodeoxycholic acid for treatment of primary biliary cirrhosis. A dose-response study. A. Crosignani, P. M. Battezzati, K. D. Setchell, P. Invernizzi, G. Covini, M. Zuin, M. Podda. Dig Dis Sci. 1996 (https://www.ncbi.nlm.nih.gov/pubmed/8674405)
  4. Tauroursodeoxycholic Acid May Improve Liver and Muscle but Not Adipose Tissue Insulin Sensitivity in Obese Men and Women. Marleen Kars, Ling Yang, Margaret F. Gregor, B. Selma Mohammed, Terri A. Pietka, Brian N. Finck, Bruce W. Patterson, Jay D. Horton, Bettina Mittendorfer, Gökhan S. Hotamisligil, Samuel Klein. Diabetes. 2010 (https://www.ncbi.nlm.nih.gov/pubmed/20522594)
  5. Chemical Chaperones Reduce ER Stress and Restore Glucose Homeostasis in a Mouse Model of Type 2 Diabetes. Umut Özcan, Erkan Yilmaz, Lale Özcan, Masato Furuhashi, Eric Vaillancourt, Ross O. Smith, Cem Z. Görgün, Gökhan S. Hotamisligil. Science. Author manuscript; available in PMC 2016 Feb 4.. Published in final edited form as: Science. 2006 (https://www.ncbi.nlm.nih.gov/pubmed/16931765)
  6. Glucose-induced beta cell dysfunction in vivo in rats: link between oxidative stress and endoplasmic reticulum stress. C. Tang, K. Koulajian, I. Schuiki, L. Zhang, T. Desai, A. Ivovic, P. Wang, C. Robson-Doucette, M. B. Wheeler, B. Minassian, et al. Diabetologia. 2012 (https://www.ncbi.nlm.nih.gov/pubmed/22396011)
  7. Bile acids induce energy expenditure by promoting intracellular thyroid hormone activation. Mitsuhiro Watanabe, Sander M. Houten, Chikage Mataki, Marcelo A. Christoffolete, Brian W. Kim, Hiroyuki Sato, Nadia Messaddeq, John W. Harney, Osamu Ezaki, Tatsuhiko Kodama, et al. Nature. 2006 (https://www.ncbi.nlm.nih.gov/pubmed/16400329)
  8. Differences in the metabolism and disposition of ursodeoxycholic acid and of its taurine-conjugated species in patients with primary biliary cirrhosis. P. Invernizzi, K. D. Setchell, A. Crosignani, P. M. Battezzati, A. Larghi, N. C. O’Connell, M. Podda. Hepatology. 1999 (https://www.ncbi.nlm.nih.gov/pubmed/9918905)
  9. Does tauroursodeoxycholic acid (TUDCA) treatment increase hepatocyte proliferation in patients with chronic liver disease? C. Panella, E. Ierardi, M. F. De Marco, M. Barone, F. W. Guglielmi, L. Polimeno, A. Francavilla. Ital J Gastroenterol. 1995 (https://www.ncbi.nlm.nih.gov/pubmed/8541578)
  10. TUDCA and UDCA are incorporated into hepatocyte membranes: different sites, but similar effects. U. Leuschner, S. Guldutuna, S. Bhatti, A. Elze, M. Imhof, T. You, G. Zimmer. Ital J Gastroenterol. 1995 (https://www.ncbi.nlm.nih.gov/pubmed/8563010)
  11. Effects of prolonged glucose infusion on insulin secretion, clearance, and action in normal subjects. G. Boden, J. Ruiz, C. J. Kim, X. Chen. Am J Physiol. 1996 (https://www.ncbi.nlm.nih.gov/pubmed/8779946)
]]>
A Lot More On HMB Part 1 https://redcon1online.com/hmb-part-1/ Thu, 11 May 2017 04:00:24 +0000 https://redcon1online.com/?p=3589 I previously wrote an article answering the very common question about HMB and is correlation to being as effective as anabolic steroids. But now that that simple question is answered, we can look further into HMB itself and the benefits it does offer and why I recommend it as a very potent ergogenic aid. HMB is a leucine metabolite. Roughly only 5% of leucine is actually oxidized into HMB. There are two supplement forms of HMB. Those being calcium HMB or as a free acid (which simply means its HMB without the calcium salt.) Between these two forms, we see that the free acid form of HMB is the superior option as it is more readily absorbed while simultaneously reaching a higher serum peak level (1.) Fuller et al looked at the free acid gel form of β-hydroxy-β-methylbutyrate and its clearance rates. Two studies were conducted and in each study four males and four females were given three treatments in a randomised, cross-over design. Treatments were CaHMB (gelatin capsule, 1 g), equivalent HMB free acid gel swallowed (FASW) and free acid gel held sublingual for 15 s then swallowed (FASL). Plasma HMB was measured for 3 h following treatment in study 1 and 24 h with urine collection in study 2. In both the studies, the times to peak plasma HMB were 128 (sem 11), 38 (sem 4) and 38 (sem 1) min (P < 0·0001) for CaHMB, FASW and FASL, respectively. The peak concentrations were 131 (sem 6), 249 (sem 14) and 239 (sem 14) μmol/l (P < 0·0001) for CaHMB, FASW and FASL, respectively. The areas under the curve were almost double for FASW and FASL (P < 0·0001). Daily urinary HMB excretion was not significantly increased resulting in more HMB retained (P < 0·003) with FASW and FASL. Half-lives were 3·17 (sem 0·22), 2·50 (sem 0·13) and 2·51 (sem 0·14) h for CaHMB, FASW and FASL, respectively (P < 0·004). Free acid gel resulted in quicker and greater plasma concentrations (+185%) and improved clearance (+25%) of HMB from plasma. In conclusion, HMB free acid gel could improve HMB availability and efficacy to tissues in health and disease.

HMB acts within the body very similarly to leucine meaning that they both inhibit muscle protein breakdown as well as increasing muscle protein synthesis. Maintenance of skeletal muscle mass is contingent upon the dynamic equilibrium (fasted losses-fed gains) in protein turnover. Of all nutrients, the single amino acid leucine (Leu) possesses the most marked anabolic characteristics in acting as a trigger element for the initiation of protein synthesis. While the mechanisms by which Leu is ‘sensed’ have been the subject of great scrutiny, as a branched-chain amino acid, Leu can be catabolized within muscle, thus posing the possibility that metabolites of Leu could be involved in mediating the anabolic effect(s) of Leu. Our objective was to measure muscle protein anabolism in response to Leu and its metabolite HMB. Using [1,2-(13)C2]Leu and [(2)H5]phenylalanine tracers, and GC-MS/GC-C-IRMS we studied the effect of HMB or Leu alone on MPS (by tracer incorporation into myofibrils), and for HMB we also measured muscle proteolysis (by arteriovenous (A-V) dilution). Orally consumed 3.42 g free-acid (FA-HMB) HMB (providing 2.42 g of pure HMB) exhibited rapid bioavailability in plasma and muscle and, similarly to 3.42 g Leu, stimulated muscle protein synthesis (MPS; HMB +70% vs. Leu +110%). While HMB and Leu both increased anabolic signalling (mechanistic target of rapamycin; mTOR), this was more pronounced with Leu (i.e. p70S6K1 signalling 90 min vs. 30 min for HMB). HMB consumption also attenuated muscle protein breakdown (MPB; -57%) in an insulin-independent manner. We conclude that exogenous HMB induces acute muscle anabolism (increased MPS and reduced MPB) albeit perhaps via distinct, and/or additional mechanism(s) to Leu (2.)

References

  1. Free acid gel form of β-hydroxy-β-methylbutyrate (HMB) improves HMB clearance from plasma in human subjects compared with the calcium HMB salt. John C. Fuller, Jr, Rick L. Sharp, Hector F. Angus, Shawn M. Baier, John A. Rathmacher. Br J Nutr. 2011 Feb; 105(3): 367–372. Published online 2010 Dec (https://www.ncbi.nlm.nih.gov/pubmed/21134325)
  2. Effects of leucine and its metabolite β-hydroxy-β-methylbutyrate on human skeletal muscle protein metabolism. D J Wilkinson, T Hossain, D S Hill, B E Phillips, H Crossland, J Williams, P Loughna, T A Churchward-Venne, L Breen, S M Phillips, T Etheridge, J A Rathmacher, K Smith, N J Szewczyk, P J Atherton. J Physiol. 2013 Jun 1; 591(Pt 11): 2911–2923. Published online 2013 Apr (https://www.ncbi.nlm.nih.gov/pubmed/23551944)
  3. Does leucine, leucyl-tRNA, or some metabolite of leucine regulate protein synthesis and degradation in skeletal and cardiac muscle? M. E. Tischler, M. Desautels, A. L. Goldberg. J Biol Chem. 1982 Feb (https://www.ncbi.nlm.nih.gov/pubmed/6915936)
  4. Mechanism of attenuation by beta-hydroxy-beta-methylbutyrate of muscle protein degradation induced by lipopolysaccharide. Steven T. Russell, Michael J. Tisdale. Mol Cell Biochem. 2009 Oct; 330(1-2): 171–179. Published online 2009 Apr (https://www.ncbi.nlm.nih.gov/pubmed/19404720)
  5. Beta-hydroxy-beta-methylbutyrate (HMB) stimulates myogenic cell proliferation, differentiation and survival via the MAPK/ERK and PI3K/Akt pathways. Reut Kornasio, Ingo Riederer, Gillian Butler-Browne, Vincent Mouly, Zehava Uni, Orna Halevy. Biochim Biophys Acta. 2009 May; 1793(5): 755–763. Published online 2009 Jan (https://www.ncbi.nlm.nih.gov/pubmed/19211028)
  6. Effects of nine weeks of beta-hydroxy-beta- methylbutyrate supplementation on strength and body composition in resistance trained men. Jasmine S. Thomson, Patricia E. Watson, David S. Rowlands. J Strength Cond Res. 2009 May (https://www.ncbi.nlm.nih.gov/pubmed/19387396)
  7. The effects of 12 weeks of beta-hydroxy-beta-methylbutyrate free acid supplementation on muscle mass, strength, and power in resistance-trained individuals: a randomized, double-blind, placebo-controlled study. Jacob M. Wilson, Ryan P. Lowery, Jordan M. Joy, J. C. Andersen, Stephanie M. C. Wilson, Jeffrey R. Stout, Nevine Duncan, John C. Fuller, Shawn M. Baier, Marshall A. Naimo, John Rathmacher. Eur J Appl Physiol. 2014 (https://www.ncbi.nlm.nih.gov/pubmed/24599749)
  8. The effect of HMB ingestion on the IGF-I and IGF binding protein response to high intensity military training. Redd et al. 2017. (http://www.growthhormoneigfresearch.com/article/S1096-6374(16)30061-2/fulltext)
  9. Serum insulin-like growth factor-1 and its binding protein-7: potential novel biomarkers for heart failure with preserved ejection fraction. Barroso, M. C., Kramer, F., Greene, S. J., Scheyer, D., Köhler, T., Karoff, M., … Dinh, W. (2016). BMC Cardiovascular Disorders, 16, 199. (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5073807/)
  10. IGFBP7 reduces breast tumor growth by induction of senescence and apoptosis pathways. Tania Benatar, Wenyi Yang, Yutaka Amemiya, Valentina Evdokimova, Harriette Kahn, Claire Holloway, Arun Seth. Breast Cancer Res Treat. 2012 (https://www.ncbi.nlm.nih.gov/pubmed/21997538)
  11. Insulin growth factor binding protein 7 is a novel target to treat dementia. Hope Y. Agbemenyah, Roberto C. Agis-Balboa, Susanne Burkhardt, Ivana Delalle, Andre Fischer. Neurobiol Dis. 2014 (https://www.ncbi.nlm.nih.gov/pubmed/24075854)
  12. Effect of β-hydroxy-β-methylbutyrate Supplementation During Energy Restriction in Female Judo Athletes. Wei Hung et al. Journal of Exercise Science & Fitness 2010. (http://www.sciencedirect.com/science/article/pii/S1728869X1060007X)
  13. Effects of Calcium β-HMB Supplementation During Training on Markers of Catabolism, Body Composition, Strength and Sprint Performance. Kreider et al. WAYNE STATE NUTRITION AND FOOD SCIENCE FACULTY RESEARCH PUBLICATIONS. 2013 (http://digitalcommons.wayne.edu/nfsfrp/7/)
]]>
The Drive To Succeed: Your Brain on Dopamine https://redcon1online.com/your-brain-on-dopamine/ Wed, 15 Feb 2017 05:00:53 +0000 https://redcon1online.com/?p=2389 The Drive To Succeed: Your Brain on Dopamine

Most people are not entirely sure what their cup of coffee does, all they really know is that they need it. Got a tough task ahead? “Let me just make some coffee first…” But what is it that gives coffee its charm? & what is it that Dopamine gives its charm?

Coffee contains the world’s most popular stimulant, caffeine. Caffeine has a whole host of beneficial effects, most notable is its ability to promote wakefulness (adenosine receptor modulator) as well as increased focus, motivation and wellbeing.  These last three benefits stem from the fact that caffeine is effective at increasing the amounts of the neurotransmitter dopamine in the brain. When it comes to experiencing pleasure and motivation, dopamine is the king of neurotransmitters. But what is dopamine really?

What is Dopamine?

Neurotransmitters are your brains messengers. They transmit stimuli across nerve gaps and either elicit inhibitory effects (for example GABA) or stimulating effects (Dopamine). That exhilarating feeling of excitement you can experience from video games? Yes, you can thank dopamine for that. Dopamine is responsible for all feelings of pleasure from the senses, everything from stuffing potato chips to having sex. However, dopamine is not all about enjoyment; it has other benefits too:

Motivation and Concentration: Remember how boring all those classes was back in high school? Ever tried to do something you don’t enjoy just to end up procrastinating for hours? Well, concentration is enhanced when the prefrontal cortex has the right levels of neurotransmitters, and dopamine plays a crucial part in that. When dopamine levels are high, it means you are enjoying what you are doing and often experiencing a state of flow, where things just seem to flow through with ease. In other words, the more dopamine you have when you try to do something, the easier and more focused you will be at the task. When you do something, you really don’t enjoy doing or have a lack of dopamine, that feeling of rather going off to procrastinate comes from your brain seeking more dopamine stimulation. Having a hard time to focus when you are surrounded by a bunch of beautiful ladies? Well, that’s dopamine to flooding your synapses and cueing you to run off and do “other” things.

Drive: without dopamine, there would simply be no wish to do anything, pure apathy. This can clearly be seen in a model of drug addiction, from example stimulants such as cocaine or amphetamine where there is a down-regulation of dopamine receptors. Without the drug, there is no willpower to do much of anything. In other words, in a healthy brain, you can prime yourself for doing tasks more effectively by making sure you take good care of your dopamine levels. Do the most boring tasks when they are at their highest concentrations in the brain, for most people that would be early in the morning just after waking up. Ever heard somebody say that the first 3 hours of your day are considered the most productive? Well, this is why!

Dopamine and Resistance Training: Testosterone and Growth Hormone

Another aspect of dopamine that most would be interested to know about is its effects on hormone levels. Testosterone and dopamine share a relationship in that more of one, also equals more of the other. Both are considered to be highly correlated with sex drive and libido, hence if you suffer from low libido but your hormone levels check out fine? Well, then it is most likely your dopamine that is the problem. We will talk about issues that can arise with fluctuating low dopamine later in the article.

Dopamine boosts the expression of GnRH (gonadotropin releasing hormone) which is the hormone that signals the testes to produce more testosterone. Do doctors check dopamine levels of patients with low testosterone? Unfortunately, not, the medical community is often lagging behind 5-10 years with the research, which is why it is important to educate yourself.

Dopamine is also a reliable booster of growth hormone. Growth hormone is responsible for all tissue growth and healing in the body. Want to build more muscle? More growth hormone will help. However, it is more complicated than just drinking coffee and thinking you will grow an inch on your biceps from the dopamine stimulation.

Dopamine stimulates the production of hormones, but constant dopamine stimulation is not possible since that would desensitize your receptors. However, boosting your dopamine at the right time, such as post workout, can greatly help increase your growth hormone response from the exercise and improve your ability to build muscle. More about this later.

The Side Effects of Low Dopamine Levels

The catch 22 with dopamine is that no matter what you do, it is not possible to keep them consistently elevated. Ever noticed how those 2 shots of expresso feel fantastic the first couple of days, and after that you suddenly find yourself downing 4 in one go to feel anything? Yeah, that’s desensitization talking.

To be able to keep a healthy response to dopamine stimulation, you need to cycle that stimulation. Let’s say you were stranded on a deserted island for 20 years, then all of a sudden you get a whiff of a woman perfume. Yes, that would be enough to get you going, however being surrounded by the most beautiful women in the world 24/7 will eventually bore you, that’s how evolution has created your brain, and it is important to understand.

 

Lack of stimulation will increase sensitivity, and increased stimulation will lower sensitivity, everything is good in moderation! Your brain will always be seeking more stimuli; this is how humans are able to evolve, always chasing the next thing. This is also why consumerism, blockbusters movies and constant high-speed internet porn is slowly sucking out the soul and intelligence of the human race, but we’ll save that one for another article.

Let’s say you’re a coffee addict with a severe gambling problem (this is dopamine related as well), what issues might arise concerning your dopamine?

Low Dopamine Symptoms:
  • Low libido
  • Inability to experience joy or pleasure
  • Depression
  • Memory loss
  • Inability to concentrate
  • Chronic procrastination
  • Fatigue, lethargy

At it’s worst, Parkinson’s Disease is a model of chronically low dopamine levels and even results in disruption of motor functions. Parkinson’s Disease is a condition of continuous degradation of your dopamine receptors and your body’s ability to use dopamine. It is thought to be caused by genetic factors and triggered by poor lifestyle and nutritional choices.

Luckily for most, low dopamine levels are a passing condition that often just last for a short period because of poor lifestyle choices such as overindulgence, chronic stress, overtraining or poor nutrition. Better yet, there are plenty of tools and techniques that can be used to take control of your dopamine, and this is the core subject of this article.

The Dopamine Diet

Dopamine is created from the amino acid Tyrosine which is both available in foods as well as supplements. The body converts Tyrosine into the dopamine precursor L-Dopa which then passes the blood brain barrier and eventually increases dopamine levels in the brain. Many dietary choices can influence neurotransmitter concentrations in the brain. A diet high in carbohydrates and sugars will stimulate dopamine receptors too much and eventually start to desensitize them. It is many researches option that this is how Parkinson’s Disease eventually begins to evolve.

A diet high in healthy fats and protein, however, such as the ketogenic diet, has been seen to optimize the dopamine pathways and be beneficial for your brain. This is why the ketogenic diet is widely known as a diet that comes with profound mental benefits. It is also known to be able to stop seizures, which is a condition of too high sensitivity to dopamine and an inability to control this sensitivity. So the ketogenic diet indeed also has a regulatory action on dopamine pathways both able to increase and decrease transmission.

Also, the specific food choices you make can influence your availability of building blocks for neurotransmitters such as dopamine. The following foods are high in Tyrosine for example:

  • Almonds
  • Apples
  • Avocados
  • Bananas
  • Watermelon
  • Animal products (meat, milk, cheese, etc.)
  • Dark leafy vegetables

Some other notable beverage choices that increase dopamine are:

  • Chocolate
  • Tea
  • Coffee

However, the above beverages mostly influence dopamine by stimulating the brain to produce more, and remember what we discussed before; chronic stimulation eventually results in degradation of receptors and their function. Tea is an interesting one though since it contains a non-essential amino acid called Theanine, which boosts dopamine but is also calming, balancing the stimulating effects of the small amounts of caffeine also present in the plant. This is why tea is not considered a stimulant in most people’s eyes and rather something you drink for relaxation.

 

Probiotics:

There is also research that suggests that the gut microbiome also plays a role in dopamine regulation. As we know the ratio of different microorganism in the gut is dependent on your food choices, where “bad” bacteria often take over and colonize when you feed it lots of junk such as sugar. One of the metabolites of “bad” bacteria’s, lipopolysaccharides, has been shown to cause a reduction in dopamine in the brain. This clearly illustrates the connection between everything in the body as a whole, but many people already experienced this in ways such as digestion related issues during periods of stress. Digestion should have nothing to do with the looming pressure rof that deadline at work right? Wrong.

Mucuna Pruriens:

A recurring superstar in many of our articles here at Redcon1 is the amazing Velvet Bean (Latin, Mucuna Pruriens). The reason why Mucuna is so special is that it is one of the only natural sources of pure L-Dopa. As we mentioned previously, L-Dopa is the primary building block for neurotransmitters such as dopamine and other catecholamine’s (adrenaline, noradrenaline, etc.). Supplementing with Mucuna will directly increase dopamine levels, and it has been extensively studied as a treatment for Parkinson’s Disease.

As we also previously mentioned about dopamine’s ability to stimulate hormone production, the effects of Mucuna on hormones is hence no exception. Mucuna has been shown to both increase growth hormone as well as increase production of testosterone by stimulating the release of luteinizing hormone from the pituitary. This explains Mucuna’s strong effects on increasing libido and also boosting mood and feelings of pleasure. You could view the herb as an overall enhancer of your senses. Mucuna is one of the core ingredients in our sleep formula Fade Out because you guessed it, dopamine also has a function in making sure you get a proper nights rest. Taking Mucuna before bed not only helps increase the length and depth of your sleep, it will also increase your testosterone levels while you sleep!

We also include Mucuna in our nootropic formula Mental Trigger, but more on that in a minute.

Cold Showers, aka James Bond Showers

A very effective way of reversing desensitization is subjecting your brain to more sensations, sensations of cold that is! Bond had it right all along. Cold showers can help you feel more manly, happier and improve your performance and stress tolerance. This works by stimulation of dopaminergic transmission pathways in areas of the brain known as the mesocorticolimbic and nigrostriatal pathways. In other words, it is not by stimulating the receptors themselves, rather, by increasing the stimulating effect of the transmission. Signal strength if you will.

This pathway in the brain is closely rated to emotions and feelings of happiness and wellbeing. We like to explain it simply in this way, if you subject your brain to though challenges such as ice baths, it will grow stronger and this strength translates into other areas of life, such as your emotional wellbeing. Studies have even shown cold showers to be able to treat depression.

Nootropics and Stimulants

Most pharmaceuticals and supplements which are said to boost cognition does that through exerting their effects on the levels of dopamine, dopamine receptors or signal transmission in dopamine pathways. There are many interesting supplements you can use to enhance dopaminergic function, but remember to be careful with stimulants, more is not always better when it comes to stimulation.

The following are our favorite ingredients when it comes to enhancing dopaminergic function in a safe and sustainable way:

Theanine + Caffeine:

If you’re a lover of caffeine, the best gift you can give yourself is a bottle of Theanine. We briefly discussed this amino acid earlier in the article as the substance in tea that makes it less stimulating and more calming. However, don’t get this wrong because Theanine is no sedative. What Theanine does is counteracts the adverse effects of caffeine, such as increased heart rate, jitters, a rise in blood pressure, etc., while still enabling you to maintain the energy and focus you get from it. In other words, it makes everything about caffeine better! We suggest a dose of 100mg-200mg with a strong cup of coffee.

Teacrine:

Talking about tea, here is another amazing compound that comes from a rare variant in the tea genus. Teacrine is the patented name for 1,3, 7, 9-tetramethyluric acid,  a purine type analog found in the Camelia assamica variety of tea plant. What makes Teacrine unique is that it too can provide much of the dopamine stimulating effects of caffeine, but without any of its side effects. It also blocks adenosine receptors in the same way as caffeine and hence, promotes feelings of wakefulness and alertness. However, the absolutely amazing thing that makes Teacrine one of the best stimulants, is that it is entirely void of tolerance. Simply put, you cannot build a tolerance to the effects of Teacrine, which enables you to use it as much as you want! We are huge fans of Teacrine and have included it in our nootropic supplement Mental Trigger, as well as our fat burner product Double Tap.

Noopept:

This is the current absolute superstar in the world of nootropics. Noopept, a peptide derived smart drug that is related to the popular nootropic Piracetam, was researched and developed in Russia. It acts in a similar way to Piracetam, just at an incredible 1000 times the potency. It appears to be able to repair damaged cells and receptor sites which are why similar to Mucuna; it has been researched for use in the treatment of Parkinson’s Disease.  Noopept stimulates dopamine receptors in the brain without causing downregulation. It is a psychostimulant that does not affect other areas of the body such as the heart, with its stimulating action. This makes it a very safe supplement and the perfect core ingredient in a nootropic stack for dopamine function. Noopept is included in our Mental Trigger formula.

]]>
6 Ways To Increase Growth Hormone Levels https://redcon1online.com/6-ways-increase-growth-hormone-levels/ Tue, 14 Feb 2017 05:00:04 +0000 https://redcon1online.com/?p=2257 6 Ways To Increase Growth Hormone Levels

A lot of people know that lifting heavy weights builds muscle, that’s  simple enough. Do you really know what process in the body is responsible for this muscle growth? HGH (human growth hormone) is the hormone in the body that is responsible for the growth of all its tissues. When you get older, your HGH levels naturally start to decline, which is why it becomes harder and harder to maintain and grow muscle mass with age.

If you completely lack HGH in your body, you’ll be suffering from dwarfism. The reason why some people are born as dwarfs is that they lack functioning receptors for HGH in their body, preventing growth. There is also the opposite condition gigantism, where people have too much HGH because of an overactive pituitary gland.

You might think that too much HGH sounds awesome right? Wrong, too much-generalized HGH unrelated to specific muscle growth processes will cause the heart to grow too big, and eventually, you run the risk of a heart attack because the heart outgrows its system. Next time you consider taking large amounts of synthetic HGH injections (somatropin) consider your heart first. HGH injections in normal physiological doses are however safe and an excellent anti-ageing remedy.

To show you just how anabolic of a hormone HGH is, here is the benefits of high HGH levels:

  • Increases insulin sensitivity
  • Inhibits the stress hormone cortisol (anti-catabolic)
  • Stimulates bone growth (healing)
  • Increases core strength
  • Burns fat regardless of exercise
  • Repairs muscle mass and increases protein synthesis (muscle growth)

If you want to make sure you keep your HGH levels at a healthy max or want to reverse the age-related decline, there is many natural treatments and lifestyle changes you can apply to reap these benefits.

Here’s our top 6:

Velvet Bean (Mucuna Pruriens)

Velvet Bean is a natural source of the dopamine precursor L-dopa. L-dopa is usually produced in the body from the amino acid L-tyrosine, which is abundant in foods such as hard cheese and other dairy products. Dopamine is essential for many functions in the body and especially affects mental processes such as focus, motivation, sex drive and ability to experience pleasure from everyday activities. Dopamine is also highly correlated with the hormones testosterone and HGH.

Supplementing with Velvet Bean has been shown to increase levels of testosterone and growth hormone because of its direct effects on dopamine production. Velvet Bean is included in our sleep formula Fade Out.

Body Fat & Intermittent Fasting

The amount of body fat you have is closely related to how much HGH your body can produce. Meaning, the more fat you have, the less HGH you will have. Weight loss is a simple strategy for increasing HGH levels, and one of the best ways to do it is through the use of another HGH increasing strategy, intermittent fasting.

Intermittent fasting is when you limit your daily eating hours within usually an 8-hour window. Meaning, you eat all your daily calories during this time frame. Eating in this way is not only a more natural way to eat (3 meals per day are the invention of an industrialized society, do you think stone age humans could eat like that?), it also helps you burn more fat and keep your insulin levels down. Insulin and HGH are directly correlated, the less insulin you produce, the more HGH you can produce. Persistently high insulin levels are also the source of many modern chronic diseases such as diabetes and obesity.

The following study found that from 3 days of fasting, HGH levels increased over 300%, and after 1 week a massive 1250% increase was seen. This clearly shows that eating less often equals more HGH.

Reduce Simple Sugars

Some bodybuilders are under the impression that you can build muscle eating just about anything, and even though it is true to some degree, you will mess up other processes in your body if you try to bulk on only Twinkies for example. A clean and targeted diet is king for building muscle. As we mentioned previously, insulin levels and HGH are highly correlated. If you want more HGH to maximize your muscle growth, stay away from simple sugars and foods of high glycemic index. Focus on complex carbs and don’t eat too close to bed time. HGH is produced during your sleep, and eating before bed means you will be surfing on a wave of insulin through half of the night, inhibiting HGH.

Whey Protein

A diet high in protein is beneficial not only for your HGH levels but also thyroid hormones and insulin sensitivity. The most popular fitness supplement of all time, Whey protein, is one of the best additions you can include in your diet for naturally maximizing HGH levels.

The following study showed that dairy based protein powders increased levels of IGF-1, helping muscle cells expand and multiply. IGF-1 is a hormone that is highly correlated with HGH levels and responsible for the muscle growth effects of HGH. If you increase HGH, you will also increase IGF-1. Aim for consuming at least 100-150 grams of protein per day. We produce a very high-quality Whey protein powder called Isotope.

Get More Sleep:

As we mentioned above, it is during your sleep that hormones such as HGH and also testosterone are produced. In other words, the more you sleep, the more time you give your body for hormone production. Getting by on 6 hours of sleep or less is a sure way of decreasing your levels of not only HGH, but also testosterone.

Anything that increases your sleep quality or time asleep can hence also be seen as an HGH booster. We suggest trying the following:

 

  • Avoid blue lights 2 hours before bed (computer screens, tv, cell phones etc.)
  • Melatonin (part of our product Fade Out)
  • Don’t consume caffeine too late in the day
  • Keeping a cooler temperature in your bedroom increases sleep quality

Focus On HIIT Workouts

Since exercise triggers growth in the body, exercising is one of the best ways to increase HGH. Of course, the increase is dependent on what kind of exercise you do (yoga won’t reap you any godlike HGH powers). Resistance training and anything form of exercise done with very high intensity are the best since it has the largest hormonal effect. Perform heavy weight lifting sessions with limited rest periods and practice high-intensity sprints and interval training (HIIT). It is important to keep sprints in short high-intensity bursts since endurance like cardio training does your hormones no good (decreases testosterone and growth hormone, catabolic). A good protocol is to replace all your current cardio based training with high-intensity sprints and perform them every day in-between your lifting days.

 

Growth Hormone Levels

Growth Hormone Levels

Growth Hormone Levels

Growth Hormone Levels

Growth Hormone Levels

]]>
RedCon1 – DMHA (2-Aminoisoheptane) https://redcon1online.com/redcon1-dmha/ Mon, 13 Feb 2017 19:26:01 +0000 https://redcon1online.com/?p=2256 RedCon1 – DMHA

I know what you’re thinking and no its not a typo. I meant to title this DMHA and not DMAA. DMHA is slowly being introduced more and more into the market as a somewhat “replacement” for DMAA (which may potentially become a banned substance.) Just as with any ingredient that gets banned, someone much smarter than myself finds a way to replicate it and, in most cases, improve it to allow it to be purchased legally. This article is going to focus on DMHA, its application, its finer details, and some of the literature we have available to us (no matter how somewhat weak that literature may be.)

DMHA (2-Aminoisoheptane) works in a very similar manner to the popular DMAA. From a structural standpoint, DMHA’s structural relations are known as monoamine releasing agents. These are compounds that have the capability of increasing levels of certain monoamines. These are dopamine and noradrenaline. It works by boosting dopamine and noradrenaline uptake while simultaneously slowing down reuptake through activation of trace amine associated receptor 1 (1, 2.) This essentially stops their binding ability to their receptors keeping these monoamines active longer. That is why you have a longer lasting, stimulated effect. Another commonality seen between DMAA and DMHA is the addition of a methyl group on the alpha carbon which limits the effect of monoamine oxidase (MAO), increases the amphiphilic nature of this ingredient, as well as its affinity for the catecholamine transporters (3, 4, 5.) What this means is the compound’s half life will be longer, it will pass through the blood brain barrier much easier, and it will have a greater stimulatory effect overall.

Even of further interest is its classification as an alpha-1 adrenergic. Although the following literature is over fifty years old, it still holds some bearing (as I previously mentioned, the literature on 2-Aminoisoheptane is very sparse and is mostly animal research. But, it is all we have to go off of and learn from so we will utilize what literature we have. Just remember to keep these studies in context.) This first study from Hutcheon et al looked at octylamines and 2-aminoheptane was one of the compounds studied. They summarized the following. In rabbits and cats with breathing depressed by sodium pentobarbitone, 1- amino-octane and 2-amino-octane increased the rate of respiration and the volume of gas moved in and out of the lungs per minute. Second, the ratio of analeptic activity of amphetamine to 1-amino-octane in rabbits was 2.51 ±0.25, and of amphetamine to 2-amino-octane 1.84±0.22. Finally, although 1-amino-octane and 2-amino-octane were less toxic than amphetamine, the therapeutic ratio was still in favor of amphetamine as a respiratory stimulant. The observation that amphetamine was more effective than 1-amino-octane and 2-amino-octane in restoring depressed respirations to normal indicated that the presence of a benzene ring in an amine may be necessary for optimum analeptic activity. It was interesting to find, however, that a liphatic amines possessed as much stimulant activity as they did. Because they were found to have a long duration of action as amphetamine and were less toxic, it is suggested that 1-amino- octane and 2-amino-octane may have a place in the treatment of some cases of respiratory depression. An analeptic should increase the circulations that the removal of the substances which are depressing the vital centers is hastened. Of the drugs used in this study, amphetamine was the most active cardiovascular stimulant, although it was less effective than 1-amino-octane in dilating the coronary vessels. In man,2-aminoheptane and 2-methylaminoheptane were reported to be active circulatory stimulants by Roma-Vega and Adriani (1944), who found that they were effective vasopressor agents in combating hypotension during spinal anesthesia (6, 7.)

Moving beyond that study, we begin to understand how its pharmacology leads it to be the ingredient it is with the list of potential ergogenic aids it is touted to have. Within the Journal of pharmacology and experimental therapeutics, DMHA was shown to increase the pain threshold, raise blood pressure, and increase cardiac rate (8.) This is all again, done in animal studies and needs to be taken with a grain of salt. Anecdotally from the clients I’ve had implement it, it seems that many either metabolize DMAA or DMHA better than the other. I personally cannot tolerate DMAA but experimenting with DMHA has proven to be vastly beneficial. I suggest you exercise caution with this new ingredient and proceed accordingly. Once more literature on humans is available to us, I will be releasing a follow up article.

 

References

  1. Rasmussen, N., & Keizers, P; “History Full Circle: Novel sympathomimetics in supplements” Drug testing and analysis; 2015; Retrieved from http://onlinelibrary.wiley.com/doi/10.1002/dta.1852/abstract
  2. Millan, M; “The role of monoamines in the actions of established and novel antidepressant agents: a critical review”; European Journal of Pharmacology; 500(1): 371-384; 2004. Retrieved from http://www.sciencedirect.com/science/article/pii/S0014299904007472
  3. Sullivan, J., & Tipton, K; “The interactions of monoamine oxidase with some derivatives of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)”; Journal of Neural Transmission, 29: 269-277; 1990. Retrieved from http://www.ncbi.nlm.nih.gov/pubmed/2358804
  4. Vauzour D, Vafeiadou K, Rodriguez-Mateos A, Rendeiro C, and Spencer JPE; “The neuroprotective potential of flavonoids:a multiplicity of effects”; Genes Nutr. 3(3-4): 115–126; 2008. Retrieved from http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2593006/
  5. Svenningsson P, Nomikos GG, Fredholm BB; “The stimulatory action and the development of tolerance to caffeine is associated with alterations in gene expression in specific brain regions”; J Neurosci; 19(10):4011–4022; 1999. Retrieved from http://www.jneurosci.org/content/19/10/4011.full.pdf
  6. Hutcheon, D, McCullough, L; “The Respiratory Stimulant Action of Octylamines”; British Journal of Pharmacology; 7, 42; 1952; Retrieved from http://onlinelibrary.wiley.com/doi/10.1111/j.1476-5381.1952.tb00688.x/pdf
  7. Charlier, R; “Pharmacology of 2-amino-6-methyl-heptane”; Archives internationales de pharmacodynamie et de thérapie; 85(1-2):144-51; January 1951; Retrieved from https://www.ncbi.nlm.nih.gov/pubmed/14820395
  8. Fellows, E; “The pharmacology of 2-amino-6-methylheptane”; The Journal of pharmacology and experimental therapeutics; 90(4):351-8; August 1947; Retrieved from https://www.ncbi.nlm.nih.gov/pubmed/20265812
]]>