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Abliderate AMMO

Have not heard. I thought we were on go for last week, but may have hit a small snag?

I'll try and figure out for you.
 
It's a banner year at the old Bender house. My old man tossed me a carton of smokes and said "Hey, Smoke up Johhny"...but make sure you take your AMMO.

This is a great product to hit belly fat, most especially if you are a drinker.


Invalid Link Removed
 
Well technically its recommended to cycle AbAb so its not surprising here. Looks good, simple dosing schedule
 
Here a quick wiki article for those of us...err, I mean YOU, that like to toss a few back on the weekends.

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Some studies on Emodin, one of the key ingredients:

Inflammation. 2013 Jun 1. [Epub ahead of print]
Therapeutic Effect of Emodin on Collagen-Induced Arthritis in Mice.
Zhu X, Zeng K, Qiu Y, Yan F, Lin C.
Source

Department of Oral and Maxillofacial Surgery, The First Affiliated Hospital, Fujian Medical University, Fuzhou, China.
Abstract

Emodin, an anthraquinone isolated from the Chinese herb Radix et Rhizoma Rhei, has been reported to have anti-inflammatory, antibacterial, and antitumor activities. However, the effect of emodin on collagen-induced arthritis (CIA) has not yet been investigated. The purpose of this study was to investigate whether emodin has a protective effect against collagen-induced arthritis in mice and its possible mechanisms. CIA was induced in mice by immunization with bovine type II collagen. The mice were treated with emodin (5, 10, and 20 mg/kg/day, i.g.) from days 21 to 42 after immunization. The clinical scores and hind paw swelling were evaluated. The expression of prostaglandin E2 (PGE2) and cyclooxygenase-2 (COX-2) in synovial tissues was determined. The levels of tumor necrosis factor alpha (TNF-α) and interleukin-6 (IL-6) in the plasma were measured by enzyme-linked immunosorbent assay. The results showed that emodin treatment significantly alleviated the severity of the disease, based on the reduced hind paw swelling and clinical scores, compared with untreated CIA mice. Comparing with untreated CIA mice, emodin treatment inhibited the levels of TNF-α and IL-6 in the plasma, PGE2 production, and COX-2 protein expression in synovial tissues in a dose manner. In conclusion, our results suggest that anti-inflammatory effects of emodin against collagen-induced arthritis in mice may be due to its ability to inhibit pro-inflammatory mediators. Emodin may be a promising potential therapeutic reagent for arthritis treatment.

PMID:
23729279
[PubMed - as supplied by publisher]

Inhibition comparison for 11b-HSD

Zhongguo Yao Li Xue Bao. 1997 May;18(3):240-4.
Inhibition of 11 beta-hydroxysteroid dehydrogenase obtained from guinea pig kidney by some bioflavonoids and triterpenoids.
Zhang YD, Wang MS.
Source

Department of Pharmacology, Cornell University Medical College, New York, NY 10021, USA.
Abstract
AIM:

To study the inhibitory effect of some bioflavonoids and triterpenoids on 11 beta-hydroxysteroid dehydrogenase (11 beta-OHSD) from guinea pig kidney.
METHOD:

The 11 beta-OHSD of kidney cortex microsomes in addition of cortisol was incubated in the presence of NADP, Triton DF-18, and the test compounds at 37 degrees C for 1 h. The enzyme activity was assayed by measuring the rate of conversion of cortisol to cortisone eluted with HPLC gradient analysis.
RESULTS:

The IC50 (95% confidence limits) values of glycyrrhizic acid, naringenin, fisetin, emodin were 254 (202-320), 336 (270-418), 470 (392-564), and 527 (425-653) mumol.L-1, respectively. The inhibitory effect of oleanolic acid was 2-fold stronger than that of astramembranin I. The mode of action of naringenin was competitive inhibition.
CONCLUSION:

The test compounds inhibited the 11 beta-OHSD in kidney cortex with different potencies as glycyrrhizic acid did.

PMID:
10072942
[PubMed - indexed for MEDLINE
 
The Euphorbia Kansui (recognized also from Absolutely Abliderated) is really the star of the show here. Potency is really off the charts.

Molecules. 2012 Oct 9;17(10):11826-38. doi: 10.3390/molecules171011826.
Inhibition of 11b-HSD1 by tetracyclic triterpenoids from Euphorbia kansui.
Guo J, Zhou LY, He HP, Leng Y, Yang Z, Hao XJ.
Source

Laboratory of Chemical Genomics, School of Chemical Biology and Biotechnology, Peking University Shenzhen Graduate School, Shenzhen 518055, Guangdong, China.
Abstract

The roots of Euphorbia kansui are considered an important traditional folk medicine. In this study the ethanol extracts of E. kansui were investigated. A new tetracyclic triterpenoid, euphane-3b,20-dihydroxy-24-ene, in addition to five known triterpenoids with euphane skeletons were isolated. Their structures were elucidated on the basis of physical and spectral techniques (1D-, 2D-NMR and MS, respectively). Furthermore, these compounds 1-6 exhibited strong inhibitory activity against human 11b-hydroxysteroid dehydrogenase type 1 (11b-HSD1), with IC(50) values of 34.86 nM, 1.115 mM, 16.08 nM, 2.815 nM, 26.47 nM, 15.99 nM, and 41.86 nM, respectively. The docking results show that the ring part of compounds can insert into the hydrophobic core of h11b-HSD1 and the alkane chain orientates toward the outside. The results presented herein provide a scientific explanation for the usage of the E. kansui in clinical treatment of diabetes.

PMID:
23047483
[PubMed - indexed for MEDLINE]
 
Those of you that follow my work, you know I am a big fan of Bitter Melon.

J Steroid Biochem Mol Biol. 2012 Jan;128(1-2):51-5. doi: 10.1016/j.jsbmb.2011.09.003. Epub 2011 Oct 1.
Momordica charantia extract, a herbal remedy for type 2 diabetes, contains a specific 11β-hydroxysteroid dehydrogenase type 1 inhibitor.
Blum A, Loerz C, Martin HJ, Staab-Weijnitz CA, Maser E.
Source

Institute of Toxicology and Pharmacology for Natural Scientists, University Medical School Schleswig-Holstein, Campus Kiel, Kiel, Germany.
Abstract

11β-Hydroxysteroid dehydrogenase type 1 (11β-HSD1) catalyzes the intracellular regeneration of active cortisol from inert cortisone in key metabolic tissues, thus regulating ligand access to glucocorticoid receptors. There is strong evidence that increased adipose 11β-HSD1 activity may be an important aetiological factor in the current obesity and diabetes type 2 epidemics. Hence, inhibition of 11β-HSD1 has emerged as a promising anti-diabetic strategy, a concept that is largely supported by numerous studies in rodent models as well as limited clinical data with prototype inhibitors. Momordica charantia (also known as bitter melon, bitter gourd or karela) is traditionally used for treatment of diabetes in Asia, South America, the Caribbean, and East Africa. In the present study, we show that M. charantia extract capsules contain at least one ingredient with selective 11β-HSD1 inhibitory activity. The finding constitutes an interesting additional explanation for the well-documented anti-diabetic and hypoglycaemic effects of M. charantia.

Copyright © 2011 Elsevier Ltd. All rights reserved.

PMID:
22001161
[PubMed - indexed for MEDLINE]
 
And here we start to cross over into the role of inflammation (central and adipocyte based) in obesity.

J Neuroinflammation. 2011 Jun 3;8:64. doi: 10.1186/1742-2094-8-64.
Momordica charantia (bitter melon) attenuates high-fat diet-associated oxidative stress and neuroinflammation.
Nerurkar PV, Johns LM, Buesa LM, Kipyakwai G, Volper E, Sato R, Shah P, Feher D, Williams PG, Nerurkar VR.
Source

Laboratory of Metabolic Disorders and Alternative Medicine, Department of Molecular Biosciences and Bioengineering, College of Tropical Agriculture and Human Resources, University of Hawaii at Manoa, Honolulu, HI 96822, USA. [email protected]
Abstract
BACKGROUND:

The rising epidemic of obesity is associated with cognitive decline and is considered as one of the major risk factors for neurodegenerative diseases. Neuroinflammation is a critical component in the progression of several neurological and neurodegenerative diseases. Increased metabolic flux to the brain during overnutrition and obesity can orchestrate stress response, blood-brain barrier (BBB) disruption, recruitment of inflammatory immune cells from peripheral blood and microglial cells activation leading to neuroinflammation. The lack of an effective treatment for obesity-associated brain dysfunction may have far-reaching public health ramifications, urgently necessitating the identification of appropriate preventive and therapeutic strategies. The objective of our study was to investigate the neuroprotective effects of Momordica charantia (bitter melon) on high-fat diet (HFD)-associated BBB disruption, stress and neuroinflammatory cytokines.
METHODS:

C57BL/6 female mice were fed HFD with and without bitter melon (BM) for 16 weeks. BBB disruption was analyzed using Evans blue dye. Phosphate-buffered saline (PBS) perfused brains were analyzed for neuroinflammatory markers such as interleukin-22 (IL-22), IL-17R, IL-16, NF-κB1, and glial cells activation markers such as Iba1, CD11b, GFAP and S100β. Additionally, antioxidant enzymes, ER-stress proteins, and stress-resistant transcription factors, sirtuin 1 (Sirt1) and forkhead box class O transcription factor (FoxO) were analyzed using microarray, quantitative real-time RT-PCR, western immunoblotting and enzymatic assays. Systemic inflammation was analyzed using cytokine antibody array.
RESULTS:

BM ameliorated HFD-associated changes in BBB permeability as evident by reduced leakage of Evans blue dye. HFD-induced glial cells activation and expression of neuroinflammatory markers such as NF-κB1, IL-16, IL-22 as well as IL-17R were normalized in the brains of mice supplemented with BM. Similarly, HFD-induced brain oxidative stress was significantly reduced by BM supplementation with a concomitant reduction in FoxO, normalization of Sirt1 protein expression and up-regulation of Sirt3 mRNA expression. Furthermore, plasma antioxidant enzymes and pro-inflammatory cytokines were also normalized in mice fed HFD with BM as compared to HFD-fed mice.
CONCLUSIONS:

Functional foods such as BM offer a unique therapeutic strategy to improve obesity-associated peripheral inflammation and neuroinflammation.

PMID:
21639917
[PubMed - indexed for MEDLINE]
PMCID:
PMC3129574
 
This is a great compound. I'm not going to explain this study too deeply, as this is a brand new area of research for EvoMuse. When I release the full details, you will see.

Note the control of inflammation...




Abstract

Send to:
Eur J Pharmacol. 2013 Jan 5;698(1-3):57-66. doi: 10.1016/j.ejphar.2012.08.013. Epub 2012 Sep 14.
The natural flavonoid galangin inhibits osteoclastic bone destruction and osteoclastogenesis by suppressing NF-κB in collagen-induced arthritis and bone marrow-derived macrophages.
Huh JE, Jung IT, Choi J, Baek YH, Lee JD, Park DS, Choi DY.
Source

Oriental Medicine Research Center for Bone & Joint Disease, East-West Bone & joint Research Institute, Kyung Hee University, 1 Hoegidong, Dongdaemungu, Seoul 130-701, Korea. [email protected]
Abstract

We investigated the effect of galangin, a natural flavonoid, on osteoclastic bone destruction in collagen-induced arthritis and examined the molecular mechanisms by which galangin affects osteoclastogenesis in bone marrow derived macrophages. In mice with collagen-induced arthritis, administration of galangin significantly reduced the arthritis clinical score, edema and severity of disease without toxicity. Interestingly, galangin treatment during a later stage of collagen-induced arthritis, using mice with a higher clinical arthritis score, still significantly slowed the progression of the disease. Extensive cartilage and bone erosive changes as well as synovial inflammation, synovial hyperplasia and pannus formation were dramatically inhibited in arthritic mice treated with galangin. Furthermore, galangin-treated arthritic mice showed a significant reduction in the concentrations of IL-1β, TNF-α and IL-17. We found that galangin inhibited osteoclastogenic factors and osteoclast formation in bone marrow-derived macrophages and osteoblast co-cultured cells, and increased osteoprotegerin (OPG) levels in osteoblasts. Galangin and NF-κB siRNA suppressed RANKL-induced phosphorylation of the c-jun N-terminal kinase (JNK) and p38 mitogen-activated protein kinase (MAPK), but not AKT and extracellular signal-regulated kinase 1/2 (ERK1/2). Also, the JNK inhibitor SP600125 and p38 inhibitor SB203580 reduced RANKL-induced expressions of phospho-c-Jun, c-fos and NFATc1 genes during osteoclast development. In addition, galangin suppressed RANKL-induced phosphorylation of NF-κB, phospho-IκBα, inflammatory cytokines and osteoclast formation in bone marrow-derived macrophages. Our data suggest that galangin prevented osteoclastic bone destruction and osteoclastogenesis in osteoclast precursors as well as in collagen-induced arthritis mice without toxicity via attenuation of RANKL-induced activation of JNK, p38 and NF-κB pathways.

Copyright © 2012. Published by Elsevier B.V.

PMID:
22985747
[PubMed - indexed for MEDLINE]
 
You will also note quite a few uses for Magnolol...

J Pharm Pharmacol. 1994 Apr;46(4):305-9.
A novel 11 beta-hydroxysteroid dehydrogenase inhibitor contained in saiboku-to, a herbal remedy for steroid-dependent bronchial asthma.
Homma M, Oka K, Niitsuma T, Itoh H.
Source

Department of Clinical Pharmacology, Tokyo College of Pharmacy, Japan.
Abstract

To identify the inhibitor of prednisolone metabolism contained in Saiboku-To, we conducted in-vitro experiments of 11 beta-hydroxysteroid dehydrogenase (11 beta-HSD), using rat liver homogenate and cortisol as a typical substrate. We studied the effects of ten herbal constituents on 11 beta-HSD. Five herbal extracts showed inhibitory activity with Glycyrrhiza glabra > Perillae frutescens > Zizyphus vulgaris > Magnolia officinalis > Scutellaria baicalensis. This suggests that unknown 11 beta-HSD inhibitors are contained in four herbs other than G. glabra which contains a known inhibitor, glycyrrhizin (and glycyrrhetinic acid). Seven chemical constituents which have been identified as the major urinary products of Saiboku-To in healthy and asthmatic subjects were studied; magnolol derived from M. officinalis showed the most potent inhibition of the enzyme (IC50, 1.8 x 10(-4) M). Although this activity was less than that of glycyrrhizin, the inhibition mechanism (non-competitive) was different from a known competitive mechanism. These results suggest that magnolol might contribute to the inhibitory effects of Saiboku-To on prednisolone metabolism through inhibition of 11 beta-HSD.

PMID:
8051615
[PubMed - indexed for MEDLINE]
 
These pathways will be addressed in the full writeup....

Mol Nutr Food Res. 2013 Jul 31. doi: 10.1002/mnfr.201300113. [Epub ahead of print]
Long-term supplementation of honokiol and magnolol ameliorates body fat accumulation, insulin resistance, and adipose inflammation in high-fat fed mice.
Kim YJ, Choi MS, Cha BY, Woo JT, Park YB, Kim SR, Jung UJ.
Source

Department of Food Science and Nutrition, Kyungpook National University, Daegu, Republic of Korea.
Abstract
SCOPE:

This study investigated the effect of honokiol (HON) and magnolol (MAG), phenolic compounds in Magnolia plants, on adiposity and adiposity-related metabolic disturbances in mice fed high-fat diet (HFD), and the potential underlying mechanisms focusing on the lipid metabolism and inflammatory response.
METHOD AND RESULTS:

C57BL/6J mice were fed HFD (45 kcal% fat) with or without HON (0.02%, w/w) or MAG (0.02%, w/w) for 16 wk. Despite no changes in body weight, food intake, and hepatic fat accumulation, HON and MAG significantly lowered the weight of white adipose tissue (WAT) as well as adipocyte size and protected against insulin resistance induced by HFD. These effects were associated with increases in energy expenditure and adipose fatty acid oxidation and decreases in fatty acid synthase activity and expression of genes related to fatty acid synthesis, desaturation, and uptake, as well as adipocyte differentiation in WAT. Moreover, HON and MAG significantly lowered the expression of proinflammatory genes in WAT and elevated the plasma IL-10 level. Particularly, HON significantly decreased the plasma resistin level and increased the plasma adiponectin level compared to the control group.
CONCLUSION:

HON and MAG have potential as novel agents for amelioration of adiposity and associated insulin resistance and inflammation.

© 2013 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.
KEYWORDS:

Adipogenesis, Antiobesity, Honokiol, Inflammation, Magnolol

PMID:
23901038
[PubMed - as supplied by publisher]
 
Inflammation. 2012 Jun;35(3):1204-12. doi: 10.1007/s10753-012-9430-0.
Magnolol protects osteoblastic MC3T3-E1 cells against antimycin A-induced cytotoxicity through activation of mitochondrial function.
Choi EM.
Source

Department of Food and Nutrition, Education Graduate School, Kyung Hee University, 1, Hoegi-dong, Dongdaemun-gu, Seoul 130-701, South Korea. [email protected]
Abstract

Antimycin A treatment of cells blocks the mitochondrial electron transport chain and leads to elevated ROS generation. In the present study, we investigated the protective effects of magnolol, a hydroxylated biphenyl compound isolated from Magnolia officinalis, on antimycin A-induced toxicity in osteoblastic MC3T3-E1 cells. Osteoblastic MC3T3-E1 cells were pre-incubated with magnolol before treatment with antimycin A. Cell viability and mineralization of osteoblasts were assessed by MTT assay and Alizarin Red staining, respectively. Mitochondrial dysfunction in cells was measured by mitochondrial membrane potential (MMP), complex IV activity, and ATP level. The cellular antioxidant effect of magnolol in osteoblastic MC3T3-E1 cells was assessed by measuring cardiolipin oxidation, mitochondrial superoxide levels, and nitrotyrosine content. Phosphorylated cAMP-response element-binding protein (CREB ) was evaluated using ELISA assay. Pretreatment with magnolol prior to antimycin A exposure significantly reduced antimycin A-induced osteoblast dysfunction by preventing MMP dissipation, ATP loss, and CREB inactivation. Magnolol also reduced cardiolipin peroxidation, mitochondrial superoxide, and nitrotyrosine production induced by antimycin A. These results suggest that magnolol has a protective effect against antimycin A-induced cell damage by its antioxidant effects and the attenuation of mitochondrial dysfunction. All these data indicate that magnolol may reduce or prevent osteoblast degeneration in osteoporosis or other degenerative disorders.

PMID:
22281543
[PubMed - indexed for MEDLINE]
 
Gotta click the link on this one guys...sorry

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bananaClip said:
dammnnn why do u need to cycle AMMO?
Click to expand...

We usually recommending cycling all our supplements at some point for the same reasons most of us cycle pretty much anything.

This is our oral cortisol control beast. Used as directed it's two months of product for 27 bucks. I think that's a pretty nice deal :) We are well aware some people are going to do their own experiments and stuff (we are all our own guinea pigs after all :))
 
Geoforce said:
We usually recommending cycling all our supplements at some point for the same reasons most of us cycle pretty much anything.

This is our oral cortisol control beast. Used as directed it's two months of product for 27 bucks. I think that's a pretty nice deal :) We are well aware some people are going to do their own experiments and stuff (we are all our own guinea pigs after all :))
Click to expand...


It's 60 caps at 2 a day. Or am I wrong?
 
domore said:
Those two doses weren't on our original label, so I'll check into it. The original doses were 100mg phosphatidylserine and 10mg zinc gluconate.
Click to expand...
Correct. Looks like a typo on the product page.

I would never waste my time or yours with 100mcg of PS.
 
mr.cooper69 said:
Awesome, I love the looks of this. I was more concerned about enough zinc to put me in the hospital :D
Click to expand...

Now where's your adventurous spirit?
 
Another study on Emodin
Keep in mind when reading Emodin studies that this compound has an ATROCIOUS oral availability. This is what took so long, as we were forced to complex it.


Invalid Link Removed

Planta Med. 2012 Jun;78(10):943-50. doi: 10.1055/s-0031-1298626. Epub 2012 Jun 6.
Emodin protects against high-fat diet-induced obesity via regulation of AMP-activated protein kinase pathways in white adipose tissue.
Tzeng TF, Lu HJ, Liou SS, Chang CJ, Liu IM.
Source

Department of Internal Medicine, Pao Chien Hospital, Ping Tung City, Pingtung County, Taiwan. [email protected]
Abstract

Emodin is an active herbal component traditionally used in China for treating a variety of diseases. The aim of this study was to examine the effect of emodin on the reducing lipid accumulation in white adipose tissue of high-fat diet-fed rats, and on the regulation of the expression of the genes involved in lipid metabolism to elucidate the mechanisms. After being fed a high-fat diet for two weeks, rats were dosed orally with emodin (20, 40, 80 mg/kg/day) or pioglitazone (20 mg/kg/day), once daily for eight weeks. Changes in body weight, feeding pattern, serum lipids, coronary artery risk index, and atherogenic index were investigated. Subcutaneous white adipose tissues were isolated for pathology histology and Western blot analyses. Changes of triglyceride accumulation in differentiated 3 T3-L1 adipocytes were also investigated. Emodin exhibited a significant concentration-dependent decrease in the intracellular accumulation of triglyceride in 3 T3-L1 adipocytes. Emodin (80 mg/kg/day) displayed similar characteristics to pioglitazone (20 mg/kg/day) in reducing body weight gain and plasma lipid levels as well as the coronary artery risk and atherogenic indices of high-fat diet-fed rats. Emodin also caused dose related reductions in epididymal white adipose tissue sizes in high-fat diet-fed rats. Emodin and pioglitazone enhanced the phosphorylation of AMP-activated protein kinase and its primary downstream targeting enzyme, acetyl-CoA carboxylase, upregulated gene expression of carnitine palmitoyl transferase 1, and downregulated sterol regulatory element binding protein 1 and fatty acid synthase protein levels in the epididymal white adipose tissue of high-fat diet-fed rats. Our findings suggest that emodin could attenuate lipid accumulation in white adipose tissue through AMP-activated protein kinase activation.

Georg Thieme Verlag KG Stuttgart · New York.

PMID:
22673833
[PubMed - indexed for MEDLINE]
 
Only a Sith deals in Absolutes...much wiser to deal in Abliderates.
 
Down and Dirty...err, Clean
 
bananaClip said:
ammo is safe for females right? can females stack ammo n sleephoria?
Click to expand...

Yes for both questions...safe for all users and safe to stack with Sleephoria.
 
Started AMMO this morning....5/3/1+sprints+ammo=

bye bye belly fat.
 
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