I've got a doctor's appointment on Wednasday and I'd like to fenagle a script for 200mg beza;I'm thinking some studies showing it to be useful for fat loss and more importantly,overall health,would convince him.
Anyone have any abstracts they can post up?
Full Version: Getting an RX for bezafibrate
I'll start posting some tomorrow... In the mean time check out the anabolism thread. I think there are a couple good ones there. That'd be bitch'n if you can pull this off... It'll also be interesting to see what dosage and protocol he recommends if it actually happens.
Colin, you are the true heir to BrooklynJuice and will follow suite if you don't stop what the hell you are doing.
What ever happened to diet and excersize? Immediate gratifiction culture at work...
If you live in the United States it is not available. The only fibric acid derivatives available in the US are fenofibrate and gemfibrozil
QUOTE (Jakeshorts @ Apr 20 2008, 08:50 PM) 
I'll start posting some tomorrow... In the mean time check out the anabolism thread. I think there are a couple good ones there. That'd be bitch'n if you can pull this off... It'll also be interesting to see what dosage and protocol he recommends if it actually happens.
Well,according to nTbonz beza isn'tavailable in the US.
Kinda sucks but gem is safer than beza anyway so if you can hook me up with some bonafide studies on gem for fat loss/health/lipid levels(whatever will make it look on the up and up ) it'd be much appreciated.I'll send you a special secret surprise if you come through on this.
Do you have dyslipidaemia?
QUOTE (GhostfaceKillah @ Apr 21 2008, 02:37 PM)
Do you have dyslipidaemia?
I can't say with certainty but I highly doubt I have this.
Found a couple but nothing so far showing fat loss but these might be enough to convince my doc.
And Jake,the first abstract paints TZD's in a good light so I might be able to kill two birds with one stone,getting a rx for a TZD too would be fucking money.I recall that troglitizone was the money shot of TZD's so I'll try to dig some shit up on that too.
Should We Use PPAR Agonists to Reduce Cardiovascular Risk?
Robinson JG.
Departments of Epidemiology & Medicine, University of Iowa, Iowa City, IA 52242, USA.
Trials of peroxisome proliferator-activated receptor (PPAR) agonists have shown mixed results for cardiovascular prevention. Fibrates are PPAR-alpha agonists that act primarily to improve dyslipidemia. Based on low- and high-density lipoprotein cholesterol (LDL and HDL) effects, gemfibrozil may be of greater cardiovascular benefit than expected, fenofibrate performed about as expected, and bezafibrate performed worse than expected. Increases in both cardiovascular and noncardiovascular serious adverse events have been observed with some fibrates. Thiazolidinediones (TZDs) are PPAR-gamma agonists used to improve impaired glucose metabolism but also influence lipids. Pioglitazone reduces atherosclerotic events in diabetic subjects, but has no net cardiovascular benefit due to increased congestive heart failure risk. Rosiglitazone may increase the risk of atherosclerotic events, and has a net harmful effect on the cardiovascular system when congestive heart failure is included. The primary benefit of TZDs appears to be the prevention of diabetic microvascular complications. Dual PPAR-alpha/gamma agonists have had unacceptable adverse effects but more selective agents are in development. PPAR-delta and pan-agonists are also in development. It will be imperative to prove that future PPAR agonists not only prevent atherosclerotic events but also result in a net reduction on total cardiovascular events without significant noncardiovascular adverse effects with long-term use.
PMID: 18288293
Relative safety of gemfibrozil and fenofibrate in the absence of concomitant cerivastatin use.
Holoshitz N, Alsheikh-Ali AA, Karas RH.
Molecular Cardiology Research Institute and Division of Cardiology, Department of Medicine, Tufts-New England Medical Center and Tufts University School of Medicine, Boston, Massachusetts, USA.
Previous analyses of fibrate safety may have been driven by a higher propensity for gemfibrozil to interact with cerivastatin, which is currently off the market because of safety concerns. We reviewed gemfibrozil- and fenofibrate-associated adverse event reports (AERs) submitted to the US Food and Drug Administration over a 5-year period. To control for cerivastatin's impact on fibrate-associated AERs, reports with concomitant cerivastatin use were excluded. Rates per million prescriptions were calculated for all AERs, serious AERs, rhabdomyolysis AERs, muscle-related AERs without rhabdomyolysis, and liver AERs. The rates of all AERs (odds ratio [OR] 0.76, 95% confidence interval [CI] 0.69 to 0.83), serious AERs (OR 0.72, 95% CI 0.65 to 0.81), and liver AERs (OR 0.37, 95% CI 0.28 to 0.50) were significantly lower for gemfibrozil compared with fenofibrate (p <0.001 for each). In contrast, rates of rhabdomyolysis AERs (OR 2.67, 95% CI 2.11 to 3.39, p <0.001) and muscle-related AERs without rhabdomyolysis (OR 1.36, 95% CI 1.12 to 1.71, p = 0.002) were significantly higher for gemfibrozil compared with fenofibrate. In conclusion, the safety profiles of fibrates differ, with a higher rate of liver-related AERs associated with fenofibrate and a higher rate of muscle-related AERs associated with gemfibrozil. Rates of all AERs and serious AERs were higher with fenofibrate, but well within the range observed with commonly used lipid-altering medications.
PMID: 18157972
Peroxisome proliferator-activated receptors (PPARs) and the human skin: importance of PPARs in skin physiology and dermatologic diseases.
Sertznig P, Seifert M, Tilgen W, Reichrath J.
Department of Dermatology, The Saarland University Hospital, Homburg/Saar, Germany.
Peroxisome proliferator-activated receptors (PPARs) are members of the nuclear receptor superfamily that regulate lipid, glucose, and amino acid metabolism. More recently, PPARs and corresponding ligands have been shown in skin and other organs to regulate important cellular functions, including cell proliferation and differentiation, as well as inflammatory responses. These new functions identify PPARs and corresponding ligands as potential targets for the treatment of various skin diseases and other disorders.It has been shown that in inflammatory skin disorders, including hyperproliferative psoriatic epidermis and the skin of patients with atopic dermatitis, the expression of both PPARalpha and PPARgamma is decreased. This observation suggests the possibility that PPARalpha and PPARgamma activators, or compounds that positively regulate PPAR gene expression, may represent novel NSAIDs for the topical or systemic treatment of common inflammatory skin diseases such as atopic dermatitis, psoriasis, and allergic contact dermatitis. Moreover, recent findings indicate that PPAR-signaling pathways may act as a promising therapeutic target for the treatment of hyperproliferative skin diseases including skin malignancies. Studies in non-diabetic patients suggest that oral thiazolidinediones, which are synthetic ligands of PPARgamma, not only exert an antidiabetic effect but also may be beneficial for moderate chronic plaque psoriasis by suppressing proliferation and inducing differentiation of keratinocytes; furthermore, they may even induce cell growth arrest, apoptosis, and terminal differentiation in various human malignant tumors. It has been reported that PPARalpha immunoreactivity is reduced in human keratinocytes of squamous cell carcinoma (SCC) and actinic keratosis (AK), while PPARdelta appears to be upregulated. Additionally, the microvessel density is significantly higher in AK and SCC that express high levels of PPARdelta. PPARdelta has been demonstrated to have an anti-apoptotic role and to maintain survival and differentiation of epithelial cells, whereas PPARalpha and PPARgamma activators induce differentiation and inhibit proliferation and regulate apoptosis. In melanoma, the growth inhibitory effect of PPARgamma activation is independent of apoptosis and seems to occur primarily through induction of cell cycle arrest in the G1 phase of the cell cycle or induction of re-differentiation. PPARalpha activation causes inhibition of migration of melanoma cells and anchorage-independent growth, whereas primary tumor growth remains unaltered. In clinical trials of gemfibrozil, a PPARalpha ligand, significantly fewer patients treated with this lipid-lowering drug were diagnosed with melanoma as compared to those in the control group.In conclusion, an increasing body of evidence indicates that PPAR signaling pathways may represent interesting therapeutic targets for a broad variety of skin disorders, including inflammatory skin diseases such as psoriasis and atopic dermatitis, and skin malignancies.
PMID: 18092840
Trog,this is just ref for me to print shit out later:
Troglitazone up-regulates vascular endothelial argininosuccinate synthase.
Goodwin BL, Corbin KD, Pendleton LC, Levy MM, Solomonson LP, Eichler DC.
Department of Molecular Medicine, College of Medicine, University of South Florida, 12901 Bruce B. Downs Boulevard, MDC Box 7, Tampa, FL 33612-4799, USA; Johnnie B. Byrd, Sr. Alzheimer’s Center and Research Institute, University of South Florida, Tampa, FL 33612, USA.
Vascular endothelial nitric oxide (NO) production via the citrulline-NO cycle not only involves the regulation of endothelial nitric oxide synthase (eNOS), but also regulation of caveolar-localized endothelial argininosuccinate synthase (AS), which catalyzes the rate-limiting step of the cycle. In the present study, we demonstrated that exposure of endothelial cells to troglitazone coordinately induced AS expression and NO production. Western blot analysis demonstrated an increase in AS protein expression. This increased expression was due to transcriptional upregulation of AS mRNA, as determined by quantitative real time RT-PCR and inhibition by 1-d-ribofuranosylbenzimidazole (DRB), a transcriptional inhibitor. Reporter gene assays and EMSA analyses identified a distal PPARgamma response element (PPRE) (-2471 to -2458) that mediated the troglitazone increase in AS expression. Overall, this study defines a novel molecular mechanism through which a thiazolidinedione (TZD) like troglitazone supports endothelial function via the transcriptional up-regulation of AS expression.
PMID: 18375203
Role of PPAR in cardiovascular diseases.
Das SK, Chakrabarti R.
Metabolic Disorders Group, Dr. Reddy's Lab, Discovery Research, Bollaram Road, Miyapur, Hyderabad 500049, India. saibal99@yahoo.com
Cardiovascular disease (CVD) is the most critical global health threat, which contributes more than one third of global morbidity. CVD includes heart disease, vascular disease, atherosclerosis, stroke and hypertension. The most important independent risk factors for CVD include dyslipidemia along with hypertension, obesity, sedentary lifestyle, diabetes and chronic inflammation. These factors are directly regulated by diet, metabolism and physical activity. Diets rich in fat and carbohydrate coupled to sedentary lifestyles have contributed to the increase in dyslipidemia, type 2 diabetes, obesity and CVD in the world. Discovery of Peroxisome Proliferator Activated Receptors (PPARs) as a key regulator of metabolic pathways has led to significant insight into the mechanisms regulating these processes. Three PPAR subtypes, encoded by distinct genes, are designated as PPAR-alpha, PPAR-delta (also know as beta) and PPAR-gamma. PPARs act as nutritional sensors that regulate a variety of homeostatic functions including metabolism, inflammation and development. PPAR-alpha is the main metabolic regulator for catabolism whereas PPAR-gamma regulates anabolism or storage. PPARs are expressed in the cardiovascular system such as endothelial cells, vascular smooth muscle cells and monocytes/macrophages. It has been shown that they play an important role in the modulation of inflammatory, fibrotic and hypertrophic responses. In 1997, a Glaxo patent described that Troglitazone (first PPAR-gamma ligand to reach market) reduced TNF-induced VCAM1 expression in HUVECs indicating the potential benefit in atherosclerosis. A series of patents from Eli Lilly and Dr. Reddy's Laboratories Ltd. between 1999 and 2005 described a variety of PPAR-alpha and -alpha,gamma dual ligands in a number of patents having glucose, triglyceride, cholesterol lowering, HDL elevating and body weight reducing activity. Patents from Metabolex and Tularik in 2001 and 2002 described the beneficial effects of SPPARM molecules for insulin resistance and diabetes, without showing concern on PPAR-gamma related side effects such as edema and body weight. GSK and Takeda described the potential effects of PPAR-delta modulators during 2001 to 2004 in few patents. Several clinical and preclinical studies have demonstrated the beneficial effects of PPAR ligands on various cardiovascular risk factors. This review intends to capture some of the key studies in this area as is described in some recent patents and literature.
PMID: 18221086
And Jake,the first abstract paints TZD's in a good light so I might be able to kill two birds with one stone,getting a rx for a TZD too would be fucking money.I recall that troglitizone was the money shot of TZD's so I'll try to dig some shit up on that too.
Should We Use PPAR Agonists to Reduce Cardiovascular Risk?
Robinson JG.
Departments of Epidemiology & Medicine, University of Iowa, Iowa City, IA 52242, USA.
Trials of peroxisome proliferator-activated receptor (PPAR) agonists have shown mixed results for cardiovascular prevention. Fibrates are PPAR-alpha agonists that act primarily to improve dyslipidemia. Based on low- and high-density lipoprotein cholesterol (LDL and HDL) effects, gemfibrozil may be of greater cardiovascular benefit than expected, fenofibrate performed about as expected, and bezafibrate performed worse than expected. Increases in both cardiovascular and noncardiovascular serious adverse events have been observed with some fibrates. Thiazolidinediones (TZDs) are PPAR-gamma agonists used to improve impaired glucose metabolism but also influence lipids. Pioglitazone reduces atherosclerotic events in diabetic subjects, but has no net cardiovascular benefit due to increased congestive heart failure risk. Rosiglitazone may increase the risk of atherosclerotic events, and has a net harmful effect on the cardiovascular system when congestive heart failure is included. The primary benefit of TZDs appears to be the prevention of diabetic microvascular complications. Dual PPAR-alpha/gamma agonists have had unacceptable adverse effects but more selective agents are in development. PPAR-delta and pan-agonists are also in development. It will be imperative to prove that future PPAR agonists not only prevent atherosclerotic events but also result in a net reduction on total cardiovascular events without significant noncardiovascular adverse effects with long-term use.
PMID: 18288293
Relative safety of gemfibrozil and fenofibrate in the absence of concomitant cerivastatin use.
Holoshitz N, Alsheikh-Ali AA, Karas RH.
Molecular Cardiology Research Institute and Division of Cardiology, Department of Medicine, Tufts-New England Medical Center and Tufts University School of Medicine, Boston, Massachusetts, USA.
Previous analyses of fibrate safety may have been driven by a higher propensity for gemfibrozil to interact with cerivastatin, which is currently off the market because of safety concerns. We reviewed gemfibrozil- and fenofibrate-associated adverse event reports (AERs) submitted to the US Food and Drug Administration over a 5-year period. To control for cerivastatin's impact on fibrate-associated AERs, reports with concomitant cerivastatin use were excluded. Rates per million prescriptions were calculated for all AERs, serious AERs, rhabdomyolysis AERs, muscle-related AERs without rhabdomyolysis, and liver AERs. The rates of all AERs (odds ratio [OR] 0.76, 95% confidence interval [CI] 0.69 to 0.83), serious AERs (OR 0.72, 95% CI 0.65 to 0.81), and liver AERs (OR 0.37, 95% CI 0.28 to 0.50) were significantly lower for gemfibrozil compared with fenofibrate (p <0.001 for each). In contrast, rates of rhabdomyolysis AERs (OR 2.67, 95% CI 2.11 to 3.39, p <0.001) and muscle-related AERs without rhabdomyolysis (OR 1.36, 95% CI 1.12 to 1.71, p = 0.002) were significantly higher for gemfibrozil compared with fenofibrate. In conclusion, the safety profiles of fibrates differ, with a higher rate of liver-related AERs associated with fenofibrate and a higher rate of muscle-related AERs associated with gemfibrozil. Rates of all AERs and serious AERs were higher with fenofibrate, but well within the range observed with commonly used lipid-altering medications.
PMID: 18157972
Peroxisome proliferator-activated receptors (PPARs) and the human skin: importance of PPARs in skin physiology and dermatologic diseases.
Sertznig P, Seifert M, Tilgen W, Reichrath J.
Department of Dermatology, The Saarland University Hospital, Homburg/Saar, Germany.
Peroxisome proliferator-activated receptors (PPARs) are members of the nuclear receptor superfamily that regulate lipid, glucose, and amino acid metabolism. More recently, PPARs and corresponding ligands have been shown in skin and other organs to regulate important cellular functions, including cell proliferation and differentiation, as well as inflammatory responses. These new functions identify PPARs and corresponding ligands as potential targets for the treatment of various skin diseases and other disorders.It has been shown that in inflammatory skin disorders, including hyperproliferative psoriatic epidermis and the skin of patients with atopic dermatitis, the expression of both PPARalpha and PPARgamma is decreased. This observation suggests the possibility that PPARalpha and PPARgamma activators, or compounds that positively regulate PPAR gene expression, may represent novel NSAIDs for the topical or systemic treatment of common inflammatory skin diseases such as atopic dermatitis, psoriasis, and allergic contact dermatitis. Moreover, recent findings indicate that PPAR-signaling pathways may act as a promising therapeutic target for the treatment of hyperproliferative skin diseases including skin malignancies. Studies in non-diabetic patients suggest that oral thiazolidinediones, which are synthetic ligands of PPARgamma, not only exert an antidiabetic effect but also may be beneficial for moderate chronic plaque psoriasis by suppressing proliferation and inducing differentiation of keratinocytes; furthermore, they may even induce cell growth arrest, apoptosis, and terminal differentiation in various human malignant tumors. It has been reported that PPARalpha immunoreactivity is reduced in human keratinocytes of squamous cell carcinoma (SCC) and actinic keratosis (AK), while PPARdelta appears to be upregulated. Additionally, the microvessel density is significantly higher in AK and SCC that express high levels of PPARdelta. PPARdelta has been demonstrated to have an anti-apoptotic role and to maintain survival and differentiation of epithelial cells, whereas PPARalpha and PPARgamma activators induce differentiation and inhibit proliferation and regulate apoptosis. In melanoma, the growth inhibitory effect of PPARgamma activation is independent of apoptosis and seems to occur primarily through induction of cell cycle arrest in the G1 phase of the cell cycle or induction of re-differentiation. PPARalpha activation causes inhibition of migration of melanoma cells and anchorage-independent growth, whereas primary tumor growth remains unaltered. In clinical trials of gemfibrozil, a PPARalpha ligand, significantly fewer patients treated with this lipid-lowering drug were diagnosed with melanoma as compared to those in the control group.In conclusion, an increasing body of evidence indicates that PPAR signaling pathways may represent interesting therapeutic targets for a broad variety of skin disorders, including inflammatory skin diseases such as psoriasis and atopic dermatitis, and skin malignancies.
PMID: 18092840
Trog,this is just ref for me to print shit out later:
Troglitazone up-regulates vascular endothelial argininosuccinate synthase.
Goodwin BL, Corbin KD, Pendleton LC, Levy MM, Solomonson LP, Eichler DC.
Department of Molecular Medicine, College of Medicine, University of South Florida, 12901 Bruce B. Downs Boulevard, MDC Box 7, Tampa, FL 33612-4799, USA; Johnnie B. Byrd, Sr. Alzheimer’s Center and Research Institute, University of South Florida, Tampa, FL 33612, USA.
Vascular endothelial nitric oxide (NO) production via the citrulline-NO cycle not only involves the regulation of endothelial nitric oxide synthase (eNOS), but also regulation of caveolar-localized endothelial argininosuccinate synthase (AS), which catalyzes the rate-limiting step of the cycle. In the present study, we demonstrated that exposure of endothelial cells to troglitazone coordinately induced AS expression and NO production. Western blot analysis demonstrated an increase in AS protein expression. This increased expression was due to transcriptional upregulation of AS mRNA, as determined by quantitative real time RT-PCR and inhibition by 1-d-ribofuranosylbenzimidazole (DRB), a transcriptional inhibitor. Reporter gene assays and EMSA analyses identified a distal PPARgamma response element (PPRE) (-2471 to -2458) that mediated the troglitazone increase in AS expression. Overall, this study defines a novel molecular mechanism through which a thiazolidinedione (TZD) like troglitazone supports endothelial function via the transcriptional up-regulation of AS expression.
PMID: 18375203
Role of PPAR in cardiovascular diseases.
Das SK, Chakrabarti R.
Metabolic Disorders Group, Dr. Reddy's Lab, Discovery Research, Bollaram Road, Miyapur, Hyderabad 500049, India. saibal99@yahoo.com
Cardiovascular disease (CVD) is the most critical global health threat, which contributes more than one third of global morbidity. CVD includes heart disease, vascular disease, atherosclerosis, stroke and hypertension. The most important independent risk factors for CVD include dyslipidemia along with hypertension, obesity, sedentary lifestyle, diabetes and chronic inflammation. These factors are directly regulated by diet, metabolism and physical activity. Diets rich in fat and carbohydrate coupled to sedentary lifestyles have contributed to the increase in dyslipidemia, type 2 diabetes, obesity and CVD in the world. Discovery of Peroxisome Proliferator Activated Receptors (PPARs) as a key regulator of metabolic pathways has led to significant insight into the mechanisms regulating these processes. Three PPAR subtypes, encoded by distinct genes, are designated as PPAR-alpha, PPAR-delta (also know as beta) and PPAR-gamma. PPARs act as nutritional sensors that regulate a variety of homeostatic functions including metabolism, inflammation and development. PPAR-alpha is the main metabolic regulator for catabolism whereas PPAR-gamma regulates anabolism or storage. PPARs are expressed in the cardiovascular system such as endothelial cells, vascular smooth muscle cells and monocytes/macrophages. It has been shown that they play an important role in the modulation of inflammatory, fibrotic and hypertrophic responses. In 1997, a Glaxo patent described that Troglitazone (first PPAR-gamma ligand to reach market) reduced TNF-induced VCAM1 expression in HUVECs indicating the potential benefit in atherosclerosis. A series of patents from Eli Lilly and Dr. Reddy's Laboratories Ltd. between 1999 and 2005 described a variety of PPAR-alpha and -alpha,gamma dual ligands in a number of patents having glucose, triglyceride, cholesterol lowering, HDL elevating and body weight reducing activity. Patents from Metabolex and Tularik in 2001 and 2002 described the beneficial effects of SPPARM molecules for insulin resistance and diabetes, without showing concern on PPAR-gamma related side effects such as edema and body weight. GSK and Takeda described the potential effects of PPAR-delta modulators during 2001 to 2004 in few patents. Several clinical and preclinical studies have demonstrated the beneficial effects of PPAR ligands on various cardiovascular risk factors. This review intends to capture some of the key studies in this area as is described in some recent patents and literature.
PMID: 18221086
Just get it overseas. I'm sure it's relatively cheap and customs would see it's as "cholesterol treatment" medication.
Or drive to Canada or something.
Or drive to Canada or something.
Colin I agree with Liorrh
I heard of some Avnat lab somewhere selling some-kinda liquid sesame seeds or something that did something similar...
Something
Something
sesamin isn't even close to as strong as Beza.
FYI - I wouldn't use TZD without beza. TZD will induce weight gain in a big way without beza.
I'll see what i can do about gem.
FYI - I wouldn't use TZD without beza. TZD will induce weight gain in a big way without beza.
I'll see what i can do about gem.
QUOTE (Colin @ Apr 21 2008, 08:40 PM)
I can't say with certainty but I highly doubt I have this.
You could always take Superdrol/M1T/Havoc for a few days prior to getting a blood test, and I suspect your HDL will be less than stellar.
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