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PGF2a in adipose tissue in love handles?
- Thread starter bigtasty25
- Start date
Dr James Daemon
New member
As for the legal status of PGF in the US- Not sure, I don't live there!Anthony would probably be the best person to ask about that.
As for "I call bullshit". I get this all the time. Its funny for me. Really funny. It means- "I've never heard of anyone doing it, so it must be rubbish" kind of the same mentality that causes superstion etc.
Anyway- Years and years ago, probably before many of you even dreamed of touching Deca, IP labs, made a product called Superclen, which he still makes to this day. Now (Children!
) we were cottening onto the idea that Clen caused massive b2 receptor degradation, rendering each successive dose less effective- this why you hear about 2 days on, 2 off etc. Well, being the clever sods we were, we noted that UK doctors administered a substance called Ketotifen to asthmatics, alongside salbutamol (structurally Clen, but with a shorter half life- similra relationship of T3 - T4 on a mcg for mcg potency basis, but with an inverse realtionship for half life!) but no-one had realised why. Even the texts that I later made an update on were stumped (Pharmacology-ritter dale,rang-2000), they said the reason for it is unclear. Well the reason is, as youve probably guessed, that it allowed receptors to regenerate, allowing a virtually consistant dose to be administered for long periods.
So, IP Made a version of clen called superclen, which contained 500mcg of clen, with 10mg of ketotifen, which is (If memory serves) an antihistamine and makes you very sleepy. He sold alot because most people needed only a quarter of a tab a day to get the shakes, and it sold for $1 a tab, do the maths.
He withdrew it though because there was always some pratt who thought "Its not really that strong, it cant be, because Ive never heard of it etcetc" and received loads of complaints.
Someone in England Had realised the virtue of these magic pills and invested in a few. He has been on them ever since, and can tolerate a full tab or more. Ive seen someone on DNP take 4 and not shake at all (because of the DNP)
So even more unbeleviable, is as within the first 1 minutes after administration of a b2 agonist, up to 90% of the recptors can dissapear, so just imagine the effect of the two combined.
He now makes a 200mcg version and sells ketotifen seperatley.
Ive been on it for longer than most have been on gear- so if you take into account that, its not really unbeleivable- its called "Attenuation", I beleive.
Hope that clears that up!
As for "I call bullshit". I get this all the time. Its funny for me. Really funny. It means- "I've never heard of anyone doing it, so it must be rubbish" kind of the same mentality that causes superstion etc.
Anyway- Years and years ago, probably before many of you even dreamed of touching Deca, IP labs, made a product called Superclen, which he still makes to this day. Now (Children!
) we were cottening onto the idea that Clen caused massive b2 receptor degradation, rendering each successive dose less effective- this why you hear about 2 days on, 2 off etc. Well, being the clever sods we were, we noted that UK doctors administered a substance called Ketotifen to asthmatics, alongside salbutamol (structurally Clen, but with a shorter half life- similra relationship of T3 - T4 on a mcg for mcg potency basis, but with an inverse realtionship for half life!) but no-one had realised why. Even the texts that I later made an update on were stumped (Pharmacology-ritter dale,rang-2000), they said the reason for it is unclear. Well the reason is, as youve probably guessed, that it allowed receptors to regenerate, allowing a virtually consistant dose to be administered for long periods.So, IP Made a version of clen called superclen, which contained 500mcg of clen, with 10mg of ketotifen, which is (If memory serves) an antihistamine and makes you very sleepy. He sold alot because most people needed only a quarter of a tab a day to get the shakes, and it sold for $1 a tab, do the maths.
He withdrew it though because there was always some pratt who thought "Its not really that strong, it cant be, because Ive never heard of it etcetc" and received loads of complaints.
Someone in England Had realised the virtue of these magic pills and invested in a few. He has been on them ever since, and can tolerate a full tab or more. Ive seen someone on DNP take 4 and not shake at all (because of the DNP)
So even more unbeleviable, is as within the first 1 minutes after administration of a b2 agonist, up to 90% of the recptors can dissapear, so just imagine the effect of the two combined.
He now makes a 200mcg version and sells ketotifen seperatley.
Ive been on it for longer than most have been on gear- so if you take into account that, its not really unbeleivable- its called "Attenuation", I beleive.
Hope that clears that up!
Dr James Daemon
New member
Why,why why-(delila?!)
Hi- This is a cut and paste:
QFS Dinoprost-Gel Transdermal Fat Reduction PGF-2a
QFS Dinoprost-Gel, Transdermal Fat Reduction active ingredients
Dinoprost Tromethamine 150mg ( Prostraglandin F2 alpha) and Dimethylsulfoxide (DMSO 25%)
Prostaglandin F2alpha is a potent inhibitor of adipocyte precursor differentiation and a physiological negative modulator of adipocyte function (ie triglyceride accumulation) through stimulation of transforming growth factor-alpha mRNA expression. It initiates a cascade of effects in the adipoctes which have physiological importance to reducing the size and it appears number of mature cells,long after PGf-2a is cleared from the system
Mature adipose cells only shrink in size in response to restricted caloric intake or increased metabolic demand. Before now the only method of reducing the number of fat cells was liposuction. It now appears that Pgf-2a applied topically can have the same same effecst as diet and liposuction. Pgf-2a can reduce the size of mature adipocytes and the number of mature adipocytes through negative modulation and reversing the process of differentiation
There are no studies on topical application. DMSO does carry PGF-2a through the dermal layers and the low concentration spread over a large area is ideal for the intended purpose. One cannot spread PGf-2a (or anyother substance) over the surface area that one can with DMSO topical application. The idea being that you need to interact as many molecules of PGF-2a with as many mature fat cells as possible. The biggest asset to DMSO as a carrier is the ability to spread the PGF-2a applicatiion over a large surface area, thereby maximising the interactuion of the number PGF-2a molucules with the maximum number of fat cells. This is where the DMOS method really shines. QFS is not masking the smell of the DMSO. It is not that bad and goes away in about 5 minutes.
It is important to remember that dinoprost tromethamine does not burn the released fatty acids, aerobic exercise and or T3 will take care of that. PGF-2a only changes the way fats are stored and the formation and function of adipose tissue. As well I find that about half of the time I feel a tickle in the back of my throat and sometimes I have a full out cou***ng fit. This says to me that I have applied a good dosage.
Here are some studies that support PGF-2a and negative modulation of adipose tissue.
Endocrinology 1995 Aug;136(8):3222-9
Prostaglandin F2 alpha stimulates transforming growth factor-alpha expression in adipocyte precursors.
Lepak NM, Serrero G.
W. Alton Jones Cell Science Center, Inc., Lake Placid, New York 12946, USA.
Transforming growth factor-alpha (TGF alpha) and prostaglandin F2 alpha (PGF2 alpha) are potent inhibitors of adipocyte differentiation. We demonstrate here that TGF alpha messenger RNA (mRNA) is expressed in freshly isolated fat pads and in primary culture of adipocyte precursors cultivated in defined medium before and after differentiation. We show that PGF2 alpha stimulated TGF alpha mRNA expression in a dose-dependent manner. PGF2 alpha also stimulated TGF alpha production in the culture medium of adipocyte precursors in primary culture. PGF2 alpha stimulated TGF alpha mRNA expression in both undifferentiated and differentiated cells. 9 alpha,11 beta-PGF2 alpha, which also inhibited adipose differentiation, stimulated TGF alpha mRNA expression similarly to PGF2 alpha, whereas other PGs had no effect on TGF alpha mRNA expression. The time-course experiment indicates that the stimulation of TGF alpha mRNA expression by PGF2 alpha is observed within 6 h of exposure to PGF2 alpha and is inhibited by treatment of the cells with actinomycin D. The effect of PGF2 alpha on TGF alpha expression did not require activation of protein kinase C and was fully reversible. As both TGF alpha and PGF2 alpha are inhibitors of adipose differentiation, it is suggested that stimulation of TGF alpha expression by PGF2 alpha could represent an amplification mechanism to modulate adipocyte precursor differentiation and adipocyte function within the adipose tissue.
Int J Obes Relat Metab Disord 1996 Mar;20 Suppl 3:S58-64 R
Endocrine and paracrine negative regulators of adipose differentiation.
Serrero G, Lepak N.
W Alton Jones Cell Science Center, Inc, Lake Placid, NY 12946, USA.
Obesity which is characterized by an abnormal adipose tissue development is a first degree public health hazard in industrialized countries. One important aspect in the study of adipose tissue development is to investigate the hormonal control of proliferation and differentiation. Any qualitative or quantitative change in these hormones or their receptors can result in abnormalities in the process of proliferation and/or differentiation possibly leading to obesity. Therefore, it is important to identify these factors and investigate their mechanism of action. We have concentrated our efforts in the study of factors triggering differentiation (positive regulators) and also of factors inhibiting differentiation (negative regulators). The present paper provides evidence of the importance of EGF/TGF-alpha and of PGF2 alpha as differentiation inhibitors for adipocyte precursors in primary culture. Data presented here also demonstrate that TGF-alpha is expressed in adipose tissue and that its expression is specifically stimulated by PGF2 alpha, thus suggesting the existence of an amplification mechanism between two differentiation inhibitors within the adipose tissue. The importance of these two types of differentiation inhibitors in the regulation of adipose tissue development is discussed.
-------------------------
I should mention a few points- Authors account of bronchoconstriction is indeed consistent with a good dose. This is one of the reasons to stack with with a bronchodilator such as Clenbuterol, or as mentioned in another thread by Anthony, Albuterol (which has a relationship to clen much akin to T4- T3. We get salbutamol inhalers over here and pre training there great- you do need a higher dose (( see previous t4/t3 statement)) but its over before the shakes start to piss you off!) as it prevents this becoming a problem.
The other IMO is the relative futility, both pharmacoldynamically, and financially of using
a) PGF2 and
b) PGF2 Transdermally.
Please allow me to elucidate! (ive been dying to use that word for a while now)
PGF2 according to the literature, is effective in doses of 1mg.
The first experimental dose of PGCL sent to me by IP was ( 75mcg per ml) effective in 15mcg. Anybody unfamiliar with the difference- simply move the decimal place.
1mg= 1000mcg.
And its cheaper.
Point a pt2: The new version of PGCL is 500mcg per ml and retails for $30.
Point b: Here you have a drug that not only will burn fat systemically. I know Ive said it before, But if you look at my pictures posted in this thread and my avatar ( which I will get resized so you can actually see what I look like) I am even leaner than that now. The drug will affect you systemically- its as simple as that. As I type this one hour 40 minutes after a bicep shot, Im sitting here in the freezing cold UK with sweat running off my forehead.
You cannot help but lose the fat everywhere. Stubborn fat depositis are the result of 'hormonal protection' if you like, and genetic predisposition. A great observation was made about fat deposition in women- Asian women put fat on the stomach, mediteranean women on the hips, and black women on the rear.
If you are having problems with 'love handles' Bang in some Test/fluoxymesterone/stanozolol/furazabol/Drostanolone with an inhibtor such as Letrozole or Anastrozole (Anastrozole itself at 1mg inb the absence of eogneous test is enough to cause hot flushes akin to the menopause.) then start injecting the PGCL with some T3 and Clen, and watch the fat melt.
My point is here you have a drug with incredible GROWTH and Fat loss potential, but by using it Transdermally, you are preferntially targeting the fat cells, and denying yourself 50% of the fucking incredible effects of this revolutionary compound.
As for dose, We settled on 0.5mcg per kilo per day. But After a few weeks I can tolerate 75 mcg per day. I just finsihed a bicep tricep shoulder workout, and have just sited 15mcg in each bicep with 10 mcg of IGF in the same (insulin) needle and put another 10mcg in each rear delt. The heat- oh the fucking heat! Im probably using a ml a day which is 75mcg, which is equiv. to <> 7-8ml of straight,expensive PGF2.
Having said that, in error the first shot I did, was 1ml- and the effects were awesome.
These doese will need tinkering with, but theyre a good starting guide. Try the first one shot at 7.5mcg 3 times daily, then go up from there.
Speaking of errors- Another one I rectified recently, off topic, was my use of HMG, for some reason I was shooting it before bedtime. It then occured to me (see http://www.synergy-solutions.org/articlestraining.html) that as Ive battered people for years, that the objective is to restore NATURAL test production and circaidian patterns-, well, peak LH/ISCSH is midday, so I was actually a good 12 hours off naturalm restoration. Doing it in morning now.
Check out: http://www.synergy-solutions/links.html
Read the articles, watch the funny videos-be told!!!!!
Hope this helps!
Hi- This is a cut and paste:
QFS Dinoprost-Gel Transdermal Fat Reduction PGF-2a
QFS Dinoprost-Gel, Transdermal Fat Reduction active ingredients
Dinoprost Tromethamine 150mg ( Prostraglandin F2 alpha) and Dimethylsulfoxide (DMSO 25%)
Prostaglandin F2alpha is a potent inhibitor of adipocyte precursor differentiation and a physiological negative modulator of adipocyte function (ie triglyceride accumulation) through stimulation of transforming growth factor-alpha mRNA expression. It initiates a cascade of effects in the adipoctes which have physiological importance to reducing the size and it appears number of mature cells,long after PGf-2a is cleared from the system
Mature adipose cells only shrink in size in response to restricted caloric intake or increased metabolic demand. Before now the only method of reducing the number of fat cells was liposuction. It now appears that Pgf-2a applied topically can have the same same effecst as diet and liposuction. Pgf-2a can reduce the size of mature adipocytes and the number of mature adipocytes through negative modulation and reversing the process of differentiation
There are no studies on topical application. DMSO does carry PGF-2a through the dermal layers and the low concentration spread over a large area is ideal for the intended purpose. One cannot spread PGf-2a (or anyother substance) over the surface area that one can with DMSO topical application. The idea being that you need to interact as many molecules of PGF-2a with as many mature fat cells as possible. The biggest asset to DMSO as a carrier is the ability to spread the PGF-2a applicatiion over a large surface area, thereby maximising the interactuion of the number PGF-2a molucules with the maximum number of fat cells. This is where the DMOS method really shines. QFS is not masking the smell of the DMSO. It is not that bad and goes away in about 5 minutes.
It is important to remember that dinoprost tromethamine does not burn the released fatty acids, aerobic exercise and or T3 will take care of that. PGF-2a only changes the way fats are stored and the formation and function of adipose tissue. As well I find that about half of the time I feel a tickle in the back of my throat and sometimes I have a full out cou***ng fit. This says to me that I have applied a good dosage.
Here are some studies that support PGF-2a and negative modulation of adipose tissue.
Endocrinology 1995 Aug;136(8):3222-9
Prostaglandin F2 alpha stimulates transforming growth factor-alpha expression in adipocyte precursors.
Lepak NM, Serrero G.
W. Alton Jones Cell Science Center, Inc., Lake Placid, New York 12946, USA.
Transforming growth factor-alpha (TGF alpha) and prostaglandin F2 alpha (PGF2 alpha) are potent inhibitors of adipocyte differentiation. We demonstrate here that TGF alpha messenger RNA (mRNA) is expressed in freshly isolated fat pads and in primary culture of adipocyte precursors cultivated in defined medium before and after differentiation. We show that PGF2 alpha stimulated TGF alpha mRNA expression in a dose-dependent manner. PGF2 alpha also stimulated TGF alpha production in the culture medium of adipocyte precursors in primary culture. PGF2 alpha stimulated TGF alpha mRNA expression in both undifferentiated and differentiated cells. 9 alpha,11 beta-PGF2 alpha, which also inhibited adipose differentiation, stimulated TGF alpha mRNA expression similarly to PGF2 alpha, whereas other PGs had no effect on TGF alpha mRNA expression. The time-course experiment indicates that the stimulation of TGF alpha mRNA expression by PGF2 alpha is observed within 6 h of exposure to PGF2 alpha and is inhibited by treatment of the cells with actinomycin D. The effect of PGF2 alpha on TGF alpha expression did not require activation of protein kinase C and was fully reversible. As both TGF alpha and PGF2 alpha are inhibitors of adipose differentiation, it is suggested that stimulation of TGF alpha expression by PGF2 alpha could represent an amplification mechanism to modulate adipocyte precursor differentiation and adipocyte function within the adipose tissue.
Int J Obes Relat Metab Disord 1996 Mar;20 Suppl 3:S58-64 R
Endocrine and paracrine negative regulators of adipose differentiation.
Serrero G, Lepak N.
W Alton Jones Cell Science Center, Inc, Lake Placid, NY 12946, USA.
Obesity which is characterized by an abnormal adipose tissue development is a first degree public health hazard in industrialized countries. One important aspect in the study of adipose tissue development is to investigate the hormonal control of proliferation and differentiation. Any qualitative or quantitative change in these hormones or their receptors can result in abnormalities in the process of proliferation and/or differentiation possibly leading to obesity. Therefore, it is important to identify these factors and investigate their mechanism of action. We have concentrated our efforts in the study of factors triggering differentiation (positive regulators) and also of factors inhibiting differentiation (negative regulators). The present paper provides evidence of the importance of EGF/TGF-alpha and of PGF2 alpha as differentiation inhibitors for adipocyte precursors in primary culture. Data presented here also demonstrate that TGF-alpha is expressed in adipose tissue and that its expression is specifically stimulated by PGF2 alpha, thus suggesting the existence of an amplification mechanism between two differentiation inhibitors within the adipose tissue. The importance of these two types of differentiation inhibitors in the regulation of adipose tissue development is discussed.
-------------------------
I should mention a few points- Authors account of bronchoconstriction is indeed consistent with a good dose. This is one of the reasons to stack with with a bronchodilator such as Clenbuterol, or as mentioned in another thread by Anthony, Albuterol (which has a relationship to clen much akin to T4- T3. We get salbutamol inhalers over here and pre training there great- you do need a higher dose (( see previous t4/t3 statement)) but its over before the shakes start to piss you off!) as it prevents this becoming a problem.
The other IMO is the relative futility, both pharmacoldynamically, and financially of using
a) PGF2 and
b) PGF2 Transdermally.
Please allow me to elucidate! (ive been dying to use that word for a while now)
PGF2 according to the literature, is effective in doses of 1mg.
The first experimental dose of PGCL sent to me by IP was ( 75mcg per ml) effective in 15mcg. Anybody unfamiliar with the difference- simply move the decimal place.
1mg= 1000mcg.
And its cheaper.
Point a pt2: The new version of PGCL is 500mcg per ml and retails for $30.
Point b: Here you have a drug that not only will burn fat systemically. I know Ive said it before, But if you look at my pictures posted in this thread and my avatar ( which I will get resized so you can actually see what I look like) I am even leaner than that now. The drug will affect you systemically- its as simple as that. As I type this one hour 40 minutes after a bicep shot, Im sitting here in the freezing cold UK with sweat running off my forehead.
You cannot help but lose the fat everywhere. Stubborn fat depositis are the result of 'hormonal protection' if you like, and genetic predisposition. A great observation was made about fat deposition in women- Asian women put fat on the stomach, mediteranean women on the hips, and black women on the rear.
If you are having problems with 'love handles' Bang in some Test/fluoxymesterone/stanozolol/furazabol/Drostanolone with an inhibtor such as Letrozole or Anastrozole (Anastrozole itself at 1mg inb the absence of eogneous test is enough to cause hot flushes akin to the menopause.) then start injecting the PGCL with some T3 and Clen, and watch the fat melt.
My point is here you have a drug with incredible GROWTH and Fat loss potential, but by using it Transdermally, you are preferntially targeting the fat cells, and denying yourself 50% of the fucking incredible effects of this revolutionary compound.
As for dose, We settled on 0.5mcg per kilo per day. But After a few weeks I can tolerate 75 mcg per day. I just finsihed a bicep tricep shoulder workout, and have just sited 15mcg in each bicep with 10 mcg of IGF in the same (insulin) needle and put another 10mcg in each rear delt. The heat- oh the fucking heat! Im probably using a ml a day which is 75mcg, which is equiv. to <> 7-8ml of straight,expensive PGF2.
Having said that, in error the first shot I did, was 1ml- and the effects were awesome.
These doese will need tinkering with, but theyre a good starting guide. Try the first one shot at 7.5mcg 3 times daily, then go up from there.
Speaking of errors- Another one I rectified recently, off topic, was my use of HMG, for some reason I was shooting it before bedtime. It then occured to me (see http://www.synergy-solutions.org/articlestraining.html) that as Ive battered people for years, that the objective is to restore NATURAL test production and circaidian patterns-, well, peak LH/ISCSH is midday, so I was actually a good 12 hours off naturalm restoration. Doing it in morning now.
Check out: http://www.synergy-solutions/links.html
Read the articles, watch the funny videos-be told!!!!!
Hope this helps!
Now the fat loss, if im not mistaken is due to not only fat cell release of FFAs but also from induction of apoptosis in the fat tissue?
How available is this PGCL? Isnt 500mcg/ml a lot? One would have to cut the ml WAY down before they shot it?
Im currently taking tren enth at 400mg a week, 50mg oral masteron (methyl-DHT) ED, 20mg nolva ED and letro at .625mg ED. My problem area is the handles and hips and ass.....it goes back there SOOOO easy after i loose it that i need to kill those fat cells so i dont rebound all the time.
THinking of adding a fat burner and CLA at about 5 grams a day (CLA has been noted to cause apoptosis in adipose as well).
How available is this PGCL? Isnt 500mcg/ml a lot? One would have to cut the ml WAY down before they shot it?
Im currently taking tren enth at 400mg a week, 50mg oral masteron (methyl-DHT) ED, 20mg nolva ED and letro at .625mg ED. My problem area is the handles and hips and ass.....it goes back there SOOOO easy after i loose it that i need to kill those fat cells so i dont rebound all the time.
THinking of adding a fat burner and CLA at about 5 grams a day (CLA has been noted to cause apoptosis in adipose as well).
