AAS Research Mega Thread (not pro hormones)

[Joedoubledose]

Subb'd , nice info BeastFitness & DavidDunn

 

[BeastFitness]

How do you feel about NPP as a Kickstarter while running Deca entire time but adjust dose of each accordingly?

I'd also like to know his thoughts on also dropping the decanoate ester towards the end of the cycle and adding NPP back in. Thinking this mighht give the longer estered nandrolone more time to clear the system and allow for an easier transition into PCT for guys that get hit hard on the longer estered Nandrolone.

I'm a big fan of using various esters to either kick start or as a taper IF the person has a history of usage (meaning they've run at least a few proper cycles.) Obviously depending on the source and quality your getting your deca from, that can determine how long it truly takes to kick in at full force and can vary from 3-4+ weeks depending on the person (I have seen some very poor responders take 5 weeks for deca to reach peak levels and begin taking effect.)

The reason I say they must have a known cycle history is for that very reason, if you know someone is a hyper responder, you can gauge how long to actually use NPP as a kickstart and when to taper deca and same thing vise versa for poor responders. If its a first time user I would use plain old deca and keep specific track to see how long it takes to kick in so you can plan your taper accordingly with NPP (This will also allow a first time user to gauge the negative side effects and is a safer option.)

At the end of the day, it truly comes down to the individual. IF someone is a poor responder with high sides to a particular compound, stick to short esters so you can drop it immediately if needed and not have any clearance time.

Subb'd , nice info BeastFitness & DavidDunn

Right on man!

 

[Gutterpump]

The candidness in this thread is great guys. Solid thread.

 

[BeastFitness]

The candidness in this thread is great guys. Solid thread.

I agree! I love how everyone is truly interested in learning AND asking questions!

My plan is to post at least 1 AAS research related paper per day and then answer any and all questions that come along! Everyone feel free and don't be shy if you have a question or what to see research about a specific topic. My Master's program is HEAVILY based in research so I have access to databases and search engines many do not (and this will only get better once I begin my PhD.) Gotta love the perks of staying in the academic world! haha

 

[Dma378]

BeastFitness is cycle support needed/recommend for orals such as dbol if ONLY used for up to 6 weeks?

Yes. An excerpt from Steroidal.com:

The Effects of Dianabol (D-Bol)

Dianabol does succumb to some limitations of its own, with the first being its C17-Alpha Alkylated property. As previously mentioned, C17-Alpha Alkylation allows an anabolic steroid to become orally active and bioavailable – without it, the anabolic steroid would not survive liver metabolism. However, the negative downside in this case is that of increased hepatotoxicity (increased liver toxicity). C17-Alpha Alkylation allows an anabolic steroid to become more resistant to hepatic breakdown, and any compound that is further resistant to hepatic breakdown with always have greater hepatotoxicity associated with it. As a result, it is a smart choice to run Dianabol for periods no greater than 4-6 weeks at any given time in a cycle. This is to ensure healthy liver function, and for proper liver recovery following the cycle. It is because of the risk of hepatotoxicity that Dianabol’s main function in a cycle is to serve as a supportive kickstarting compound.

 

[datsthat]

I agree! I love how everyone is truly interested in learning AND asking questions!

My plan is to post at least 1 AAS research related paper per day and then answer any and all questions that come along! Everyone feel free and don't be shy if you have a question or what to see research about a specific topic. My Master's program is HEAVILY based in research so I have access to databases and search engines many do not (and this will only get better once I begin my PhD.) Gotta love the perks of staying in the academic world! haha

Then you will need to change your name to Doctor Beast Fitness. School is not easy. Congrats for making it this far.

 

[Dma378]

Subbed. Great thread.

In regards to the post above and cycle support with Dbol, I will also agree with BeastFitness in saying that "cycle support" can be achieved through many health conscious/dietary means other than a "cycle support product". Protect yourself however you find best.

 

[datsthat]

Is it safe to assume that injectable dbol is just as hepatotoxic as the oral version?

 

[Dma378]

Is it safe to assume that injectable dbol is just as hepatotoxic as the oral version?

From ppcss.weebly.com:

Both forms of the drug can be toxic to the liver, especially with over-usage; however, injectable dbol seems to be a bit less toxic. It can, however, be more toxic to the kidneys. Because Dbol increases glycogen breakdown, the body increases protein breakdown to compensate. All those excess amino acids have to get out of the body somehow, and that somehow is through your kidneys, which can cause problems.

 

[B5150]

Hepatoxicty: Fact or Fiction
by Roy Harper

We all know that the alpha alkylated steroids are hepatotoxic, right….. But, is there actually any truth to this? We’ve been told for years that if you take 17 alpha-alkylated steroids, you will eventually run into liver problems. Never combine 17 aa’s, never go beyond 50mg day, never go longer than 4 weeks, etc. All of this is crap! As I we walk you through some studies, today, you’ll see 17 alpha-alkylated steroids can be hepatotoxic but not to the degree you would think.

To make a steroid hepatotoxic, you need only a small change to a steroid molecule; A strong bond that cannot readily be down broken by enzymes in the liver. This may be a bond at the 17th position, or even at the 1st position (as in methenolone or proviron ). Because the liver cannot easily break the steroid down before it is released in to the blood stream, this also results in the steroid to becoming more orally bio-available.

We can see that the liver has to work harder to break down these steroids. Enzymes in the blood and tissue easily metabolize other steroids such as Testosterone . Commonly, this increase in liver activity has been viewed as a harmful process, but as you will see, this increase is, in and of itself, irrelevant. The liver is THE filter of the human body -- it can figure out what to do with just about anything. The only real problem comes in when one keeps their liver at full blast for long periods of time.

Let’s look at some studies showing the hepatotoxicity of steroids. Here's one of my favorites, a study published in 1979[1]. Essentially, researches did a study of deaths caused by hepatic angiosarcoma (a malignant tumor of vascular tissue in the liver) between 1964 and 1974. Researchers found 131 reported cases of death from hepatic angiosarcoma. Out of the 131 cases, 3.1% (4 cases) were reported to be at all related to the use of androgenic -anabolic steroids. Keep in mind that these 4 people could have liver complications before any steroids were used, aka a genetic disposition. In fact there is no proof, in this study at least, that the anabolic-androgenic steroids even caused the hepatic angiosarcoma.

This is the classic case of associating a cause with an effect, without any evidence, aside from both existing. Furthermore, based on the above numbers, there are only 0.4 cases of hepatic angiosarcoma reported each year, by those using AAS. Now consider the number of people on steroids at this time. Now factor in all the people that don’t know their ass from a hole in the ground when it comes to using AAS, properly. Clearly, this is very week evidence. Lastly there has not been a real increase in hepatic angiosarcoma since the early seventies. Meanwhile, there has been a huge, almost exponential, increase in steroid use during this period.

Another study, that somewhat supports the previous hepatotoxicity case, showed the possibilities of hepatic adenomas(cysts in the liver) caused by androgenic-anabolic steroids [2]. In this study, a Japanese girl was found to have multiple liver lesions after the use of the drug oxymetholone (aka Anadrol ). Most everyone “knows” that Anadrol is linked with liver problems, but a closer inspection into this study shows more.

Apparently, this girl, starting at the age of 14, was diagnosed with aplastic anemia. She was prescribed oxymetholone at 30mg per day. This continued for 6 years until the lesions first appeared. Assuming that the girl was most likely around 100 lbs., this was a pretty heavy dosage. If you extrapolated this data out to a 200 - 250lbs. male, that would be taking approximately 60 - 90mg of anadrol per day for 6 years. Ouch!

The researchers also stated that there were only 17 other cases of hepatic adenomas, found in English literature between 1975 and 1998. They failed to mention the causes of these 17 cases, but there is no reason to believe they were all using 17-AA androgens and 17 is certainly miniscule compared to the number of people who have used them. The authors’ finish off the study by saying the following: "This report may be helpful in identifying the population who is at risk of developing hepatic sex hormone-related tumors." So remember, if you're a small 14-year-old girl taking 30mg of Anadrol per day for 6 years, you may be at risk!

Let's move on to some more useful studies. Take for example a 1995 study that showed the toxic effects of anabolic-androgenic steroids in primary rat hepatic cell cultures[3]. In this study the researchers used the following drugs and dosages:

Steroid
*1x10^-8M
**1x10^-6M
***1x10^-4M

19-nortestosterone
0.002744mg*
0.2744mg**
27.44mg***

Fluoxymesterone
0.003365mg*
0.3365mg**
33.65mg***

Testosterone cypionate
0.004126mg*
0.4126mg**
41.26mg***

Stanozolol
0.003285mg*
0.3285mg**
32.85mg***

Danazol
N/A
N/A
N/A

Oxymetholone
0.003325mg*
0.3325mg**
33.25mg***

Testosterone
0.002884mg*
0.2884mg**
28.84mg***

Estradiol
0.0027424mg*
0.2724mg**
27.24mg***

Methyltestosterone
0.003024mg*
0.3024mg**
30.24mg***


As proof of the hepatoxicity they used Lactate dehydrogenase release, neutral red retention, and glutathione depletion to determine plasma membrane damage, cell viability, and possible oxidative injury, respectively.

What they showed was that the 17 alpha-alkylated steroids, methyltestosterone, stanozolol and oxymetholone, significantly increased Lactate dehydrogenase release and decreased neutral red retention at the 1x10^-4M dosage for 24h. Both methyltestosterone and oxymetholone also showed depleted glutathione at the 1x10^-4M dosage after 2h, 6h and 8h treatments. In other words they increased liver activity. You may also note that the other, non-alkylated steroids showed no significant difference in any levels. All in all this not only shows that 17 alpha-alkylated steroids are directly “hepatotoxic”, but also non-alkylated steroids are note hepatotoxic at all. But is this a real measure of hepatotoxicity? There is yet to be any correlation between the increase of the above-mentioned measurement and “hepatotoxicity”. Obviously, high dosages of the 17 alpha-alkylated steroids are potentially dangerous, but upon closer inspection, the study reveals more.

Take a look, the researchers took cell cultures from the liversse of 60-day-old Sprague-Dawley rats. Not only are rat livers much smaller than human livers, but these were merely cultures. Furthermore, it was the 1x10^-4M concentrations that caused the most changes, but these are approximately 1 to a 1/3 of a full, daily human dosage -- at least for the 17 alpha-alkylated steroids. Even at the 1x10^-6M concentration, there were no significant changes observed. It's apparent that the levels of 17 alpha-alkylated steroids used were potentially toxic, but for a human to take the same amount would be insane. I'm guessing this could translate to maybe 4 grams every 24 hours or 28 grams a week if not more.

What is common so far is we can only prove that any steroid, that is believed to be hepatotoxic, only increases liver activity. I’ll say it again, where is the correlation to hepatotoxicity? We know that if the liver is running at 100% for long periods this may cause complications, but this is akin to any other chemical, which is metabolized by the liver. Ever noticed that liver cancer due to alcoholism takes decades of constant alcohol abuse? It’s apparent that the possibility for hepatotoxicity is there, but for the smart steroid user this is nearly an impossible task.

Another study done in 1999, attempted to show the acute and chronic effects of stanozolol on the liver[4]. In acute treatments of stanozolol, dosages not mentioned, both cytochrome P456 and b5 (microsomal enzymes) levels dropped after 48 hours, and then at 72 hours, levels significant increased. On the other hand, with chronic treatments, time or dosage not mentioned, these microsomal enzymes showed a decrease in levels. Researchers showed that both acute and chronic treatments resulted in "slight to moderate inflammatory or degenerative lesions in centrilobular hepatocytes", but the authors did not note true hepatotoxicity.

How about we look at the other side of the story, the good studies. For instance, in a 1999 study, which looked at the effects of an 8-week cycle of 17 alpha-alkylated steroids[5]. The researchers used fluoxymesterone, methylandrostanolone, or stanozolol on rats at 2mg/kg-body weight, five times a week for 8 weeks. That's 182mg per dosage, for a 200lb man, or 910mg per week. Half of the rats were sedentary and the other were trained on a treadmill.

Levels of NADH-cytochrome c reductase, succinate cytochrome c reductase, and cytochrome oxidase (showing liver activity), increased in the steroid-administered rats, while citrate synthase showed no change. Comparatively, in vitro, the "cytochrome oxidase and citrate synthase activities were insensitive to the AAS, whereas NADH-cytochrome c reductase and succinate cytochrome c reductase activities were partly inhibited."

Furthermore, in vivo, each rat had liver enzyme levels that were within normal range. From this, the researchers determined that the steroid-administered rats, trained or sedentary, did not show "...classical serum indicators of hepatic function". Extrapolating this, 910mg a week for 8 weeks could potentially have little to no effect on the liver in humans.

As for human studies, in 1999 researchers tried to prove that the hepatotoxicity of steroids is overstated[6]. In this study, 15 of the participants were bodybuilders using self-administered steroid dosages and 10 were non-steroid bodybuilders. Serum data was compared to 49 patients with viral hepatitis, and 592 exercising and non-exercising medical students. [

All of the bodybuilders showed increases in aspartate aminotransferase (AST), alanine aminotransferase (ALT) and creatine kinase (CK) while gamma-glutamyltranspeptidase (GGT) levels were in the normal range. In comparison, hepatitis patients showed increased ALT, AST, and GGT levels while the control exercising medical students showed increased CK levels. From this, the researchers suggested that it is the correlation between AST, ALT and GGT that shows true liver dysfunction. Keep in mind, we can only guess that the 15 steroid users were using 17 alpha-alkylated steroids, and we do not know what the dosages that were used., but common sense tells us the results are likely relevant.

Last but not least, a simple study done in 1996, showed the long term benefits after taking a 3 month break from steroids[7]. 16 bodybuilders using steroids were compared to 12 bodybuilders that were not. After a three-month drug withdrawal, the researchers showed that levels of liver enzymes, types not mentioned, returned to the same as the non users. Again the dosages are left to the reader’s imagination and we can only guess that the 16 steroid users were using 17 alpha-alkylated steroids.

So what can we conclude from all of this? First off, 17 alpha-alkylated steroids are hepatotoxic in high dosages taken for a long time. On the other hand, short cycles and small dosages appear to be perfectly safe. I suggest that maximum dosages should be 500mg to 900mg per day. They should be cycled for perhaps 8 weeks at a time, and if needed a 3-month break from them should be used. Using the above-mentioned techniques, your liver can be healthy for a long time. Simply put, the hysteria surrounding “hepatoxic” steroids, is based mainly on folk lore.


References:

[1] Lancet 1979 Nov 24;2(8152):1120-3, Hepatic angiosarcoma associated with androgenic-anabolic steroids. Falk H, Thomas LB, Popper H, Ishak KG.

[2] J Gastroenterol 2000;35(7):557-62, Multiple hepatic adenomas caused by long-term administration of androgenic steroids for aplastic anemia in association with familial adenomatous polyposis. Nakao A, Sakagami K, Nakata Y, Komazawa K, Amimoto T, Nakashima K, Isozaki H, Takakura N, Tanaka N.

[3] J Pharmacol Toxicol Methods 1995 Aug;33(4):187-95, Toxic effects of anabolic-androgenic steroids in primary rat hepatic cell cultures. Welder AA, Robertson JW, Melchert RB.

[4] Arch Toxicol 1999 Nov;73(8-9):465-72, Evaluation of acute and chronic hepatotoxic effects exerted by anabolic-androgenic steroid stanozolol in adult male rats. Boada LD, Zumbado M, Torres S, Lopez A, Diaz-Chico BN, Cabrera JJ, Luzardo OP.

[5] Med Sci Sports Exerc. 1999 Feb;31(2):243-50, Rat liver lysosomal and mitochondrial activities are modified by anabolic-androgenic steroids. Molano F, Saborido A, Delgado J, Moran M, Megias A.

[6] Clin J Sport Med 1999 Jan;9(1):34-9, Anabolic steroid-induced hepatotoxicity: is it overstated? Dickerman RD, Pertusi RM, Zachariah NY, Dufour DR, McConathy WJ.

[7] Int J Sports Med 1996 Aug;17(6):429-33, Body composition, cardiovascular risk factors and liver function in long-term androgenic-anabolic steroids using bodybuilders three months after drug withdrawal. Hartgens F, Kuipers H, Wijnen JA, Keizer HA.

 

[B5150]

I bolded the references. If someone wants to find (Google came up with the first in pubmed) them and post them here individually that would be great.

 

[Dma378]

It makes a lot of sense. And I have also considered the alcohol induced liver disease/failure comparison. Now I totally support anything that can help minimize sides and/or damage at any level. But it seems the extent of it is quite overstated!!

 

[B5150]

Dma378 I believe it's very overstated!

Here's my SuperDrol beta tester log. My liver values actually improved while using up to 50mg. Only liver support supplements were 600mg ALA and 1800mg NAC

The scanned blood work is at the end of cycle while ON 50mg of SuperDrol!

Invalid Link Removed

Here is the pre and post comparative.

Invalid Link Removed

Holy ****! Its been 12 years now :shocked1:

 

[BamBam0319]

Dma378 I believe it's very overstated!

Here's my SuperDrol beta tester log. My liver values actually improved while using up to 50mg. Only liver support supplements were 600mg ALA and 1800mg NAC

The scanned blood work is at the end of cycle while ON 50mg of SuperDrol!

Invalid Link Removed

Here is the pre and post comparative.

Invalid Link Removed

Holy ****! Its been 12 years now :shocked1:

Wow. This is good news lol, I have 100 10mg Superdrol caps stashed away, I've been wanting to use them but wasn't sure how best to do it.

 

[Dma378]

Dma378 I believe it's very overstated!

Here's my SuperDrol beta tester log. My liver values actually improved while using up to 50mg. Only liver support supplements were 600mg ALA and 1800mg NAC

The scanned blood work is at the end of cycle while ON 50mg of SuperDrol!

Invalid Link Removed

Here is the pre and post comparative.

Invalid Link Removed

Holy ****! Its been 12 years now :shocked1:

I was wondering how the cholesterol would be effected. Not dramatic it doesn't seem.

And yeah the liver values speak for themselves.

 

[B5150]

Keep in mind that as I mentioned within that journal that I had also recently used M1T.

I hate to say it but the hysteria about the adverse effects are not substantiated and are captitized upon by the supplement industry. I'm not saying don't use caution but adverse effects are sensationalized for the profit of the support product manufacturers. Not to mention even if there are adverse effects the supplements do not hinder their ability to influence those biological parameters during the use of said hormone.

Sadly we all see kids are spending hundreds on ancillaries while running a $30-40 OTC cycle of said anabolic from same company </rant>

 

[BeastFitness]

Yes. An excerpt from Steroidal.com:

The Effects of Dianabol (D-Bol)

Dianabol does succumb to some limitations of its own, with the first being its C17-Alpha Alkylated property. As previously mentioned, C17-Alpha Alkylation allows an anabolic steroid to become orally active and bioavailable – without it, the anabolic steroid would not survive liver metabolism. However, the negative downside in this case is that of increased hepatotoxicity (increased liver toxicity). C17-Alpha Alkylation allows an anabolic steroid to become more resistant to hepatic breakdown, and any compound that is further resistant to hepatic breakdown with always have greater hepatotoxicity associated with it. As a result, it is a smart choice to run Dianabol for periods no greater than 4-6 weeks at any given time in a cycle. This is to ensure healthy liver function, and for proper liver recovery following the cycle. It is because of the risk of hepatotoxicity that Dianabol’s main function in a cycle is to serve as a supportive kickstarting compound.

I've actually read this before and definitely feel anyone beginning dbol should understand what their getting themselves into

Then you will need to change your name to Doctor Beast Fitness. School is not easy. Congrats for making it this far.

HAHAHA! I like the sound of that Definitely not easy but I love it! Thanks man!

Subbed. Great thread.

In regards to the post above and cycle support with Dbol, I will also agree with BeastFitness in saying that "cycle support" can be achieved through many health conscious/dietary means other than a "cycle support product". Protect yourself however you find best.

Thanks man! Theres no way you can get EVERYTHING from one product…its just not realistic. Glad you agree!

Is it safe to assume that injectable dbol is just as hepatotoxic as the oral version?

From ppcss.weebly.com:

Both forms of the drug can be toxic to the liver, especially with over-usage; however, injectable dbol seems to be a bit less toxic. It can, however, be more toxic to the kidneys. Because Dbol increases glycogen breakdown, the body increases protein breakdown to compensate. All those excess amino acids have to get out of the body somehow, and that somehow is through your kidneys, which can cause problems.

Hepatoxicty: Fact or Fiction
by Roy Harper

We all know that the alpha alkylated steroids are hepatotoxic, right….. But, is there actually any truth to this? We’ve been told for years that if you take 17 alpha-alkylated steroids, you will eventually run into liver problems. Never combine 17 aa’s, never go beyond 50mg day, never go longer than 4 weeks, etc. All of this is crap! As I we walk you through some studies, today, you’ll see 17 alpha-alkylated steroids can be hepatotoxic but not to the degree you would think.

I bolded the references. If someone wants to find (Google came up with the first in pubmed) them and post them here individually that would be great.

LOVED that post David! I'll post them up all below!

It makes a lot of sense. And I have also considered the alcohol induced liver disease/failure comparison. Now I totally support anything that can help minimize sides and/or damage at any level. But it seems the extent of it is quite overstated!!

Dma378 I believe it's very overstated!

Here's my SuperDrol beta tester log. My liver values actually improved while using up to 50mg. Only liver support supplements were 600mg ALA and 1800mg NAC

The scanned blood work is at the end of cycle while ON 50mg of SuperDrol!

Invalid Link Removed

Here is the pre and post comparative.

Invalid Link Removed

Holy ****! Its been 12 years now :shocked1:

Wow. This is good news lol, I have 100 10mg Superdrol caps stashed away, I've been wanting to use them but wasn't sure how best to do it.

I was wondering how the cholesterol would be effected. Not dramatic it doesn't seem.

And yeah the liver values speak for themselves.

Keep in mind that as I mentioned within that journal that I had also recently used M1T.

I hate to say it but the hysteria about the adverse effects are not substantiated and are captitized upon by the supplement industry. I'm not saying don't use caution but adverse effects are sensationalized for the profit of the support product manufacturers. Not to mention even if there are adverse effects the supplements do not hinder their ability to influence those biological parameters during the use of said hormone.

Sadly we all see kids are spending hundreds on ancillaries while running a $30-40 OTC cycle of said anabolic from same company </rant>

I'm glad you brought this up David because even though I am a huge proponent of health, there obviously is a limit and the amount of ancillaries should be kept to the MINIMUM needed to keep blood markers within optimal ranges. This is kind of the area people do not seem to take into consideration whether they run orals or injectables….blood levels need to be monitored. I have some people that take ZERO ancillaries simply because they do not need them (obviously these guys are genetic freaks) but the point is still there. Don't put anything in your body unless you need to.






Here's the actual PubMed studies from David's post about Hepatoxicity

Lancet 1979 Nov 24;2(8152):1120-3, Hepatic angiosarcoma associated with androgenic-anabolic steroids. Falk H, Thomas LB, Popper H, Ishak KG.
Abstract
A retrospective epidemiological study of deaths from hepatic angiosarcoma (HAS) in the U.S. showed that during 1964--74 there were 168 such cases, of which 37 (22%) were associated with previously known causes (vinyl chloride, 'Thorotrast', and inorganic arsenic) and 4 (3.1%) of the remaining 131 cases with the use of androgenic-anabolic steroids. It is suggested that the long-term use of androgenic-anabolic steroids is the fourth cause of HAS, the majority of cases still being of unknown aetiology. Moreover, the presented cases serve as a link in a spectrum of hepatic disorders recently recognised to be caused by environmental agents such as vinyl chloride, arsenic, and thorotrast, and by contraceptive and anabolic steroids. Similar precursor stages, usually not recognised by clinical laboratory tests and consisting of areas of hyperplasia of hepatocytes and sinusoidal cells and sinusoidal dilatation, lead potentially to hepatic adenoma, carcinoma, peliosis, and angiosarcoma.


J Gastroenterol 2000;35(7):557-62, Multiple hepatic adenomas caused by long-term administration of androgenic steroids for aplastic anemia in association with familial adenomatous polyposis. Nakao A, Sakagami K, Nakata Y, Komazawa K, Amimoto T, Nakashima K, Isozaki H, Takakura N, Tanaka N.

Abstract
We report a rare case of hepatic adenomas (HA), in a 20-year-old Japanese girl treated for 6 years with anabolic androgens for aplastic anemia. In a review of the world literature using computer MEDLINE search, we found only 17 cases of androgen-induced HA published between 1975 and 1998 in the English-language literature. The patient was referred to us because of liver lesions detected during a follow-up examination for familial adenomatous polyposis. After being diagnosed with aplastic anemia at 14 years of age, she had been treated with oxymetholone (30 mg/day) for 6 years. Laboratory evaluation revealed normal liver function. Ultrasonography (US) and computed tomography (CT) demonstrated multiple liver lesions. Histopathological examinations of biopsied specimens from the liver tumor showed HA. After the patient was diagnosed with HA, oxymetholone was tapered off. Patients taking androgenic-anabolic steroids should be carefully monitored with US and CT and tumor markers should be measured. This report may be helpful in identifying the population who is at risk of developing hepatic sex hormone-related tumors.

J Pharmacol Toxicol Methods 1995 Aug;33(4):187-95, Toxic effects of anabolic-androgenic steroids in primary rat hepatic cell cultures. Welder AA, Robertson JW, Melchert RB.

Abstract
Hepatic complications in athletes and bodybuilders after abusing anabolic-androgenic steroids (AAS) have been reported. Hepatic injury, including cholestasis, peliosis hepatis, hyperplasia, and tumors, have been attributed to abuse of the 17 alpha-alkylated AAS. Some of these pathological conditions have been reversed when individuals were converted to nonalkylated AAS regimens. The purpose of this study was to determine and compare the direct toxic effects of commonly abused AAS (both 17 alpha-alkylated and nonalkylated) in primary hepatic cell cultures. Primary cultures, established from 60-day-old Sprague-Dawley rats, were exposed to doses of 1 x 10(-8), 1 x 10(-6), and 1 x 10(-4)M 19-nortestosterone, fluoxymesterone, testosterone cypionate, stanozolol, danazol, oxymetholone, testosterone, estradiol, and methyltestosterone for 1, 4, and 24 hr. Lactate dehydrogenase (LDH) release, neutral red (NR) retention, and glutathione (GSH) depletion were evaluated to determine plasma membrane damage, cell viability, and possible oxidative injury, respectively. Those cultures exposed to the 17 alpha-alkylated AAS, methyltestosterone and stanozolol, at doses of 1 x 10(-4) M for 24 hr and the 17 alpha-alkylated AAS, oxymetholone, at 1 x 10(-4) M for 4 and 24 hr showed significant increased in LDH release and decreases in NR retention while there were no significant differences with the nonalkylated steroids (testosterone cypionate, 19-nortestosterone, testosterone, and estradiol). GSH depletion was evaluated in cultures treated with 1 x 10(-8), 1 x 10(-6), and 1 x 10(-4) M concentrations of methyltestosterone, stanozolol, and oxymetholone for 1, 2, 4, and 6 hr. Cultures exposed to 1 x 10(-4) M oxymetholone were significantly depleted of GSH at 2, 4, and 6 hr; cultures exposed to 1 x 10(-4) M methyltestosterone were significantly depleted of GSH at 4 and 6 hr; and cultures exposed to stanozolol were not significantly depleted of GSH at any of the time periods tested. These data indicate that the 17 alpha-alkylated steroids (methyltestosterone, oxymetholone, and stanozolol) are directly toxic to hepatocytes, whereas the nonalkylated steroids (testosterone cypionate, 19-nortestosterone, testosterone, and estradiol) show no effects at similar doses. These data demonstrate a trend toward a structural-activity relationship to AAS-induced toxicity in primary cultures of rat hepatocytes.

Arch Toxicol 1999 Nov;73(8-9):465-72, Evaluation of acute and chronic hepatotoxic effects exerted by anabolic-androgenic steroid stanozolol in adult male rats. Boada LD, Zumbado M, Torres S, Lopez A, Diaz-Chico BN, Cabrera JJ, Luzardo OP.

Abstract
Stanozolol (ST) is a 17alpha-alkyl anabolic-androgenic steroid (17alpha-AAS) often misused by athletes and bodybuilders. The use of anabolic-steroids by sportsmen and teenagers has increased dramatically, thus raising the question about their hepatotoxicity, specially those such as ST which are orally administered. Previously, we have reported diverse in vivo effects exerted by this steroid and published the existence of a highly specific ST-binding site in male rat liver microsomes. The existence of this binding site, the reported hepatic effects exerted in humans, and the very limited information about its potential hepatotoxicity led us to treat adult male rats acutely and chronically with ST and study different parameters that could indicate liver damage: serum levels of transaminases, concentration of monooxygenase enzymes in liver, liver membrane lipid peroxidation products, liver histopathology, and cell cycle/ploidy status of liver cells. In our study, no changes in serum transaminases or lipid peroxidation levels were obtained. However, acute stanozolol treatment significantly decreased the levels of cytochrome P450 (Cyt. P450) and cytochrome b5 (Cyt. b5) during the first 48 h of treatment, while subsequently, at 72 and 96 h, these microsomal enzymes underwent a significant increase in their levels. In sharp contrast with this response to acute treatment, the content of these two enzymes during chronic treatment showed an important decrease. Interestingly, acutely and chronically ST-treated livers showed slight to moderate inflammatory or degenerative lesions in centrilobular hepatocytes. Flow cytometric analysis demonstrated that both acute and chronic ST treatment were capable of increasing the percentage of S-phase fraction (%SPF) of liver cells. These findings taken together clearly show that this steroid is capable of altering the liver capacity for metabolizing xenobiotics and indicate that high doses of ST could exert a proliferative effect on liver cells. Such data should be considered in risk evaluations for this compound.

Med Sci Sports Exerc. 1999 Feb;31(2):243-50, Rat liver lysosomal and mitochondrial activities are modified by anabolic-androgenic steroids. Molano F, Saborido A, Delgado J, Moran M, Megias A.

Abstract
PURPOSE:
The aim of this study was to examine the separate and combined effects of an 8-wk treatment with high doses of 17alpha-alkylated anabolic-androgenic steroids (AAS) and exercise training on selected lysosomal and mitochondrial enzyme activities in rat liver.
METHODS:
Sedentary and treadmill-trained (25 m x min(-1), 45 min x d(-1), 5 d x wk(-1)) male rats were treated with fluoxymesterone, methylandrostanolone, or stanozolol (2 mg x kg body weight(-1), 5 d x wk(-1)) for 8 wk.
RESULTS:
Acid phosphatase, arylsulfatase, beta-glucuronidase, and beta-galactosidase activities were increased in liver homogenates of sedentary and trained AAS-treated rats. The mitochondrial respiratory chain activities rotenone-sensitive NADH-cytochrome c reductase (NCCR), succinate cytochrome c reductase (SCCR), and cytochrome oxidase (COX) showed a significant decrease in steroid-administered rats, whereas citrate synthase (CS), a matrix enzyme, exhibited no changes in activity, pointing to a selective effect of AAS on mitochondrial membrane complexes. In vitro studies in mitochondrial fractions isolated from the liver of control rats showed that COX and CS activities were insensitive to the AAS, whereas NCCR and SCCR activities were partly inhibited. On the other hand, the mean values of serum parameters related to hepatic function were within normal ranges in all the experimental groups of animals.
CONCLUSIONS:
The present data show that 8-wk ingestion of three different anabolic-androgenic steroids, either with or without concurrent exercise training, affects lysosomal hydrolases and mitochondrial respiratory chain electron transport in rat liver without modifying classical serum indicators of hepatic function.

Clin J Sport Med 1999 Jan;9(1):34-9, Anabolic steroid-induced hepatotoxicity: is it overstated? Dickerman RD, Pertusi RM, Zachariah NY, Dufour DR, McConathy WJ.

Abstract
OBJECTIVE:
There have been numerous reports of hepatic dysfunction secondary to anabolic steroid use based on elevated levels of serum aminotransferases. This study was conducted to distinguish between serum aminotransaminase elevations secondary to intense resistance training and anabolic steroid-induced hepatotoxicity in elite bodybuilders.
DESIGN:
This was a case-control study of serum chemistry profiles from bodybuilders using and not using anabolic steroids with comparisons to a cohort of medical students and patients with hepatitis.
PARTICIPANTS:
The participants were bodybuilders taking self-directed regimens of anabolic steroids (n = 15) and bodybuilders not taking steroids (n = 10). Blood chemistry profiles from patients with viral hepatitis (n = 49) and exercising and nonexercising medical students (592) were used as controls.
MAIN OUTCOME MEASURES:
The focus in blood chemistry profiles was aspartate aminotransferase (AST), alanine aminotransferase (ALT), gamma-glutamyltranspeptidase (GGT), and creatine kinase (CK) levels.
RESULTS:
In both groups of bodybuilders, CK, AST, and ALT were elevated, whereas GGT remained in the normal range. In contrast, patients with hepatitis had elevations of all three enzymes: ALT, AST, and GGT. Creatine kinase (CK) was elevated in all exercising groups. Patients with hepatitis were the only group in which a correlation was found between aminotransferases and GGT.
CONCLUSION:
Prior reports of anabolic steroid-induced hepatotoxicity based on elevated aminotransferase levels may have been overstated, because no exercising subjects, including steroid users, demonstrated hepatic dysfunction based on GGT levels. Such reports may have misled the medical community to emphasize steroid-induced hepatotoxicity when interpreting elevated aminotransferase levels and disregard muscle damage. For these reasons, when evaluating hepatic function in cases of anabolic steroid therapy or abuse, CK and GGT levels should be considered in addition to ALT and AST levels as essential elements of the assessment.

Int J Sports Med 1996 Aug;17(6):429-33, Body composition, cardiovascular risk factors and liver function in long-term androgenic-anabolic steroids using bodybuilders three months after drug withdrawal. Hartgens F, Kuipers H, Wijnen JA, Keizer HA.

Abstract
The purpose of this study was to investigate in a cross-sectional design body composition, muscle fiber characteristics, cardiovascular risk factors and liver enzymes in long-term androgenic-anabolic steroids (AAS) using bodybuilders three months after drug withdrawal (AAS group; n = 16) and in non-users (CO group; n = 12). Training and dietary data were collected in all subjects. Anthropometry included weight, height, 8 skinfolds and 11 circumferences. Percentage fat (%FAT), fat mass (FM) and lean body mass (LBM) were calculated. In a muscle biopsy from the vastus lateralis muscle water content, fiber type distribution and diameters of fiber type I and type II were determined. Age, height, training characteristics, nutrition, skinfolds, %FAT and FM did not differ between the groups. The AAS group had greater BW and LBM, and larger circumferences of thorax, waist, upper arm and thigh than the CO group. Muscle biopsy data were comparable, except for muscle fiber diameter of type I which was larger in the AAS group. No differences in serum values of total cholesterol, HDL-cholesterol and triglycerides, nor in systolic and diastolic blood pressure were observed. In both groups serum alkaline phosphatase and gamma GT were within the normal range. This study suggests that in long term AAS using body-builders, after a three months AAS free period, BW is greater than in non drug users. This is reflected in larger LBM, circumferences and diameter of muscle fiber type I. In addition, no differences in fat mass, blood pressure, lipoprotein profiles and liver enzymes exist between AAS users three months after interrupted drug use and their non drug using counterparts.

 

[Quest]

thanks for brain gainz

 

[B5150]

I've posted that artical multiple times and I'm convinced that no one before us have read the references.

Thanks for being in the educated group!

 

[Dma378]

It's funny how trained our minds are when something is drilled into it. I kicked off my current Test cycle with DMZ and Halo and could have sworn my liver was twitching LOL. So stupid. For like 3 days. Obviously it was probably an abdominal muscle twitching, but my mind was like, "it's your liver dude drop the DMZ". So I did.

Yet last year I ran DMZ and Tbol (not concurrently) with no liver support, only support for BP, and felt fine. For me personally it is the BP issues that I need to combat. Also very maintainable with a clean diet, plenty of water, and a decent amount of cardiovascular exercise.

I have some Winstrol (oral) that I plan on using this Spring, any experience or info on how it may effect BP? I have looked around a bit and details are a bit vague.

 

[B5150]

BP and lipids. Poor lipids and hypertension can be precursor to heart disease. Although liver issues are overstated Orals hit the lipids pretty well as cholesterol is processed through liver metabolism.

 

[BeastFitness]

thanks for brain gainz

I'm loving it! haha

I've posted that artical multiple times and I'm convinced that no one before us have read the references.

Thanks for being in the educated group!

Thats one of the biggest things I've learned the deeper into the medical research field I get…learning research results FROM the actual research referenced within the text itself. Say you have a 2015 meta analysis that contains 20-45+ references about a certain subject, well, all that research PROBABLY dates back as far as the 1970's and seeing things from a different perspective is beyond beneficial. Its not as simple as reading the conclusion section and accepting that as fact

It's funny how trained our minds are when something is drilled into it. I kicked off my current Test cycle with DMZ and Halo and could have sworn my liver was twitching LOL. So stupid. For like 3 days. Obviously it was probably an abdominal muscle twitching, but my mind was like, "it's your liver dude drop the DMZ". So I did.

Yet last year I ran DMZ and Tbol (not concurrently) with no liver support, only support for BP, and felt fine. For me personally it is the BP issues that I need to combat. Also very maintainable with a clean diet, plenty of water, and a decent amount of cardiovascular exercise.

I have some Winstrol (oral) that I plan on using this Spring, any experience or info on how it may effect BP? I have looked around a bit and details are a bit vague.

BP and lipids. Poor lipids and hypertension can be precursor to heart disease. Although liver issues are overstated Orals hit the lipids pretty well as cholesterol is processed through liver metabolism.

So little bit on winstrol. Winstrol is not estrogenic meaning this cannot cause gyno or excess water retention that typically increases blood pressure BUT, high blood pressure levels are still possibly depending on your genetic predisposition. You can see some acne gain, hair loss, virilization in women, reduction in HDL (good cholesterol), increase in LDL (bad cholesterol), and is more hepatotoxic than anavar which is going to increase liver enzyme levels.

Since we're on the topic of winny, might as well share a relevant study. The study below looks at winstrol taken at .1mg/kg of body weight per day OR 9mg/day for a 200lb man. This type of study makes you somewhat wonder what a minimum effective dose could be (low dosing winny seems to be slightly more beneficial long term, especially when in conjunction with other synergistic compounds.)


Short-Term Modulation of the Androgen Milieu Alters Pulsatile, But Not Exercise- or Growth Hormone (GH)-Releasing Hormone-Stimulated GH Secretion in Healthy Men: Impact of Gonadal Steroid and GH Secretory Changes on Metabolic Outcomes


Gonadal steroids are known to alter GH secretion as well as tissue metabolism. The present study was designed to examine the effects of short term (2- to 3-week) alterations in gonadal steroids on basal pulsatile (nonstimulated) and exercise- and GH-releasing hormone-stimulated GH secretion, urinary nitrogen excretion, and basal and exercise-stimulated oxygen consumption. Two protocols were conducted, which reflect a total of 18 separate studies. In the first paradigm, 5 healthy young men were each studied in a double blind, randomized manner during 3 different gonadal hormone manipulations, in which serum testosterone was varied from hypogonadal (induced by leuprolide) to eugonadal (saline injections) to high levels (testosterone enanthate, 3 mg/kg.week, i.m.). There was a washout period of 8 weeks between treatments. In the second protocol, 3 of the original subjects were studied after 2 weeks of treatment with stanozolol (0.1 mg/kg.day). Two to 3 weeks after the desired changes in serum testosterone, each subject was admitted to the General Clinical Research Center for study. The hypogonadal state (serum testosterone, 33 ng/dL) increased urinary nitrogen loss (by 34%; P < 0.005) and decreased basal metabolic rate (by 12%; P < 0.02) compared with the eugonadal state (testosterone, 796 ng/dL). High dose testosterone (1609 ng/dL) further decreased urinary nitrogen loss over the eugonadal state (by 16%; P < 0.05). Stanozolol yielded the lowest urinary nitrogen excretion of all (P < 0.03). Like urinary nitrogen, the basal metabolic rate showed the greatest change between the hypogonadal and eugonadal states (12%; P < 0.02), with a lesser change during high dose testosterone treatment (4%). Analogously, end-exercise oxygen consumption rose by 11% between the hypogonadal and eugonadal states (P < 0.05). Between the hypogonadal and eugonadal states, no significant changes in pulsatile (nonstimulated), exercise-stimulated, or GRF-stimulated GH secretion or serum insulin-like growth factor I concentrations were observed. Raising testosterone to supraphysiological levels increased pulsatile GH secretion by 62% over that with leuprolide and by 22% over that with saline (P < 0.05). High dose testosterone treatment also increased serum insulin-like growth factor I concentrations by 21% and 34% over those during the eugonadal and hypogonadal states, respectively (P < 0.01). Testosterone did not affect either exercise- or GRF-stimulated GH secretion. In protocol 2, stanozolol did not affect any parameter of GH secretion. To examine the interaction between GH secretion and testosterone on urinary nitrogen excretion and basal metabolic rate, a one-way analysis of covariance was undertaken. Statistical examination of GH production as the covariate and testosterone (by tertile) as the interactive factor demonstrated significant relationships between serum testosterone levels and either urinary nitrogen (P < 0.02) or basal metabolic rate (P < 0.01), but not GH secretion (P = NS). In summary, these results demonstrate that short term modulation of the androgen milieu affects metabolic outcome without necessitating changes in GH secretion. These results have significance for both normal physiology and for the treatment of hypogonadal GH-deficient patients.

Short-Term Modulation of the Androgen Milieu Alters Pulsatile, But Not Exercise- or Growth Hormone (GH)-Releasing Hormone-Stimulated GH Secretion in Healthy Men: Impact of Gonadal Steroid and GH Secretory Changes on Metabolic Outcomes1 (PDF Download Available). Available from: Invalid Link Removed [accessed Feb 4, 2016].

 

[Gutterpump]

FWIW - cholesterol shouldn't be a problem for people who maintain clean diets and eat healthy. I know someone who cruises year round on 800mg/week of test (because of what they do) and keeps all health markers in check, including cholesterol.

 

[datsthat]

FWIW - cholesterol shouldn't be a problem for people who maintain clean diets and eat healthy. I know someone who cruises year round on 800mg/week of test (because of what they do) and keeps all health markers in check, including cholesterol.

Unless that person is using Adex as their AI and/or genetically predisposed to high cholesterol... like myself therefore I swapped Adex for Aromasin.

Edit: correction, Adex lowered my good cholesterol, not total cholesterol. I have bloods to show if anybody interested

 

[Whacked]

Similar or same study below (abstract?):

Trenbolone improves cardiometabolic risk factors and myocardial tolerance to ischemia-reperfusion in male rats with testosterone-deficient metabolic syndrome.
Donner DG1, Elliott GE1, Beck BR2, Bulmer AC1, Lam AK3, Headrick JP1, Du Toit EF1.
Author information
Abstract
The increasing prevalence of obesity adds another dimension to the pathophysiology of testosterone deficiency (TD) and potentially impairs the therapeutic efficacy of classical testosterone replacement therapy (TRT). We investigated the therapeutic effects of selective androgen receptor modulation with trenbolone in a model of TD with the metabolic syndrome (MetS). Male Wistar rats (n=50) were fed either a control standard rat chow (CTRL) or a high-fat/high-sucrose diet (HF/HS). Following 8 weeks of feeding, rats underwent sham surgery or an orchiectomy (ORX). Alzet mini-osmotic pumps containing either vehicle, 2 mg/kg/day testosterone (TEST) or 2 mg/kg/day trenbolone (TREN) were implanted in HF/HS+ORX rats. Body composition, fat distribution, lipid profile and insulin sensitivity were assessed. Infarct size was quantified to assess myocardial damage following in vivo ischaemia-reperfusion, before cardiac and prostate histology was performed. The HF/HS+ORX animals had increased subcutaneous and visceral adiposity; circulating triglycerides, cholesterol and insulin; and myocardial damage, with low circulating testosterone compared to CTRLs. Both TEST and TREN protected HF/HS+ORX animals against subcutaneous fat accumulation, hypercholesterolaemia and myocardial damage. However, only TREN protected against visceral fat accumulation, hypertriglyceridaemia and hyperinsulinaemia; and reduced myocardial damage relative to CTRLs. TEST caused widespread cardiac fibrosis and prostate hyperplasia, which were less pronounced with TREN. We propose that TRT may have contraindications for males with TD and obesity-related MetS. TREN treatment may be more effective in restoring androgen status and reducing cardiovascular risk in males with TD and MetS.

Mind blown. Assumed Tren was poison.

 

[Gutterpump]

Unless that person is using Adex as their AI and/or genetically predisposed to high cholesterol... like myself therefore I swapped Adex for Aromasin.

Edit: correction, Adex lowered my good cholesterol, not total cholesterol. I have bloods to show if anybody interested

Yup, aromasin is key. Much friendlier on lipids.

 

[BeastFitness]

FWIW - cholesterol shouldn't be a problem for people who maintain clean diets and eat healthy. I know someone who cruises year round on 800mg/week of test (because of what they do) and keeps all health markers in check, including cholesterol.

Unless that person is using Adex as their AI and/or genetically predisposed to high cholesterol... like myself therefore I swapped Adex for Aromasin.

Edit: correction, Adex lowered my good cholesterol, not total cholesterol. I have bloods to show if anybody interested

^^^THIS!!!

Please show bloods! The more bloodwork people can see and get an idea for ranges, the more people can learn and benefit!

Mind blown. Assumed Tren was poison.

No matter what AAS is taken, theres side effects and assumed risks. I just hate that tren is so demonized when its not the compound, more the abused dosage and the person's genetic predisposition

Yup, aromasin is key. Much friendlier on lipids.

The effect of exemestane on serum lipid profile in postmenopausal women with metastatic breast cancer: a companion study to EORTC Trial 10951, ‘Randomized phase II study in first line hormonal treatment for metastatic breast cancer with exemestane or tamoxifen in postmenopausal patients’

Background:

The impact of aromatase inhibitors (AIs) on non-cancer-related outcomes, which are known to be affected by oestrogens, has become increasingly important in postmenopausal women with hormone-dependent breast cancer. So far, data related to the effect of AIs on lipid profile in postmenopausal women is scarce. This study, as a companion substudy of an EORTC phase II trial (10951), evaluated the impact of exemestane, a steroidal aromatase inactivator, on the lipid profile of postmenopausal metastatic breast cancer (MBC) patients.

Patients and methods:

The EORTC trial 10951 randomised 122 postmenopausal breast cancer patients to exemestane (E) 25 mg (n = 62) or tamoxifen (T) 20 mg (n = 60) once daily as a first-line treatment in the metastatic setting. Exemestane showed promising results in all the primary efficacy end points of the trial (response rate, clinical benefit rate and response duration), and it was well tolerated with low incidence of serious toxicity. As a secondary end point of this phase II trial, serum triglycerides (TRG), high-density lipoprotein cholesterol (HDL), total cholesterol (TC), lipoprotein a (Lip a), and apolipoproteins (Apo) B and A1 were measured at baseline and while on therapy (at 8, 24 and 48 weeks) to assess the impact of exemestane and tamoxifen on serum lipid profiles. Of the 122 randomised patients, those who had baseline and at least one other lipid assessment are included in the present analysis. The patients who received concomitant drugs that could affect lipid profile are included only if these drugs were administered throughout the study treatment. Increase or decrease in lipid parameters within 20% of baseline were considered as non-significant and thus unchanged.

Results:

Seventy-two patients (36 in both arms) were included in the statistical analysis. The majority of patients had abnormal TC and normal TRG, HDL, Apo A1, Apo B and Lip a levels at baseline. Neither exemestane nor tamoxifen had adverse effects on TC, HDL, Apo A1, Apo B or Lip a levels at 8, 24 and 48 weeks of treatment. Exemestane and tamoxifen had opposite effects on TRG levels: exemestane lowered while tamoxifen increased TRG levels over time. There were too few patients with normal baseline TC and abnormal TRG, HDL, Apo A1, Apo B and Lip a levels to allow for assessment of E’s impact on these subsets. The atherogenic risk determined by Apo A1:Apo B and TC:HDL ratios remained unchanged throughout the treatment period in both the E and T arms.

Conclusions:

Overall, exemestane has no detrimental effect on cholesterol levels and the atherogenic indices, which are well-known risk factors for coronary artery disease. In addition, it has a beneficial effect on TRG levels. These data, coupled with E’s excellent efficacy and tolerability, support further exploration of its potential in the metastatic, adjuvant and chemopreventive setting.

 

[BeastFitness]

I received an email from someone on these boards that was interested in B6 research as it pertains to AAS usage and prolactin



J Clin Endocrinol Metab 1976 Mar;42(3):603-6
Effect of pyridoxine on human hypophyseal trophic hormone release: a possible stimulation of hypothalamic dopaminergic pathway.
Delitala G, Masala A, Alagna S, Devilla L.

A single dose of pyridoxine (300 mg iv) produced significant rises in peak levels of immunoreactive growth hormone GH and significant decrease of plasma prolactin PRL in 8 hospitalized healthy subjects. Serum glucose, luteinizing hormone LH, follicle stimulating hormone FSH and thyrotropin TSH were not altered significantly. In addition, in 5 acromegalic patients who were studied with both L-dopa and pyridoxine, inhibition of GH secretion followed either agent in a similar pattern. These data suggest a hypothalamic dopaminergic effect of pyridoxine.



Boll Soc Ital Biol Sper 1984 Feb 28;60(2):273-8
[influence of administration of pyridoxine on circadian rhythm of plasma ACTH, cortisol prolactin and somatotropin in normal subjects]
Barletta C, Sellini M, Bartoli A, Bigi C, Buzzetti R, Giovannini C.

The influence of vitamin B6 in a dosage of 300 mg X 2 in 24 hrs, on circadian rhythm of plasmatic ACTH, cortisol, prolactin and somatotropin have been studied in 10 normal women. After vitamin B6 24 hrs pattern of ACTH and cortisol is unchanged; prolactin levels are slightly lower, in a statistically unsignificant proportion the night peak of growth hormone is higher in a statistically significant proportion (p. 0.05). The effect of vitamin B6 is likely to me mediated by dopaminergic receptors at hypothalamic level as previous studies by other authors appear to prove.




Journal of Clinical Endocrinology & Metabolism, Vol 42, 1192-1195, Copyright © 1976 by Endocrine Society
Treatment of women with the galactorrhea-amenorrhea syndrome with pyridoxine (vitamin B6)

Three women with the galactorrhea-amenorrhea syndrome and elevated prolactin concentrations experienced a return of regular ovulatory menses within 37-94 days after starting pyridoxine treatment (200-600 mg/day). In each the galactorrhea ceased and serum prolactin levels were maintained in the normal range while taking pyridoxine. In two other women with prolonged secondary amenorrhea but without hyperprolactinemia or galactorrhea, pyridoxine at dosages up to 600 mg/day did not restore ovulatory menses. Pyridoxine treatment was also ineffective in decreasing profuse galactorrhea in one woman with normal prolactin levels and regular ovulatory menses. In the three women effectively treated with pyridoxine, the galactorrhea returned, serum prolactin levels increased, and the menses ceased after discontinuing pyridoxine. These results imply that pyridoxine, by decreasing the excessive secretion of prolactin, may be useful in the long-term medical management of women with hyperprolactinemia and the galactorrhea-amenorrhea syndrome.




Prolactin and thyrotropin responses to thyrotropin-releasing hormone in patients with secondary amenorrhea: the effect of bromocriptine
E Hirvonen, T Ranta and M Seppala

Prolactin (PRL) and thyrotropin (TSH) responses to a 200 mug intravenous thyrotropin-releasing hormone (TRH) bolus were measured by radioimmunoassay in 11 women with hyperprolactinemic amenorrhea and 9 with normoprolactinemic amenorrhea. In all cases, the tests were carried out under basal conditions and repeated during bromocriptine treatment. In women whose basal PRL level was normal; TRH caused a maximal PRL increment of 85 +/- 25.2 mug/l (mean +/- SE), while those women whose basal PRL level was raised showed a smaller increase (5.2 +/- 11.9 mug/l) (P=0.02). The peak levels were not significantly different in these two groups (95.0 +/- 26.7 and 134.6 +/- 35.9 mug/l) (P is greater than 0.1). During bromocriptine treatment, the raised PRL levels decreased in all cases, but levels over 30 mug/l remained in 3 patients, one of whom turned out to have a pituitary tumor. Prolactin responses to TRH were markedly inhibited in normoprolactinemic patients by the dose of bromocriptine used. The mean maximal net increase of PRL was 2.0 +/- 0.9 mug/l in normoprolactinemic patients and 11.0 +/- 8.1 mug/l in hyperprolactinemic patients taking bromocriptine. After TRH stimulation during bromocriptine, the peak PRL levels in hyperprolactinemic patients were higher (32.7 +/- 10.5 mug/l) than in normoprolactinemic patients (7.2 +/- 1.5 mug/l). Unlike what has been described for hypothyroid patients, the basal TSH level in euthyroid amenorrhea patients was not affected by bromocriptine, and we found that bromocriptine has no effect on the TRH-TSH response.

 

[Dma378]

Awesome ^^^^

Had never even heard either ai's relationship to lipids.

Exemestane was already my AI of choice, but this is great info.

 

[Dma378]

Also as men taking these essentially as little as possible, i.e. e3d, our doses are significantly lower than what a woman taking them for breast cancer, etc. would take them at. Which is daily correct?

 

[BeastFitness]

Awesome ^^^^

Had never even heard either ai's relationship to lipids.

Exemestane was already my AI of choice, but this is great info.

Thanks dude!

Also as men taking these essentially as little as possible, i.e. e3d, our doses are significantly lower than what a woman taking them for breast cancer, etc. would take them at. Which is daily correct?

The dosage for men VS women is honestly going to be dependent upon their blood work. I've had some males and females run it e2D, e4D, or even not at all…obviously their is going to be a huge discrepancy among gender but its still going to come down to the individual's specific blood work results…if you can't tell, I'm a HUGE fan of getting proper blood work testing done! If you don't know what going on internally, how can you expect to optimize hormone levels?

 

[Driven2lift]

Subbed late but caught up.
Solid thread here.

 

[datsthat]

I received an email from someone on these boards that was interested in B6 research as it pertains to AAS usage and prolactin.

I did a breift search but didn't find any...Do you know if anyone sells injectable b6 + b12 combined? thanks

 

[datsthat]

Adex effects on Lipid - bloodwork

Summary (See 1st pic below for standard range):
I started taking Anastrozole on Nov 1 2015 (start of TRT) which came from either Bartells or compound pharmacy. My dose was .25mg day after injection. On Jan 11th, my dose was increased to .5mg day after injection when my e2 came back higher than normal range because I accidentally pinned more than I was supposed to (oops).

Total Cholesterol decreased from 214 down to 147:yes(1):. 147 is the lowest mine has ever been. Highest was mid 300's
Good Cholesterol (HDL) deceased from 80 down to 27:aargh:
Bad Cholesterol (LDL) decreased from 121 down to 11:yes(1):
Ratio increased from 2.7 up to 5.4

What concerns me the most is the ratio.

Bloodwork on 10-10-2015
Invalid Link Removed


Bloodwork on 01-27-2016. This test was taken at my work.
Invalid Link Removed

 

[Gutterpump]

What concerns me the most is the ratio.

The ratio is always the worst part for anyone who partakes in AAS.
What I'd like to know, is if the ratio is really all that important if total cholesterol is in a healthy range.

 

[B5150]

FYI life insurance looks at ratio as part of your "category" of coverage as well lipids in general and blood pressure. We old guys know this stuff

 

[brofessorx]

good tool for those looking to understand aas
ncbi.nlm.nih.gov/pmc/articles/PMC2439524/

 

[criticalbench]

subbed

 

[Hyde]

The "short-cycling" dry short/esterless/oral article was an awesome read. Am I missing anything when I say it looks like a standard protocol was basically moderate tren ace and anavar for 2-3wks, 2 weeks of clomid, and 2 weeks neither AAS or SERM, and they never came off 2.5mg of letro daily??

 

[BeastFitness]

Subbed late but caught up.
Solid thread here.

Right on man welcome in!

I did a breift search but didn't find any...Do you know if anyone sells injectable b6 + b12 combined? thanks

They are definitely for sale, maybe not in combination unless done at a clinic but I know you can buy them individually. I've seen (anecdotally) many people respond very well to these types of injections.

[Efficacy of a combination therapy with vitamins B6, B12 and folic acid for general feeling of ill-health. Results of a non-interventional post-marketing surveillance study].

Abstract
OBJECTIVE:
In the present non-interventional postmarketing surveillance study, patients with symptoms of an inadequate supply of vitamins were tested for how a treatment with a combination vitamin injection consisting of vitamins B6, B12 and folic acid affects mood and fitness. The evaluation of the efficacy and tolerability as well as the documentation of adverse drug reactions were carried out by the physician.
METHODS:
The patient collective included 1430 patients (70.8% women, average age 67.1 years, average BMI 25.5 kg/m2). The average duration of treatment was 4.5 weeks with an average of 8.3 intramuscular injections. The principal method for determining the efficacy was the self-assessment scale of well-being (Bf-S) according to Zerssen (sum score with a value range between 0 and 56 points).
RESULTS:
The sum score of the Bf-S decreased from 37.5 (+/-10.1) points at admission to 15.6 (+/- 9.4) points after four weeks of treatment. The subjective impression improved correspondingly in 96.3% of the patients. The improvement of the Bf-S was equally good in women and men. The number of injections correlated with the improvement in the sum score. The tolerability was mainly rated as very good or good.
CONCLUSIONS:
Eight vitamin infections over four weeks led to a clear improvement in the mood and vitality of patients with symptoms of intracellular vitamin B deficiency.

Summary (See 1st pic below for standard range):
I started taking Anastrozole on Nov 1 2015 (start of TRT) which came from either Bartells or compound pharmacy. My dose was .25mg day after injection. On Jan 11th, my dose was increased to .5mg day after injection when my e2 came back higher than normal range because I accidentally pinned more than I was supposed to (oops).

THANK YOU FOR POSTING THAT!! Its a lot easier for people to understand if they can see legitimate numbers, ratios, and blood work on paper VS simply talking about it.

The ratio is always the worst part for anyone who partakes in AAS.
What I'd like to know, is if the ratio is really all that important if total cholesterol is in a healthy range.

Total cholesterol is secondary to the actual ratios. With everyone's individual genetics, you need to look at the composition OF your cholesterol and not just your total number.

FYI life insurance looks at ratio as part of your "category" of coverage as well lipids in general and blood pressure. We old guys know this stuff

Ohh I'm glad I'm not dealing with life insurance yet HAHA! I hate dealing with that kind of stuff lol

good tool for those looking to understand aas
ncbi.nlm.nih.gov/pmc/articles/PMC2439524/

Thanks man! I'll post it below so people can view it easier!

Pharmacology of anabolic steroids

Abstract
Athletes and bodybuilders have recognized for several decades that the use of anabolic steroids can promote muscle growth and strength but it is only relatively recently that these agents are being revisited for clinical purposes. Anabolic steroids are being considered for the treatment of cachexia associated with chronic disease states, and to address loss of muscle mass in the elderly, but nevertheless their efficacy still needs to be demonstrated in terms of improved physical function and quality of life. In sport, these agents are performance enhancers, this being particularly apparent in women, although there is a high risk of virilization despite the favourable myotrophic–androgenic dissociation that many xenobiotic steroids confer. Modulation of androgen receptor expression appears to be key to partial dissociation, with consideration of both intracellular steroid metabolism and the topology of the bound androgen receptor interacting with co-activators. An anticatabolic effect, by interfering with glucocorticoid receptor expression, remains an attractive hypothesis. Behavioural changes by non-genomic and genomic pathways probably help motivate training. Anabolic steroids continue to be the most common adverse finding in sport and, although apparently rare, designer steroids have been synthesized in an attempt to circumvent the dope test. Doping with anabolic steroids can result in damage to health, as recorded meticulously in the former German Democratic Republic. Even so, it is important not to exaggerate the medical risks associated with their administration for sporting or bodybuilding purposes but to emphasize to users that an attitude of personal invulnerability to their adverse effects is certainly misguided.

subbed

Welcome in dude!

 

[Burnfire]

A little late, but subbed! So much information and knowledge, thank you for starting this thread!

 

[BeastFitness]

A little late, but subbed! So much information and knowledge, thank you for starting this thread!

Welcome in brother!

 

[BeastFitness]

I have never tried anything along these lines so have no anecdotal evidence to back up any claims…has anyone tried something along these lines?


[Does grapefruit juice increase the bioavailability of orally administered sex steroids?].

To verify if and to which extent the interaction with grapefruit juice can increase bioavailability of orally administered sexual steroids.
DESIGN:
Pilot pharmacokinetics study.
SETTING:
Department of Obstetrics and Gynecology and Institute of Pharmacology, Medical Faculty, Palacký University, Olomouc; Department of Nuclear Medicine, University Hospital, Olomouc.
METHODS:
2 mg of estradiol valerate and 100 mg of micronized progesterone were given to eight healthy postmenopausal volunteers. Blood samples were collected at time 0, 2, 3, 5 and 24 hours after tablets application. The same trial was repeated a week later but tablets were swallowed with 200 ml of grapefruit juice. Serum levels of estradiol and progesterone were measured by RIA. Results were statistically evaluated using the Wilcoxon's nonparametric paired test.
RESULTS:
Though grapefruit juice on average slightly increased serum levels of estradiol (E2) and progesterone, this increase reached statistical significance only for the E2 level 24 hours after application of tablets. The mean area under curve (AUC) of estradiol rose significantly to 117%. The even greater increase in the mean AUC of progesterone (to 125%) was not statistically significant because of marked individual variability of response.
CONCLUSIONS:
Our results suggest that grapefruit juice may increase bioavailability of orally administered estradiol and progesterone. The response varies markedly between individuals. This observation may be of some importance also for users of OC and HRT.



BEYOND the abstract (if your a detail junkie like myself)

Grapefruit juice interacts with a number of medications. This unusual discovery was made serendipitously in 1989 during an experiment designed to test the effect of ethanol on a calcium-channel blocker.1 The observed response was later determined to be due to the grapefruit juice delivery vehicle rather than the alcohol. In the past decade, the list of drug interactions with grapefruit juice has expanded to include several classes of medication, precipitating a recent advisory from Health Canada. The interaction: As little as 250 mL of grapefruit juice can change the metabolism of some drugs.3 This drug?food interaction occurs because of a common pathway involving a specific isoform of cytochrome P450 ? CYP3A4 ? present in both the liver and the intestinal wall. Studies suggest that grapefruit juice exerts its effect primarily at the level of the intestine. After ingestion, a substrate contained in the grapefruit binds to the intestinal isoenzyme, impairing first-pass metabolism directly and causing a sustained decrease in CYP3A4 protein expression.5 Within 4 hours of ingestion, a reduction in the effective CYP3A4 concentration occurs, with effects lasting up to 24 hours.6 The net result is inhibition of drug metabolism in the intestine and increased oral bioavailability. Because of the prolonged response, separating the intake of the drug and the juice does not prevent interference. Individuals express CYP3A4 in different proportions, those with the highest intestinal concentration being most susceptible to grapefruit juice?drug interactions.5 An effect is seen with the whole fruit as well as its juice, so caution should be exercised with both.7 The precise chemical compound in grapefruit that causes the interaction has not been identified. There is no similar reaction with orange juice, although there is some suspicion that “sour oranges” such as the Seville variety, may have some effect.8 A recent study, however, that tested the known interference of grapefruit juice with cyclosporine showed no similar effect with Seville oranges. There is some interest in the potential therapeutic benefit of adding grapefruit juice to a drug regimen to increase oral bioavailability.3 The limitation is the individual variation in patient response. However, if the chemical that causes grapefruit’s CYP3A4 inhibition is elucidated, there may be an opportunity to modulate that pathway in a controlled fashion. What to do: Much of the data obtained on grapefruit juice?drug interactions involved measuring serum drug concentrations in small numbers of healthy volunteers. Because of the limited data and only occasional case reports,10 it is difficult to quantify the clinical significance for individual patients. One may assume that the interaction occurs primarily with oral medicines, and only with those that share the CYP3A4 metabolism pathway, with the consequence being increased oral bioavailability, higher serum drug concentrations and associated adverse effects. Physicians should review medication lists often, with the goal of warning patients about adverse interactions. A list of medicines with which patients should not consume grapefruit is provided in Table 1.3,11,12 In the case of several medications that share the CYP3A4 metabolism pathway, but for which a clinical effect has not been elucidated or is theoretical, patients should be advised to consume grapefruit cautiously and be monitored for toxicity..

Grapefruit juice drug interactions
The novel finding that grapefruit juice can markedly augment oral drug bioavailability was based on an unexpected observation from an interaction study between the dihydropyridine calcium channel antagonist, felodipine, and ethanol in which grapefruit juice was used to mask the taste of the ethanol. Subsequent investigations showed that grapefruit juice acted by reducing presystemic felodipine metabolism through selective post-translational down regulation of cytochrome P450 3A4 (CYP3A4) expression in the intestinal wall. Since the duration of effect of grapefruit juice can last 24 h, repeated juice consumption can result in a cumulative increase in felodipine AUC and Cmax. The high variability of the magnitude of effect among individuals appeared dependent upon inherent differences in enteric CYP3A4 protein expression such that individuals with highest baseline CYP3A4 had the highest proportional increase. At least 20 other drugs have been assessed for an interaction with grapefruit juice. Medications with innately low oral bioavailability because of substantial presystemic metabolism mediated by CYP3A4 appear affected by grapefruit juice. Clinically relevant interactions seem likely for most dihydropyridines, terfenadine, saquinavir, cyclosporin, midazolam, triazolam and verapamil and may also occur with lovastatin, cisapride and astemizole. The importance of the interaction appears to be influenced by individual patient susceptibility, type and amount of grapefruit juice and administration-related factors. Although in vitrofindings support the flavonoid, naringin, or the furanocoumarin, 6′,7′-dihydroxybergamottin, as being active ingredients, a recent investigation indicated that neither of these substances made a major contribution to grapefruit juice-drug interactions in humans.

Introduction
The opportunity for a food-drug interaction is an everyday occurrence. The interaction can be particularly important when total drug absorption is altered. Recently, a chance observation led to the finding that grapefruit juice can markedly increase the oral bioavailability of a number of medications [1]. This article retraces discovery of this novel interaction and reviews the mechanism of action, summaries both studied and predicted medications for an interaction, discusses possible active ingredient(s) in the juice and considers clinical implications

Discovery
Originally, a study was designed to test for an interaction between ethanol and the dihydropyridine calcium channel antagonist, felodipine [2], an analogue of nifedipine. Grapefruit juice was chosen to mask the taste of the ethanol following an assessment of every juice in a home refrigerator one Saturday evening. White grapefruit juice, particularly double-strength juice (single dilution of frozen concentrate), was the most effective. The combination of a non-intoxicating dose of ethanol and felodipine resulted in lower standing blood pressure and a high frequency of orthostatic hypotension compared with felodipine alone in patients with untreated borderline hypertension [2]. Although plasma felodipine concentrations were not different between treatments, they were several-fold higher than observed in other pharmacokinetic investigations with the same dose of drug. A systematic examination for obvious possible causes, such as incorrect dose or drug assay problems, did not resolve this discrepancy and eventually resulted in a pilot project in a single volunteer to judge the role of the juice. Plasma felodipine concentrations were more than five-fold greater with grapefruit juice compared with water .

Felodipine disposition and metabolism
Felodipine has been the most extensively studied probe for grapefruit juice?drug interactions. Normally, felodipine is completely absorbed from the gastrointestinal tract following oral administration [3]. However, it undergoes high presystemic (first-pass) metabolism resulting in low absolute bioavailability averaging 15% [3] but ranging from 4% to 36% among individuals [4]. Both the gut wall and the liver appear responsible for presystemic felodipine elimination.

Grapefruit juice effects
The first report of this interaction revealed that grapefruit juice, but not orange juice, tripled mean plasma felodipine area under the curve (AUC) compared to water in borderline hypertensive patients [12]. Blood pressure reduction, heart rate increase and frequency of vasodilatation-related adverse events were also greater. Grapefruit juice markedly elevated plasma peak felodipine concentration (Cmax) but did not alter systemic felodipine elimination half-life (t1/2) [12]. Since grapefruit juice did not change intravenous felodipine pharmacokinetics [5], it indicates that the interaction with grapefruit juice resulted from inhibition of presystemic drug metabolism.
Grapefruit juice reduced dehydrofelodipine/felodipine AUC ratio and increased absolute dehydrofelodipine AUC [1, 12]. The decrease in the AUC ratio was compatible with inhibition of the primary metabolic pathway. The absolute increase in dehydrofelodipine AUC indicated that a subsequent metabolic pathway might also be inhibited and this was supported by measurements showing that the M3 metabolite AUC was reduced [8]. Thus, grapefruit juice appeared to inhibit CYP3A4, an important isozyme of cytochrome P450 since it oxidizes a broad range of drugs and xenobiotics [13], with predominant and perhaps exclusive action on presystemic drug elimination.
Recently, the effect of grapefruit juice on drug metabolizing enzymes of the small bowel and liver was reported in an in vivoinvestigation in humans [14]. Grapefruit juice consumption for 5 days caused a mean 62% reduction of small bowel enterocyte CYP3A4 and CYP3A5 protein content associated with a greater than 3- and 5-fold increase in felodipine AUC andCmax, respectively. In contrast, liver CYP3A4 activity, as measured by the erythromycin breath test, and colon CYP3A5 protein content were not altered. Also, intestinal CYP2D6 and CYP1A1 protein content were not affected. Although these changes were measured after 5 days of grapefruit juice, preliminary data also showed that small bowel CYP3A4 can be markedly reduced 4 h after a single glass of juice. Consequently, it was concluded that grapefruit juice acted by selectively inhibiting CYP3A isozymes of the small bowel to cause greater felodipine oral bioavailability.
Decreased expression of CYP3A isoforms by grapefruit juice implied that the interaction was not simple competition for substrate metabolism. Since small bowel CYP3A4 mRNA was not changed [14], grapefruit juice likely decreased CYP3A4 protein content by a post-transcriptional mechanism, possibly involving accelerated CYP3A4 degradation through mechanism-based enzyme inhibition. Thus, the return of CYP3A4 activity would require de novo enzyme synthesis which could result in prolonged effect of grapefruit juice.
The duration of activity of grapefruit juice has been studied. In one study, consumption of a single glass (200 ml) of juice at various time intervals before felodipine showed that the extent of increase in felodipine AUC and Cmax was maximal between simultaneous and 4 h previous juice administration with drug [15]. Then, the magnitude of the interaction declined slowly with increasing time interval between grapefruit juice and felodipine administration. The half-life of effect of grapefruit juice was estimated at 12 h. Higher felodipine Cmax was still evident when grapefruit juice was consumed 24 h before felodipine. In another investigation, the effect of routine grapefruit juice consumption was evaluated [14]. One glass (250 ml) of grapefruit juice augmented mean felodipine AUC and Cmax to 267% and 345%, respectively, of that compared with water. Grapefruit juice three times daily with meals for 5 days further increased felodipine AUC and Cmax to 345% and 538% of that compared with water showing a cumulative effect of the juice.
The magnitude of the interaction was highly variable among individuals ranging from no change to six-fold greater plasma felodipine AUC and Cmax with grapefruit juice compared with water under single dose conditions [1, 8, 14, 16]. However, it was reproducible within individuals following repeat testing and thus, dependent on factors inherent to the individual [16]. Grapefruit juice reduced small bowel CYP3A4 content contingent upon pretreatment levels [14]. Individuals with the highest small bowel CYP3A4 content before grapefruit juice had the largest reduction in CYP3A4 and highest increase in felodipineCmax with grapefruit juice. Consequently, individual disparity in the magnitude of interaction with grapefruit juice appears at least partially explained by innate differences in baseline small bowel CYP3A4 protein content.

Conclusions
A single glass of grapefruit juice has the potential to augment the oral bioavailability and to enhance the beneficial or adverse effects of a broad range of medications, even by juice consumed hours beforehand. Grapefruit juice acts by inhibiting presystemic drug metabolism mediated by CYP3A isoforms in the small bowel. The interaction appears particularly relevant for medications with at least a doubling of plasma drug concentration or with a steep concentration-response relationship or a narrow therapeutic index. Patients that appear particularly susceptible have high small bowel CYP3A4 content, hepatic insufficiency or a pre-existing medical condition which predisposes to enhanced, excessive or abnormal drug effects. Since grocers do not take a drug history, physicians, pharmacists and other health professionals should educate patients about consumption of grapefruit juice with medications.
Isolation of the active ingredient(s) may lead to identification of other foods producing this interaction or to its incorporation into pharmaceutical formulations. Further research is required to understand the interaction better during routine grapefruit juice consumption, at amounts considered safe for administration with drugs and with different patient populations. Nevertheless, the serendipitous observation of increased plasma felodipine concentrations by grapefruit juice has provided fundamental new knowledge to improve pharmacotherapy and to stimulate research.

 

[datsthat]

I have never tried anything along these lines so have no anecdotal evidence to back up any claims…has anyone tried something along these lines?


[Does grapefruit juice increase the bioavailability of orally administered sex steroids?].

.

I've only tried with narcotic pain killlers back in my addicted days, but I couldn't tell if it worked or not because I was a pill junkie and my qualitative skills sucked.

 

[datsthat]

EDIT: I deleted my post as this thread about about AAS, not about personal cycle advice. I apologize for being so selfish and taking advantage of BeastFitness

 

[BeastFitness]

I've only tried with narcotic pain killlers back in my addicted days, but I couldn't tell if it worked or not because I was a pill junkie and my qualitative skills sucked.

It will be interesting to see if anyone else has any input on this

How does this cycle look Nandrolone Cycle look?

Deca 250mg/ml
NPP 250mg/ml
Test Cyp 200mg/ml
Test Prop 75mg/ml

The reason why proposed decreasing NPP after 4 weeks is because Deca will "kick" in around week 4. Or should I drop NPP after week 4 and run Deca at 400mg starting week 5. AI will be aromasin. Blood work will be done at week 5 and then week 10 to ensure AI is on point. Then going back to TRT dose once done. I will have TRT blood work E6Months so 2 months after end of this cycle.

Any pros and cons?

Should I drop Deca and run NPP the entire time so that I don't risk screwing up my TRT blood work?

What would you do differently and why?


Continual Thanks from me

Ok so an actual cycle specific question is going to depend on your training and nutritional programming during that time. I know the majority of people simply plan their cycle and allow their training and nutrition to follow…I'm the opposite. I like to plan my client's training and nutritional protocols THEN implement the cycles based off of when calories are being pushed/pulled back as well as when your training is planned for an overreaching/acclimation phase.

So lets say your training and nutritional protocols are what I view as "optimal." THEN I would look into past cycle history (compounds used, dosages, durations, etc.)

So lets say in the past you've never used these dosages and this is your proposed BLAST. There is obviously more than 1 way to skin a cat but personally, if you need to time your blood work to stay on TRT, I would go with NPP and drop deca to ensure you can time your injections properly. Its hard but a lot of this is going to be based off of your current and past history of usage so its really hard to say. I would however ask why your using both test cyp and prop.

Not a problem man! Keep em coming!

Are you planning on planning a growth phase? If so, when? More details the better haha

 

[B5150]

IMHO and I mean no disrespect but this thread is supposed to be the "research thread" and not a datsthat personal cycle advice thread.

 

[datsthat]

It will be interesting to see if anyone else has any input on this



Ok so an actual cycle specific question is going to depend on your training and nutritional programming during that time. I know the majority of people simply plan their cycle and allow their training and nutrition to follow…I'm the opposite. I like to plan my client's training and nutritional protocols THEN implement the cycles based off of when calories are being pushed/pulled back as well as when your training is planned for an overreaching/acclimation phase.

So lets say your training and nutritional protocols are what I view as "optimal." THEN I would look into past cycle history (compounds used, dosages, durations, etc.)

So lets say in the past you've never used these dosages and this is your proposed BLAST. There is obviously more than 1 way to skin a cat but personally, if you need to time your blood work to stay on TRT, I would go with NPP and drop deca to ensure you can time your injections properly. Its hard but a lot of this is going to be based off of your current and past history of usage so its really hard to say. I would however ask why your using both test cyp and prop.

Not a problem man! Keep em coming!

Are you planning on planning a growth phase? If so, when? More details the better haha

I may take this conversion via PM as I don't want this thread to be "what about my cycle" and clog this up personal inquires. I should have thought about the ramifications prior to being so selfish. For that I apologize to you and others that are following this thread.

 

[datsthat]

IMHO and I mean no disrespect but this thread is supposed to be the "research thread" and not a datsthat personal cycle advice thread.

You are abolutely correct....I just came to that realization few mins after I made my post.

EDIT: I have deleted my cycle advice inquiry

 

[BeastFitness]

Not a problem at all dats! Shoot me a message whenever!


I have an interesting bit of research I'll be posting in a little….it should get everything thinking about every cycle they've ever done