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Gold Aesthetic drug: Primobolan cycle

Phill

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Get Shredded!
I have been in for 3 weeks now.

The end is not fixed but I will go on at least throughout February and March.

Primo 700 mg/week
Test E 1 gr/week
EQ 2 gr/week

Arimidex 1 mg/ed

I'm also taking some Proviron. Primo always kills me libido.

In addition to these, Noopept / Rapofill.


All strictly as usual provided by my best source: PuritySourceLabs.ru
 
Following

Max
#primoluv
 
my receptors have been raped for years.
It's like having sex with a prostitute, you need a huge cock to make her come.

[FONT=Verdana,Arial,Tahoma,Calibri,Geneva,sans-serif]however EQ doesn't make text, you don't have to count it.
Everyone knows that it is only oil and does nothing.[/FONT]
 
[FONT=Verdana,Arial,Tahoma,Calibri,Geneva,sans-serif]however EQ doesn't make text, you don't have to count it.
Everyone knows that it is only oil and does nothing.[/FONT]

Lol EQ @2 grams? Huhmm ... similar to adding flour to beef stock to make a brown gravy, which also gives no lbm gains lol





Sent from my iPhone using Tapatalk
 
IML Gear Cream!
Phill always comes out Pins-a-Blazing. Gram here, gram there.

Give ‘em hell Phill, you always polish up real nice. Dude knows his stuff and is dedicated to his craft.
 
I always take 50mg Proviron when I take primo. Seems to help.

Max

Yeah, was just curious about the science behind his lower libido bc I was thinking the Primo has little conversion to estrogen and was the fewest on side effects overall...IDK?
 
Yeah, was just curious about the science behind his lower libido bc I was thinking the Primo has little conversion to estrogen and was the fewest on side effects overall...IDK?

It eludes me because Primobolan usually causes increased libido but, it may just be that a persons system could be suppressed or hpg axis(I read that serotonin levels being messed up can cause loss of libido). There were a lot of factors including aas, AI/Serm, supplements, and a lot of different medications; along with past med/physical background. Hope you can nip it in the bud. Good luck

Max
 
Methenolone [17beta-Hydroxy-1-methyl-5alpha-androst-1-en-3-one] also known as methylandrostenolone, known in general with old trade name Primobolan (today Rimobolan), is AAS DHT derivative with androgen/anabolic value equal to 44-57:88.
It is a natural molecule, which is found inside the adrenal glands of domestic felines in pregnancy, and is synthesized in the laboratory.

Methenolone was first described in 1960. Squibb introduced the drug (in the oral and injectable form) to the United States in 1962. This molecule was sold for a very short period of time both in its oral form (in 20 mg tablets) and in its injectable form, respectively under the brand names of Nibal® and Nibal® Depot.

Schering in western Germany (now Bayer) obtained the rights to the drug which it would sell in the same year under the name Primobolan. Nibal® (in both forms) was soon removed from the United States market without ever returning to it. Thus Schering obtained exclusive patent rights for the production of Metenolone acetate and enanthate, and would have continued to sell the drug without interruption since 1962, and it became natural for consumers to identify Metenolone as a Schering product.

Thus Primobolan has always been identified as a European steroid, and during the 1960s and 1970s it was sold in countries such as Germany, Austria, Belgium, France, the Netherlands and Finland. For a period of time Schering produced an oil-based injectable form containing 20 mg/ml of Metenolone acetate (called Primobolan Acetate), but was declared out of production since 1993. Injectable Metenolone acetate proved to be very popular for race preparation, so much so that when it was eliminated from the market, European athletes missed it. Although the oral form of Methenolone acetate continued to exist it is not the same (obviously the injectable version is much more efficient for this steroid)

Schering maintained control of the Methenolone patent until the late 1970s. Before its patents expired, Schering had rigorously protected its intellectual property rights against any potential infringement, including in the U.S. market, where the company did not distribute Primobolan. Although Methenolone has not been available for commercial sale in the United States for decades, it has technically maintained its FDA-approved drug status.

Primobolan is generally prescribed as an anabolic agent for the growth of lean tissue, often used in post-operative cases, of prolonged infections, of diseases with a strong catabolic component, following chronic administration of corticosteroids, or in convalescence. Some doctors prescribe this molecule for the treatment of osteoporosis, sarcopenia (the natural loss of muscle mass with aging), some cases of chronic hepatitis, and breast cancer (usually as a secondary drug followed by other therapies). The steroid has also been used to promote weight gain in underweight premature babies and children in clinical trials, and has been able to do this effectively and without signs of toxicity or undesirable effects. Athletes have the use of this AAS has long been favored, with its contained androgenic value and its non-estrogenic nature, characteristics that make it very favorable for beginner athletes.

Although Primobolan has shown good clinical safety margin, by the 1990s Schering had grown to become a giant pharmaceutical multinational, and was inevitably forced to review its steroid offering worldwide in light of public concerns. about doping in sports. Primobolan would have been voluntarily withdrawn from most of the countries that originally sold it. Today Primobolan is sold in a handful of countries, including Spain, Turkey, Japan, Paraguay and Ecuador. Despite its limited supply, Bayer has remained (almost) the exclusive producer of Methenolone in the global human pharmaceutical business.

Schering withdrew the oral form of the drug from most markets in the early 2000s. There are still no oral versions containing 50mg still in production, there are at most a couple of products containing 5 mg or 25 mg which can be still legally in circulation. The only confirmed sources for oral Primobolan in recent years have been in Japan and South Africa, and these have been sold under the Schering brand. It is not known whether these products were also sold under the new Bayer label. In addition to this, a small number of pharmaceutical preparations containing methenolone acetate may still be in production. In recent years, however, Methenolone is also produced and distributed by UGLs on the black market.

As previously mentioned, Methenolone is a derivative of DHT with two structural modifications, namely:
-the double bond in C1-C2, which increases the stability of the ketone in the C3 position (essential for maintaining the bond with the muscle androgen receptors, where in fact Metenolone is degraded to diol; typical of DHT which undergoes hydroxylation in muscle cells almost instantaneous) only to a lesser extent; in addition, this modification makes the molecule less similar to the bond with the SHBG, increasing its bio activity.
-the methyl in C1 which increases to some extent the resistance of the molecule to the hepatic passage; not at the level of a methylation in C17, but not as toxic as these. This feature allows its use, even oral, of the acetate form, although at much higher dosages than the enanthate form, typically administered by injection. The presence of methyl in C-1 is the only difference compared to Diidroboldenone: since it is about three times more potent as anabolic than Metenolone, it is assumed that this modification of the molecular structure, even if it increases oral bioavailability, decreases it somehow the anabolic power, most likely by increasing the affinity for SHBG, particularly high in Methenolone. In practice, methylation in C-1 partially reverses the effect of the double bond in C1-C2, making Methenolone more orally bioavailable than Boldenone, but making the first compound less bioactive.

Metenolone, being a reduced 5-alpha molecule (as derivative of DHT), does not undergo any aromatization and does not exhibit any measurable estrogenic activity. Hence, estrogen-dependent side effects should not be considered when administering this steroid alone. Sensitive individuals also need not worry about developing gynecomastia, or appreciable water retention with this drug.

Although this steroid has an androgenic activity of 44-57, the appearance of androgenic side effects is still possible. This can include oily skin, acne, body and face hair growth. Also this AAS can aggravate androgenetic alopecia where genetically predisposed. Women should be warned of the potential virilizing effects of this steroid. These can include deep voice, menstrual irregularity, changes in the structure of the skin, growth of facial hair (hirsutism), and enlargement of the clitoris. So although Metenolone is a very mild AAS, it can exhibit strong androgenic side effects at high doses.

Metenolone, not being a C-17 methylated molecule, is not considered a hepatotoxic steroid; liver toxicity is unlikely. No appreciable changes in liver stress markers were observed during the studies when the drug was administered at therapeutic doses. The oral form of Methenolone has some resistance to hepatic de-activation, and liver toxicity, insufficiency, and death have been reported in an elderly patient receiving oral methenolone acetate. Although it is unlikely, hepatotoxicity cannot be completely excluded, especially with very high oral doses.

The absence of methylation in position C-17 gives Methenolone an overall mild ability to influence the lipid balance. AAS can have deleterious effects on serum cholesterol. This includes a tendency to reduce HDL cholesterol (good) and to increase LDL cholesterol (bad), with an alteration of the balance between HDL / LDL promoting a greater risk of arteriosclerosis. The relative impact of an AAS on serum lipids depends on the dose, the route of administration (oral or injectable), the type of steroid (flavored or non-aromatizable), and the level of resistance to liver metabolism. Methenolone should have a stronger negative effect on liver cholesterol management than Testosterone or Nandrolone because of its unflavourable, but much weaker nature than AAS c-17 alpha alkylates. Due to the method of administration, oral methenolone has a slightly stronger negative effect on lipids than the injectable form. AAS can also adversely affect blood pressure and triglyceride levels, reducing endothelial relaxation, and promoting left ventricular hypertrophy, all factors with a potential to increase the risk of cardiovascular disease and myocardial infarction.

all AAS if taken in sufficient doses to promote muscle mass increase cause suppression of endogenous Testosterone. Without intervention with Testosterone-stimulating substances, and adequate PCT, Testosterone levels should return to normal within 1-4 months of the sale of the drug. Note that prolonged hypogonadotropic hypogonadism can develop secondary to the abuse of steroids, which requires medical intervention. Methenolone is generally described as having a low impact on endogenous Testosterone production.

Although this may be true with small clinical doses (20-25 mg per day), in sports, and therefore doping, things are different. In one study, more than half of patients treated with only 30-45 mg per day of methenolone acetate experienced a 15-65% suppression of gonadotropin levels. Although this molecule has a lower suppressive potential compared to other AAS, the suppression caused by Metenolone is still present and verifiable. If Methenolone is used in moderate doses for less than 8 weeks, hormonal recovery should not be a prolonged experience. As for the injectable form, at a low dosage of 100-200 mg per week, Methenolone should offer a less incisive measurable suppression than an equal dose of Testosterone and Nandrolone, probably due to its unflavourable nature.

As for the oral form, as for other oral AAS, it is recommended to take it between meals as studies have shown that taking an oral anabolic steroid with food can decrease its bioavailability. This is caused by the fat-soluble nature of the steroid hormones, which can allow part of the drug to dissolve with undigested food fats, reducing absorption from the gastrointestinal tract. For maximum bioavailability, this steroid must be taken on an empty stomach.

The injectable acetate form (from the black market) is still used as a local "fat burner" (intradermal injections), given the marked affinity for androgen receptors of Methenolone. In fact, the androgen receptors in the adipose tissue stimulate lipolysis; Furthermore, this possibility of use is reinforced by the anti-estrogenic property, common to Mesterolone and Drostanolone (both derivatives of DHT), deriving from the bond with the aromatase coenzyme P-450. Furthermore, Methenolone shows no affinity with Progesterone receptors and with Cortisol receptors; the first is obviously an advantage (no progestogenic activity) while the second is a disadvantage (no anti catabolic effect) that can be easily solved by combining the molecule with another AAS or with substances having this characteristic. Methenolone is said to have a strong affinity for liver AR receptors, a feature that would lead to a healthy enlargement of the organ (without certain source).

The half-life of Methenolone Acetate is approximately 4-6 hours while Methenolone Enanthate has a half-life of approximately 10.5 days.

Not being a particularly powerful AAS, its combination with other molecules is not easy to choose. Certainly, it would not be properly exploited if taken with strongly AR compounds such as Trenbolone, while with molecules with non-genomic activity it finds its best combination. In a beginner's "Bulk", Methenolone can be combined with Metandrostenolone (Dianabol) while in a "Cut" phase it can be combined with Stanozolol (Winstrol).
 
How does your skin handle all that oil I mean EQ ? I’d be a walking zit.
 
How does your skin handle all that oil I mean EQ ? I’d be a walking zit.
[FONT=Verdana,Arial,Tahoma,Calibri,Geneva,sans-serif]I have no obvious pimples if not the usual 2 that I have since I entered puberty.
I don't have oily skin, if not just a little in the face.
but for the skin I also have a secret: MT2 :)

I tolerate androgens well, it is estrogens that make me pimples.
arimidex every day and I'm fine with those too[/FONT]
 
Going Big! I wanna see you at the peak of your bulk!! Your always so ripped. Gotta be able to see when your totally Full Blown!!
Max
 
I have no obvious pimples if not the usual 2 that I have since I entered puberty.
I don't have oily skin, if not just a little in the face.
but for the skin I also have a secret: MT2 :)

I tolerate androgens well, it is estrogens that make me pimples.
arimidex every day and I'm fine with those too

[FONT=Verdana,Arial,Tahoma,Calibri,Geneva,sans-serif]however a couple of sides in the long run I noticed them:
-lowering of the voice. not a lot but I've been told many times
-body hair. back shoulders and a little on the chest[/FONT]
 
How does your skin handle all that oil I mean EQ ? I’d be a walking zit.
The only draw back from bold for me is the acne, my lord!
 
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