I’ve seen this graph, this isn’t the original graph. THIS is the original graph, taken from this study http://jpet.aspetjournals.org/content/281/1/93
NPP peaks higher because it exits the system faster, the same is true with any other shorter estered compounds. If you pin 100mg of testosterone propionate in one individual and 100mg of test E in another the guy on test P will have a much higher peak, however the substance will exit their system sooner too. Say one takes 100mg of nandrolone decanoate per week vs 50mg of NPP 2X/WK nandrolone concentrations will be very similar.
However that being said nandrolone phenylpropionate doesn’t seem to be as short estered as people think. The molar mass of nandrolone is 274.404g/mol (6.022x10^23 molecules (very big number) is a mole, and a mole of base nandrolone weighs 274.404 grams. Nandrolone PHENYLPROPIONATE has a molar mass of
406.566g/mol so 274.404/406.566=0.67 so 67 MG’s per 100mg of NPP is pure nandrolone, with the remaining 33mg compromised of the ester. 600mg of deca is not going to give you the same amount of gains as 200mg NPP, that’s not how science works, you need the same amount of pure base hormone to get the same effect, and even then it needs to be released over the same period of time for the effects to be exactly the same
Nandrolone decanoates molar mass is 428.657g/mol
428.657/274.404=0.64 therefore theoretically 64 mg/100mg is pure nandrolone while the rest is compromised of ester weight. Therefore theoretically PP ester isn’t nearly as short estered as people think, however it is a shorter ester than decanoate
Nandrolone also seems to be fairly harsh in terms of alteration of neurotransmitters and is likely far harsher than test towards overall detrimental effects on cardiac remodelling. It isn’t nearly as mild or safe as people make it out to be. One can get awesome gains off test alone, so why not just use more test.
Epistane (the designer steroid) isn’t the same as the anti estrogenic drug in Japan. Epitiostanol was the anti E in Japan, methylepitiostanol is the designer steroid. While there was another type of epitiostanol marketed in japan I believe it was mepitiostanol or something, it has the c-17AA group replaced with a 17-b hydroxyl group and is therefore digested via the lymphatic system, similar to prostanozolol I believe. The c17AA designer steroid version of epistane is supposedly highly toxic, and very harsh on the lipid profile based on what I’ve seen. Whether it still maintains its anti-e properties… Maybe, however once an anabolic steroid has a c-17AA alteration its behaviour is drastically changed, think dbol vs EQ. Or mast vs sdrol
Finally I forgot, ergot contains several poisonous alkaloids if taken in excess, ergot also contains lysergic acid… Sound familiar? Lysergic acid diethylamide… Otherwise known as LSD was synthesized from ergot as consumption of ergot, besides vasoconstriction leading to gangrene due to loss of blood flow to the limbs, vomiting and a plethora of other wonderful side effects, causes hallucinations. It is hypothesized the reason the Salem witch trials were a thing was because ergot fungus grew on the wheat that year, which is a far fetched hypothesis as the hallucinogenic properties of the fungus would probably be burnt off during the cooking of wheat however it is possible, and kinda funny to think the people might’ve just been expriencing drug induced psychosis. Several ergot alkaloids are used in prescription medicine (I think) however ergot itself if consumed is typically poisonous. Cabergoline is an ergot derivitave, it isn’t ergot