/fraud/

What are the problems with your health?
Also if your test is crashed just get back on lol.

>penile length
What did he mean by this?

length x girth

What steroid can I take that won't give me acne

Vitamin D
Ok boomer
what is your cycle?
post body

Can confirm. My dad took test C for 6 weeks and has been hospitalized since. I kiss him boys

I once licked an anadrol and immediately developed terminal ass cancer

>Vitamin D
lmao based

Guys. Is it better to take 400mg Primo once per week or 200mg every 3.5 days? Or doesn't it matter?

Do it twice a week. Use steroidplotter.com to see the difference.

Every 5 days
half life of Methenolone Enanthate is wrong on steroidplotter. It's ~ 10 days, not 4.5 days.

>It's ~ 10 days, not 4.5 days.
Source?

Why would the half life of an ester differ that drastically between alcohols with similar lipophilicity?

How exactly are oral steroids hepatotoxic? How is the "second pass" actually bad for the liver? How does the "second pass" cause liver damage? I don't really understand. Also why and how are some orals more toxic than others? Pic related. Thanks bros.

Attached: Metribolone.jpg (837x837, 89.5K)

Half life does not only depend on esters..books.google.de/books/about/Lowinson_and_Ruiz_s_Substance_Abuse.html?id=w4ZUJAdleTsC&redir_esc=y

Attached: 1560025954767.png (1643x826, 114.92K)

>test cyp half life 12 days
Yeah I don't think that's a good source.

>How exactly are oral steroids hepatotoxic?
The fact that an active substance can be taken orally does not make it hepatotoxic. There are orals that have absolutely no liver toxicity like Methenolone Acetate or Proviron. Whether and to what extent an AAS is toxic to the liver depends on how and whether it is methylated and which modifications have been made to the first carbon ring.
I can give you more sources. I don't know what gives you the idea that two different compounds have the same half-life just because they have the same ester. That's not how drug elimination works.

The lipophilicity of the ester (the entire thing, not only the acid) is the key factor determining half-life as higher solubility in the oil slows release from the IM depot and probably reduces substrate affinity to the esterase.

>I can give you more sources
Why aren't you? That source isn't even a real source, they didn't run a study they're just copy pasting numbers they found elsewhere.
>don't know what gives you the idea that two different compounds have the same half-life just because they have the same ester.
Are you retarded? Show me where I said that.

Thanks bro. With regards to those AAS that are methylated and which have the requisite first carbon ring modifications, do you happen to know how and why they cause liver damage? What happens during their metabolism that injures the liver? I keep hearing talk about a "second pass" that allows them to survive initial breakdown but I don't really know what "second pass" is, what it means or what it does and how it does it. Sorry not at all a biochemist or pharmacist or endocrinologist or anything of the sort

Imagine being this retarded. You're that stupid hairlet from the last thread, right? You do realize that the Methylation additionally slows down hepatic elimination and thus prolongs Methenolone's half life, right?
>Why aren't you? That source isn't even a real source, they didn't run a study they're just copy pasting numbers they found elsewhere.
Because I have to go through my books. I literally have over 100 books and Acrobat takes a while to scan that shit.
>Are you retarded? Show me where I said that.
Because you are defending steroidplotter.com and you're implying that I'm wrong. Just take a look at what the creator did. He gave every compound with an enantate ester a half life of 4.5 days. He is retarded.

Attached: 1569976186034.png (475x901, 33.63K)

do i stick the steroid needle in my asshole or in the butt cheek

someone ring my phone and give me a source please and thanks

The inability of the liver to metabolize 17aa steroids plus the high load due to all of it reaching it at once results in free radical formation and oxidative damage.
lmao obviously methylation increases lipophilicity and prolongs half life but a single methyl group isn't enough wrt to the entire compound to double the half life, so again OBVIOUSLY there will be slight differences due to the differential lipophilicity of the various alcohols.

I'm the fag that BTFO'd you on androgen upregulation you tryhard.

*AR upregulation

Thanks for the clear and concise answer, makes sense. I wonder how something like m-tren can be so destructive while something like tbol is very mild in comparison

I'll try to keep it simple. Let's compare Stanozolol and Oxandrolone. Oxandrolone is far less hepatotoxic than Stanozolol even though both are 17aa but unlike Stanozolol which has a Pyrazol group at its first ring, Oxandrolone has a simple replacement of carbon with oxygen at C2. Why does it matter because hepatic elimination relies on oxidation (I'm simplifying a lot right now). I tried to explain it as simple as possible.
>but a single methyl group isn't enough wrt to the entire compound to double the half life
Actually it is. Source? So far you've been spitting bro science knowledge.
don't listen to this retard hairlet

>I'm the fag that BTFO'd you on androgen upregulation you tryhard.
LOL what? You didn't do shit. I love how you're trying to throw terms at people which you don't even understand yourself. Fucking German hairlet. I'm not the one who was retarded enough to take Finasteride.

Next time please create a hairlett free /fraud/ thread

Attached: 1565628277705.png (1874x728, 266.69K)

Do you need a source to understand basic logP? lmfao
I never took fin and I have a full head of hair you fucking retard. You keep acting like you're the hot shit with your "pharmacology" degree, yet you were convinced exogenous T downregulates AR. lol again.