Mechanism by which AAS effect lipids?

[Studious69]

I think it’s widely known anabolic and androgens have a deleterious effect on lipid profiles in users. Why does this occur in the human body? What about these compounds causes the effect on lipids?

 

[KevTom1]

I think it has something to do with hepatic lipase expression. I read a cool thread on it here a while ago, I can never get the search function to find what I’m looking for though or I’d link it

 

[psauce]

One mechanism is a liver enzyme that tanks HDL once it’s unbound and circulating, hepatic lipase. Don’t recall many details. I don’t think a drop in HDL necessitates a rise in LDL, but maybe it’s an indirectly coupled phenomenon.

 

[Type-IIx]

From Oral Steroid and Cholesterol:

With respect to lowering HDL-C, this ↓ is caused by an ↑ hepatic triglyceride lipase activity (HTGLA). Hepatic lipase (HL) is a liver-secreted enzyme that liberates FAs from lipoprotein constitutents (e.g., including HDL), therefort this induces a shift towards breakdown ∴ reduced HDL.

The 17AAs, because they are either nonaromatizable or resistant to aromatization and thus lack estrogen benefits to lipids (estrogens ↓HTGLA), and because they are metabolized primarily in liver, having greater effects on hepatic proteins (e.g., HL), are worse than parenteral androgens (especially T).

With respect to increasing LDL, 17AAs may ↑Apo B in particular, which is associated with VLDL & gives insight into LDL actually in bloodstream circulation, perhaps by ↑ liver secretion of these lipoproteins directly.

Here is a great Table summarizing the effects of AAS (17AAs & i.m.) on lipoproteins and cholesterol efflux capacity (CEC) associated with CVD risk. I urge you to read this great paper: [link] for more information about your questions in this thread.

 

[Studious69]

From Oral Steroid and Cholesterol:


Here is a great Table summarizing the effects of AAS (17AAs & i.m.) on lipoproteins and cholesterol efflux capacity (CEC) associated with CVD risk. I urge you to read this great paper: [link] for more information about your questions in this thread.
View attachment 261346

beautifully answered!! Paper will be read tomorrow.

 

[Studious69]

From Oral Steroid and Cholesterol:


Here is a great Table summarizing the effects of AAS (17AAs & i.m.) on lipoproteins and cholesterol efflux capacity (CEC) associated with CVD risk. I urge you to read this great paper: [link] for more information about your questions in this thread.
View attachment 261346

Although, initially I see above it states 17-aa compounds are either nonaromatizable or resistant… what about something like dianabol? Methylestradiol I believe being the e2 converted from dbol in the body.

 

[Type-IIx]

Although, initially I see above it states 17-aa compounds are either nonaromatizable or resistant… what about something like dianabol? Methylestradiol I believe being the e2 converted from dbol in the body.

Right, good thinking. Among the common 17AAs (so excluding methyltestosterone) used by bodybuilders, Dianabol (p.o.) would be the least dyslipidemic or harsh on lipids, but still harsher than Test & Deca (i.m.)