Anavar Kicked In, Erection Checked Out

Funny story (or not), one doctor who Rx’d oxandrolone for me once specialized in the heart (that’s all I will say). He swore up and down he’d never had a patient who’s HDL dropped while taking oxandrolone. He recommended I try 50 mg/day for 8 weeks and repeat blood work. Ole readalot wasn’t down with that and I did blood work at 4 weeks and sure enough my HDL had dropped by 70% (SHBG, T, etc detailed in the other thread). This is the same doc who was not comfortable with Hct above 50% :-).

It’s truly scary how exposed you are if you know nothing of the pharmocology/metabolism of AAS and blindly follow doctor protocols (especially if they are in a certain state). Check that HDL!

So I looked through that other thread, and I’ll be honest, I didn’t comb through all the linked papers and such.

The conclusion you came up with goes against all the anecdotal information I have heard. Most say SHBG going down will increase Free T and E2. The crux of your argument seems to be that SHBG going down increases clearance rates of the testosterone, but how do we know that the clearance rate increasing is a bigger factor than having less SHBG to bind to?

I have seen blood work results of men with low SHBG taking low TRT doses with super high Free T. I have seen the results from men with high SHBG on larger doses with lower Free T. I guess I am not convinced, but if there is good evidence, I am willing to evaluate it.

see the link, lower SHBG —>lower TOTAL T. Where your free T lands is a function of Total T and SHBG. Competing effects. Make sure you keep track of the terms Total T and Free T. In the example I provided, my SHBG dropped markedly, Total T dropped, and free T was about the same.

Which link. There were quite a few in that other thread.

Damn at least you did the bloodwork yourself. Did you stop it right away? Or lower the dose? My HDL and LDL are good, however HDL is the lowest it can be and still be in range. So I’m curious what my labs will show

The specific post I linked in that thread.

I cover methodically the time course of Total T, SHBG and free T. The variable piece is how much your liver will be affected by the oxandrolone and the AI. My liver very sensitive, others not so much apparently. Where your free T ends up is the combination of Total T and SHBG (which are both are function of the oxandrolone and AI dosage).

Okay so AI, High T, low SHBG…for 14 weeks/3.5 months max - is this going to cause me life long issues? I am eating a VERY clean diet - 100% homemade, organic, protein, fats, veggies, and carbs mainly on workout days. Lot’s of good fruit etc. Lots of cardio. I forgot to mention - he also prescribed CJC/IPA to inject at nights. Fat is coming off fast. This is going to do lifelong damage with my HDL is crushed for 3 months?

Sorry if I am not exactly putting this together. This is the study you are referencing, correct?

No idea. Question is will it only be for 3 months? Folks on here typically cycle more frequently and TRT is the gateway to lots of other stuff. IF you do just one cycle of oxandrolone, then way to go.

You asked why you are potentially having erection issues and I tried to give you some perspective. Even cautioned you on potential heart concern. It’s difficult to communicate on here since I find a lot of times posts are made to try and justify AAS use. Good luck and best wishes.

That is a study I posted but read the post I linked above. The post I wrote detailing my SHBG, Total T and free T before and after 4 weeks of oxandrolone.

Here I will copy it verbatim:

Here’s my approximate T-values on 100 mg/week of Tcyp (50 mg twice weekly):

image

Now add on top of the TRT add the 50 mg/day of oxandrolone. After 4.5 weeks (1 week at 25 mg/day + 3.5 weeks at 50 mg/day):

image

There’s competing effects here.

  1. SHBG drops significantly which speeds up testosterone MCR and reduces total serum testosterone by about 50% (the testosterone is getting secreted more rapidly and the lower SHBG is effectively reducing half-life/binding efficiency).
  2. The lower SHBG results in less of the remaining total serum testosterone being bound vs free. So you can see I ended up with close to the same free T (18.7 ng/dL before vs 17 ng/dL after). Bioavailable went from 438 to 399.

As SHBG gets closer to zero you’ll lose even more ground. So don’t crash your SHBG (just like estradiol) otherwise you risk having no testosterone (and hence lower estradiol) to balance synthetic AAS that you may also be administering. Depending on whether synthetic AAS is aromatizing/5-alpha reduced, this may or may not be a huge deal. For the guys in article above, they had ED effects that may be attributed to significant reduction in SHBG while on exogenous T.

Here’s a hypothetical example on same 100 mg/week of Tcyp but now you’ve taken your SHBG down to 1 (your liver is extremely sensitive to oxandrolone here, let’s say your total T is now 200 ng/dL (I’m just giving example):

Almost all of your serum T is bioavailable (96.8%) but there’s not much around because you’re hyperexcreting it compared to an SHBG of 30 or 50. So another consideration to keep in mind.

I stopped right away. 6 months later (see even I couldn’t stay away) I tried 15 mg/d for 4 weeks. Again, about 60% reduction in HDL. Either I have the worst genes for AAS or my safety margin is too high. Either way, I have retired from brief provocative trials of synthetic AAS for therapeutic benefit.

So, I have heard frequent injection for low SHBG to address clearing quickly. Now I didn’t see in the study how often they were administering Test. That could be an important variable for the end Free T values. Additionally, is it possible that the anavar itself (could be that the VAR and SHBG together caused faster clearance) had an impact on clearance times? It seems like the body might clear out testosterone faster with a higher total androgen level? Not sure on it, but just asking some questions about your conclusion.

Good question. My data was based on injecting 2x/week so the T numbers I shared we’re trough right before the next injection.

2X is pretty good. So you saw your own total testosterone drop from 1054 to 494 ng/dL on the same dose, same dosing schedule, and same blood draw timing?

Sorry if I am asking a lot of questions, I just want to make sure I am justified to believe something. Especially if that thing goes against what I thought I knew.

No worries, thanks for your interest and thirst to challenge/learn.

Here’s the dosing schedule from the paper (quite the use of symbols and footnotes):

You make a very good observation about the dosing frequency of exogeneous Test while taking medication that drops your SHBG. One way to potentially work around this somewhat is increase your dosing frequency (I was only doing 2x/week). Again, depends on how sensitive your liver is.

Well, fingers crossed I don’t take quite the hit to HDL lol. I’ve liked the response so much I can see wanting to run this again and agai

Precisely! Therein lies the dilemma. Go watch the Mike Matarazzo video I posted. No one wants to think about this.

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Correct.

Hmm, thanks for that last post. I am having a bit of difficulty coming up with any conclusions from the results table from the study (what a cluster fuck).

Were you using the same testosterone? UGL? Pharma? Ester? Blood Work lab? Since it is anecdotal, I want to make sure variables are accounted for. Anecdotal evidence is evidence (sometimes the best you can get) in AAS.

I haven’t looked into this and found the particular original studies but my understanding was oxandrolone doesn’t bind to SHBG.

I don’t have a primary mechanism by which oxandrolone itself chemically interferes with Test MCR. It dropping SHBG would be a secondary mechanism.

Here’s a good study on SHBG and total T (MCR):

https://academic.oup.com/jcem/article/91/11/4669/2656842

The metabolic clearance of T and other steroid hormones can be conceptualized as consisting of two parts: hepatic clearance and clearance from other tissues or extrahepatic clearance ([23](javascript:;), [25](javascript:;), [26](javascript:;)). The observed differences in aMCR-T between older and younger men could be due to age-related changes in hepatic clearance or extrahepatic clearance. Hepatic clearance accounts for 50–65% of aMCR-T in men ([23](javascript:;), [25](javascript:;)).

Hepatic clearance is a function of hepatic blood flow and hepatic extraction from the splanchnic vascular bed, both of which decrease with age. Hepatic blood flow decreases with age and is about 15% lower in people in their 60s and 70s, compared with those under the age of 45 yr ([27](javascript:;)). Hepatic extraction is also lower in older men (45%) than young men (65%) ([28](javascript:;)). The decrease in hepatic extraction with aging is presumably related to the increase in SHBG seen with aging because the non-SHBG-bound fraction of T is presumed to approximate its hepatic extraction ([26](javascript:;)). The greater SHBG levels found in older men may be a contributing factor in the lower aMCR-T observed in this study, compared with young men. This effect would be more important at the higher doses of TE when SHBG binding of T could become saturated in the younger men with lower SHBG levels. Extrahepatic clearance has also been found to be lower in older men, compared with young men ([26](javascript:;)).

Age-related differences in serum SHBG concentrations may contribute in multiple ways to the age-related changes in aMCR-T. SHBG increases with age but decreases with increasing adiposity ([1](javascript:;), [29](javascript:;)–[32](javascript:;)). The higher SHBG levels in the older men in this study ([Fig. 4A](javascript:;)) may have contributed to lower aMCR-T and the higher total T levels observed in older men in comparison with the younger men. However, free T levels were also significantly higher in older than young men; the higher SHBG levels cannot account fully for the higher free T levels ([Fig. 2](javascript:;)). SHBG levels declined in a dose-dependent manner in younger men in response to TE, whereas the magnitude of change in SHBG levels during T treatment was lesser in older men. The greater magnitude of decrease in SHBG in young men may be reflected in their higher aMCR-T. aMCR-T correlated negatively with SHBG in this analysis.

Another possible explanation of the lower aMCR-T in older men may be differences in body composition between young and older men. Older men had a higher percent body fat than younger men at baseline ([17](javascript:;)). aMCR-T estimates were negatively correlated with total fat mass and percent body fat at baseline and during treatment. Whereas both total fat mass and percent body fat were predictive of aMCR-T, percent change in fat mass was not correlated with or predictive of aMCR-T. SHBG decreases with increasing adiposity, which would be expected to increase T clearance; therefore, it is surprising that fat mass was negatively correlated with aMCR-T in this study. aMCR-T estimates were associated positively with LBM at baseline and during treatment but not with percent change in LBM. Muscle mass is presumably a large contributor to the extrahepatic clearance of T. This observation is consistent with the positive correlation we observed between aMCR-T and LBM. These observations suggest that the etiology of age-related differences in aMCR-T is likely multifactorial and that a complex interaction of factors, including age-related changes in body composition, SHBG, hepatic blood flow, and other unknown factors, contribute to the age-related changes in aMCR-T.

These observations have significant implications for T therapy in older men. Our data suggest that T doses should be adjusted downward in older men and guided by monitoring of serum T levels. Whereas we do not advocate T therapy for older men with low T levels, should the physician choose to administer T to symptomatic older men, we suggest that the initial T dose should be 25% lower than that used in young men.