T Nation

Anavar Kicked In, Erection Checked Out

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

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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):

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.

Same bottle of Rx test cypionate, same lab, same time, same frequency, same fasting. I like to run controlled experiments!

I will say I am more convinced than before. I may have to run this experiment myself. I have heard big names in bodybuilding say that anavar (and other AAS) increase the effectiveness of testosterone by way of lowering SHBG which results in higher Free T. That makes sense, but not if lowering SHBG results in lower Total T and about the same Free T. I suppose how much SHBG gets lowered is dependent on the individual.

Correct. I don’t put a lot of stock in big name bodybuilders solving coupled non-linear equations. I’ve known of a few perceptive bodybuilders who have documented this effect. Also, I have no experience injecting 500-1000 mg of testosterone at time vs 50 mg at a time which will also add to the calculus. I tried 325 mg/week for 1.5 weeks and went into AFIB so I am just trying to recover mentally and hoping to help some folks.

I guess I have seen even some TRT doctors (IIRC, the anabolic doc mentions this effect, but he is not the only one) on YouTube say what I described in the post above. Logically it makes sense (probably why I have heard it a few times), if you don’t account for increased clearance.

Devil is in the details and I can tell you are a details person. I dont have a response surface distribution showing what fraction of people will come out ahead on free T using this method and again the inputs would be injection dose, injection frequency, oral AAS dose, bodyfat level, a few more. Glad you now consider the effect of SHBG on free T as well as the effect on total T via MCR.

Obviously the correct answer is clone @iron_yuppie DNA and go from there.

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I think with several compounds one would be wise to do blood work mid cycle to evaluate how they respond. I think before using EQ in an actual effective dose, I would run it low (with just my TRT dose which I have blood work on), and see what it does to E2, and kidney markers.

I was told I was an analytical person early on. Went into engineering which is far more tedious than analytical than I thought it would be.

Smart. It would serve the OP well with his current issue. A little extra data never hurt anyone.

Sadly there’s some issues that can’t readily be detected with bloodwork. I went and saw cardiologist prior to running ND, after 19 week ND. Before oxandrolone. Echos came back great as well as EKG. I guess you could have yourself hooked up to Zio patch the entire time you are on cycle but not really practical. My only conclusion is some people just shouldn’t participate in AAS. Take care.

And OP, definitely pull those labs.

Did you ever track down the most probable factor in the afib? IIRC, you were using T3 (cytomel), right? To me, that seems about as probable as the AAS?

I have brought my T3 dose down to a max of 10 mcg per day (using liquid stuff, so a bit hard to tell exactly), and feel about the same (was using it to bring down RT3). I have lost some weight, so I will try to get off and do blood work after a month off of the T3.

Good point. AAS + T3 + T4 + HIIT plus getting to the age where crazy exercise addicts get afib. Prior ND use.

Dropped the T3 and back to very low TRT. Zio patch results come back fine now but I can tell you the mental sides and panic/anxiety are no fun.

Blows me way guys are doing this ND-based TRT (should read HRT to be more accurate) now with a little test thrown in the mix. Wont touch ND again. I think there really is something to up-regulating beta receptors in the heart. I get these short runs of SVT now that really get one’s attention. Stress events cause my heart to race but again maybe it’s all in my head.

Many people are looking for the next thing.

Glad you dropped/dropping the T3. Duchaine’s BodyOpus manual may yield some GAINZ but long term it’s the path to ruin for folks. Even though I understood that taking T3 floods your tissues with exogenous active hormone when the body should decide how each organ should convert T4 to T3, I still took it. Took it for a few years.

I traversed the extreme range of rT3 levels and never noticed a difference on either bodyfat or energy. But I was sub 10% BF before ever taking exogenous hormones. Take care of yourself.

I’ll try. For a bit I was taking 50 mcg of T3. Hope I didn’t F myself up with that. It was only like a month, and I had done research, but not enough. I guess many are running it at those dosages and up for BBing. My chances are good, but not something I will play with again.

I am the type of person to ruminate on past decisions, and really hope I didn’t cause damage. I did get heart racing and such with the higher T3, but nothing else. Seems normal now.

Guy’s dick when it hears he’s doing a nandrolone-only trt


best case scenario! I think the prevailing notion is running 100-200 mg ND/week with 50 mg/week of Test to keep the E2 levels in range. I’ll pass.

I have no idea what happened in this thread of mine hah! So is there a temporary cure I can use for the ED during Anavar? I’m already on 75mg Sildenafil when needed. Also, someone said my E2 might have crashed. Is that really possible? I twas in the 80’s…I am prescribed 0.125mg of Anastrozole. Isn’t that a Tiny dose even at 3-4 times a week?

Sounds like you are in good shape. I ran 50 mcg/d (split up into 25 mcg 2x per day) of T3 in addition to T4 for a couple of years. Had no increased HR and no heart racing. fT4 and fT3 levels were in range. Worked up to about 380 W on my 20 min FTP so I think that combined with squats + trying a blast of Test + prior ND use probably didn’t do me any favors.

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