I watched a video today where the guy claimed Oxandrolone did attach to SHBG, but he didn’t offer anything to back that up. But he’s pretty knowledgeable.
If the ED is from the anavar—and I’m generally dubious of this, although it’s happened to enough guys to make me think it’s possible—then simply ceasing to take it would solve the problem.
Did you have issues with e2 at 80? I’m not going back and reading all the comments to see if this was mentioned, sorry. If you had no issues and you started using adex it could very well be related to that.
Guess his info is off, that’s good to know.
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I almost always read through everything, but I just didn’t have the energy to go back and find his e2 reading. Don’t take my laziness today as a reflection of the very good and important stuff you post here.
Assuming bloods showed the crashed E2 and reduced SHBG, would the solution be to up the TRT dose for a couple weeks to try bring the E2 back up?
Thanks yes. I’m asking because I finished a Var addition to TRT about 3 weeks ago. Everything is ok but libido not as good as usual and morning wood not as frequent. My first thought is higher E2 but the studies you posted cast a different light on it. Really interesting reading thanks as it’s not what I would have expected.
What you posted is solid. Don’t worry about the warning.
I am not sure how we can come to a conclusion on if Var makes FT higher or lower while on exogenous test with this data since the test subjects did not take exogenous test. We know Var will lower test production, which is another variable.
So we haven’t concluded if Var leads to an increase or decrease in FT when using test exogenously?
Have we concluded Var leading to a decrease in TT when also using test exogenously?
Table 3 has avg HDL at baseline designated at 1 mmol/l with a standard deviation of ± 0.4. Avg depression in HDL is 0.5 with a standard deviation of 0.4. One could extrapolate from this data that a certain subset of patients had abysmally low HDL (0.1-0.2) following treatment with oxandrolone. This would align with the bloods people post up when on oxandrolone, stanozolol, chlorodehydromethyltestosterone and other non aromatising c17-aa anabolic androgenic steroids. Generally speaking, there is data indicative that lipid profile alteration may not be entirely dose dependent for oxandrolone, rather it may be a byproduct of use at any dose high enough to elicit an anabolic effect.
increased postheparin hepatic lipase expression (effects HDL metabolism), cholestasis etc likely contribute to the dramatic effects seen on HDL/LDL ratios with c17-aa AAS, I could be wrong though, I’m not an expert (and oxandrolone isn’t particuarly hepatotoxic)… I get irritated when I see people using stanozolol + trenbolone as on paper it looks like the perfect combination for inducing heart disease.
“To test this hypothesis, we treated these two men and two controls with the oral androgen stanozolol (6 mg/d) for 2 weeks. Consistent with other reports, HL activity increased a mean of 277% in controls with a concomitant decrease in HDL cholesterol (49%), HDL2 cholesterol (90%), HDL3 cholesterol (16%), and apo A-I (41%) and no change in apo A-II. Although stanozolol failed to induce HL activity in the HL-deficient man, HDL cholesterol, HDL2 cholesterol, and apo A-I were reduced a mean of 20%, 48%, and 32%, respectively. In contrast to controls, HDL3 cholesterol (46%) and apo A-II (14%) increased in HL-deficient subjects. Stanozolol treatment also increased LPL activity (124% +/- 86%, n = 4) and decreased lipoprotein(a) ([Lp(a)] 66% +/- 3%, n = 3) in the three men with detectable levels.”
https://www.nejm.org/doi/full/10.1056/NEJM197506192922503
"The mean total postheparin lipolytic activity increased 100 per cent during oxandrolone treatment (p < 0.05). This change was caused mainly by postheparin hepatic lipase, whose activity increased on the average more than 2.5 times (p < 0.001). The change in postheparin plasma-lipoprotein-lipase activity was insignificant. A highly significant correlation(r = + 0.87, p < 0.01) was observed between the activities of postheparin hepatic lipase and phospholipase A1 before and during oxandrolone treatment. No relation was observed between serum triglyceride level and various postheparin lipase activities, or between the changes induced by oxandrolone in the level of serum lipids and the activities of postheparin lipases.”
Literature pertaining to anabolic steroids/atherosclerosis makes it seem somewhat likely that a distinct relationship does exist between AAS use and accelerated atherogenesis. I don’t believe the decrease in lp(a) mediated by androgen use eliminates the prospect of enhanced atherogenesis.
There are numerous ways in which AAS abuse could lead to myocardial infarction, all of which could be considered as being interlinking risk factors. Coronary calcification, the development of atherosclerosis, haematological alteration (increased blood viscosity/hyper-coagulability mediated via increased HCT/RBC count, platelet aggregation, increased TXAC2 receptor density etc), hypertension mediated vascular damage/endothelial dysfunction (20-hete production and subsequent RAAS activation) and rarely… coronary vasospasm. Interestingly quite a few reports exist within relation to stanozolol in particular inducing coronary vasospasm.
Anabolic steroids may also increase homocysteine (data conflicting). Hyperhomocystemia is strongly correlated with the development and progression of cardiovascular disease as homocysteine interferes with the structural formation of arteries (or rather interferes with the building blocks that make up arteries). Androgen receptors are present throughout the body, including vascular smooth muscle. Vascular calcification noted in bodybuilders may be mediated via direct effect induced via AR binding.
“we addressed the hypothesis that exogenous androgen treatment induces vascular calcification. Immunohistochemical analysis revealed expression of androgen receptor (AR) in the calcified media of human femoral artery tissue and calcified human valves. Furthermore, in vitro studies revealed increased phosphate (Pi)-induced mouse vascular smooth muscle cell (VSMC) calcification following either testosterone or dihydrotestosterone (DHT) treatment for 9 days. Testosterone and DHT treatment increased tissue non-specific alkaline phosphatase (Alpl) mRNA expression. Testosterone-induced calcification was blunted in VSMC-specific AR-ablated (SM-ARKO) VSMCs compared to WT. Consistent with these data, SM-ARKO VSMCs showed a reduction in Osterix mRNA expression. However, intriguingly, a counter-intuitive increase in Alpl was observed. These novel data demonstrate that androgens play a role in inducing vascular calcification through the AR. Androgen signalling may represent a novel potential therapeutic target for clinical intervention.”
“Six of the 7 calcium scores were >90th percentile.“
CRP also tends to be elevated within AAS users compared to controls. Higher CRP/homocystine is associated with systemic inflammation/oxidative stress, both of which serve as factors towards inducing a pro-atherogenic environment. Oxidative stress induced via AAS is also an important factor when accounting for the cardiac damage induced (myocardial apoptosis, subsequent fibrosis). Other mechanisms off the top of my head in relation to cardiac damage include direct AR mediated injury, enhanced capsase-3 activity, hypertension mediated LVH, excess sympathetic nervous system stimulation (also contributes towards arrhythmia/SCD)
Coronary plaque volume associated with cumulative years of anabolic-androgenic steroid exposure (taken from this study Cardiovascular Toxicity of Illicit Anabolic-Androgenic Steroid Use - PMC). I’d have to plug in each dot point individualistically to find the correlation co-efficient, but I’m not doing that. From eyeballing there appears to be a weak-moderately strong correlation between use/the development of atherosclerosis. When comparing mean plaque scores to controls the P value was significant.
Exposure to supra physiologic concentrations of androgens within themselves intrinsically induces oxidative stress, both at rest and during exercise (exacerbated response). AAS mediated medical pathology is multi-faceted. It isn’t just lipid profile alteration one needs to worry about in terms of atherosclerosis progression, there are a number of variables of which will contribute towards the risk of stroke, myocardial infarction and sudden cardiac death.
If we look here (another deca study) The Anabolic Androgenic Steroid Nandrolone Decanoate Disrupts Redox Homeostasis in Liver, Heart and Kidney of Male Wistar Rats - PMC Nandrolone appears to alter redox homeostasis within the heart (focusing on the heart). Nandrolone appears to increase NOX expression within the heart. Over expression of NOX leads to ROS imbalance, ROS imbalance induces a favourable environment for the development of atherosclerosis. Rodents obviously have differing metabolic/elimination pathways compared to humans, but I believe we have enough data to go on suggesting a direct relationship between prolonged AAS exposure and atherosclerosis. Some of the mechanisms by which AAS accelerate plaque build up aren’t solely related to dyslipidemia and many variables are interlinked with one another (hypertension can induce LVH, as can direct AR binding within cardiac myocytes etc).
I haven’t covered much, there’s a LOT to write up about when delving into AAS induced aetiology. I should state while many of these mechanisms may seem scary (and they are) but in practicality the human body can generally endure and bounce back from quite a bit of abuse.
In short, HDL vs Lp(a) isn’t enough to drive atherogenic risks down when taking into account all the other variables at hand
People also need to start talking about AAS mediated neurotoxicity and the studies (on humans) indicative of AAS mediated enhanced glutamate turnover, beta amyloid accumulation etc. Mechanisms behind proposed neurotoxicity are numerous, from NDMA receptor overactivation to dopaminergic neurotoxicity… This is something that needs to be talked about more often.
More interesting data
https://onlinelibrary.wiley.com/doi/pdf/10.1111/bcpt.13143
Human data potentially backing the concept of AAS induced beta-adrenergic receptor up-regulation.
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You’d be surprised as to how many people legitimately can’t run a mile without stopping to catch their breath.
As to being in group A or B… I’m in group C… Have you seen my lipids, there’s a damn good chance I have some form of undiagnosed familial hypercholesterolemia. My LDL runs between 130-145 and HDL runs around 45. High cholesterol runs in my family, but interestingly we don’t have much of a history regarding cardiovascular disease. A few of my relatives are on statins.
Having afrikana + ashkanazi Jewish heritage makes me the perfect candidate for FH. Unfortunately medical expertise regarding this issue is lacking and it typically goes by undiagnosed, thus I’m told my levels are borderline despite being above the 95th percentile for my age.
I bet my sub-fractions are pretty toxic…
I’m not too concerned, the constant, unrelenting pain I have to live with is far higher up on my list of priorities. Red yeast rice (monacolin K, equiv to an unregulated dose of lovastatin) allows me to have perfect lipids (LDL of around 95-100). I’ll probably get a prescription for legitimate statins soon. The prospect of citrinin contamination with RYR is concerning.
I dont get it. Taking anavar reduce total test despite injecting the same dosage??