Adjusting my dose down for longterm health reasons, will it lead to muscle loss?

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That's pretty much it -- then, retest your ferritin to confirm that it's back to pre-donation level.

The times of taking are crucial, as is avoiding Vitamins C and D (while you're doing this). No dose skipping either!

For people just jumping in:
the explanation is here.
Nice paper. Thanks for putting that in your writeup:


Aspirin will give you an anti-clotting effect, and if you believe my results a reduction in Hct, but it's not all a free lunch.

====

Aspirin's effects on the cardiovascular system other than the platelet​

Because of its primary effect in platelets, it is often forgotten that aspirin is also inhibitory at other sites within the cardiovascular system. Recent concerns about the potential pro-thrombotic effects of the COX-2-selective drugs were initially prompted by studies showing that consumption of either celecoxib [39] or rofecoxib [38] reduced urinary PGI2 metabolites, an effect that was interpreted as being consistent with an increased risk of thrombosis because of a loss in anti-thrombotic PGI2. However, aspirin was shown more than 10 years earlier to reduce urinary PGI2 metabolites, although the reduction was less marked than the reduction in TXA2 metabolites [1]. These investigators used a wide dose range of aspirin, 20–2600 mg day−1, and found that lower doses of aspirin had greater inhibitory effects upon TXA2 than PGI2 metabolites. However, they found that inhibition of platelet function was not maximal at the lower aspirin dosage and notably that aspirin at doses greater than 80 mg day−1 caused substantial inhibition of endogenous PGI2 production. They concluded that it was ‘unlikely that any dose of aspirin can maximally inhibit thromboxane generation without also reducing endogenous prostacyclin biosynthesis’. In support of this idea, local infusion of aspirin to the human coronary bed has been shown to increase coronary vascular resistance and reduce coronary blood flow [69], as has i.v. infusion of indomethacin [70]. So if it is able to reduce the intravascular production of PGI2, aspirin could also release a brake upon atherosclerotic disease progression and platelet activation, as well as promoting vasoconstriction. Taken together these could increase the risk of adverse cardiovascular events, an idea supported by the report that individuals with dysfunctional IP receptors have accelerated cardiovascular disease [71]. Further support for this concept can be derived from studies using mouse models. For example, in a mouse model of atherosclerosis, deletion of the IP receptor was found to enhance disease progression, whereas deletion of the TP receptor or treatment with a TP receptor antagonist reduced atherogenesis [72, 73]. Similarly, platelet and vascular responses following experimental injury are enhanced in knockout mice lacking the IP receptor, and may be depressed in mice lacking the TP receptor [74, 75]. Finally, a gene/dose dependent relationship between blood pressure, platelet aggregation and thrombogenesis has been demonstrated using heterozygote and homozygote knock out mice for the IP receptor [76].
The effects of aspirin at sites other than the platelet are informed by the recent understanding that inhibition of COX-2 isoforms by NSAIDs is associated with an increased risk of adverse cardiovascular events [4, 5, 8, 11, 18, 77]. While on the one hand these effects could be associated with inhibition of the vascular production of PGI2 leading directly to local increases in platelet reactivity, on the other hand it is also important to realize that aspirin and NSAIDs can increase blood pressure in normotensive subjects and in those with existing hypertension [4, 5, 9, 11, 14, 15, 18, 20, 23, 77] thereby increasing the risk of thrombotic events through exacerbation of the development of atherosclerotic disease [78]. Indeed, the use of these drugs is weakly associated with an increased risk of congestive heart failure [79] and an increased risk of hypertension [80]. As these effects are COX mechanism-driven and dose-related, it is clear that higher doses of aspirin and longer exposures have greater effects than lower doses and shorter exposures [80].
In addition to the PGI2 and TXA2 pathways, aspirin also affects the production of other prostanoids within the circulation, most notably PGE2. PGE2 has been identified as both an inhibitor and a potentiator of platelet aggregation via interaction with different isoforms of the EP receptor (see above). Interestingly, deletion of the F prostanoid receptor (FP) in mice reduces blood pressure and atherogenesis associated with disruption of renin release in the kidney [81], so it is important not to become too narrowly focused on aspirin and platelet endothelial cell interactions although this is very much where the weight of evidence lies.


Conclusion​

In summary, in vitro, ex vivo and in vivo mechanistic studies link the anti-thrombotic effects of aspirin to irreversible inhibition of platelet COX-1 and formation of TXA2. However, aspirin also produces dose-dependent inhibition of COX at other sites within the body and some of these inhibitory effects, notably reduction in endothelial cell production of PGI2 and increase in blood pressure, are associated with an increase in overall cardiovascular risk. P2Y12-receptor antagonists have also been shown to be anti-thrombotic because of their blockade of ADP-dependent pathways of platelet activation, and dual therapy with aspirin has now become standard care for many patients at risk of thrombosis. While clinical trials using clopidogrel have investigated interactions with aspirin, large outcome studies of newer and more potent P2Y12-receptor antagonists, notably prasugrel and ticagrelor, have not randomized the dose of aspirin. As potent P2Y12-receptor antagonists can strongly inhibit TXA2-dependent pathways of platelet activation, i.e. those targeted by aspirin, and sensitize platelets to the anti-thrombotic effects of endogenously produced PGI2, there is the possibility that additional dosing with aspirin, in particular high-dose aspirin, will not confer any additional cardioprotective effect. On the contrary, there is a possibility that combining a high level of P2Y12 antagonism with high doses of aspirin could unmask an effect of aspirin on the production of anti-thrombotic prostanoids, notably PGI2, increase the risk of fluid retention and hypertension, and increase the risk of bleeds, particularly gastrointestinal bleeds. Clearly this currently is only a hypothesis. However, as these effects could impair the overall therapeutic benefit of the treatment, it will be important to evaluate further this concept in pre-clinical and clinical studies.
====
 
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For years I've been on 200mg test and 100md ND a week, split into multiple shots. The deca is because I have moderate osteoarthritis and have had multiple surgeries on my shoulders, hips and knees over the years and prefer not to ever take NSAIDS if possible

As I'm turning 46 next year I feel this is a bit of a high total dose for long term health reasons, my HCT is always low 50s and even through my Cystatin C egfr is at 115 consistently, my creatinine is always terrible. I'm also concerned about long term cardiac damage from deca so a lower dose makes me happier

I've cleaned up my diet and gone keto/paleo and added in hard 30 min cardio sessions 4-5 times a week after my weight training, as well as 1500mg niacin, coq10 and fish oil daily. I take lisinopril 10mg and HCTZ at 12.5mg ed along with with trt

I've dropped to 150mg test a week and 75mg deca, I guess my question would be is this enough to hang onto the muscle I spent years building? At one point while abusing AAS I was 230lbs and 10% but these days I'm a soft 225lbs. Ideally I'd like to get down to a ripped 200ish if that's maintainable on a lower dose. I understand it's still 225mg total AAS a week but from what I understand the deca in low doses isn't especially anabolic

Any thoughts appreciated
I just want to commend you. Dropping the dose and putting health over GAINZ and vanity takes introspection and self-awareness. I did two 19 week bouts of ND along with TRT and I can say it wasn't for the better and I won't be using it again (but those vials are still in the fridge and call out to me along with the other goodies that aren't good for you).

Way to go. Unless someone can point me to the literature (which no one has yet), I'll continue to speculate that ND's joint pain improvement properties happen all in the brain along with the extra anhedonia and increased depression it caused.






And no, this article doesn't count...

It's an AI-generated article.
 
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I just want to commend you. Dropping the dose and putting health over GAINZ and vanity takes introspection and self-awareness. I did two 19 week bouts of ND along with TRT and I can say it wasn't for the better and I won't be using it again (but those vials are still in the fridge and call out to me along with the other goodies that aren't good for you).

Way to go. Unless someone can point me to the literature (which no one has yet), I'll continue to speculate that ND's joint pain improvement properties happen all in the brain along with the extra anhedonia and increased depression it caused.






And no, this article doesn't count...

It's an AI-generated article.

What were ur protocols when using Test w/ nandrolone?

Did u ever try controlling E2 and/ or prolactin while using nandrolone? From my understanding, nandrolone sensitizes estrogen and prolactin receptors. So even if ur levels of E2 and prolactin don’t increase from adding nandrolone, it can sensitize ur receptors of both and whatever E2/ prolactin being produced by the test can become more potent and cause issues

Obv everyone is different, but I know a ton of guys that didn’t do well on a test base, possibly due to E2 and prolactin issues, and feel amazing using a nandrolone base (mentally, physically, and sexually) with the minimum dose of test needed to keep their E2 where they need it to feel best and to keep their health parameters within range, and just for optimal health in general. Obv healthy E2 levels play a big part in that.

There’s a fb group based around using nandrolone only steroid cycles, and most of the guys feel great mentally. Some don’t, and just require small doses of either an aromatizing compound, or direct E2 supplementation to feel good mentally. But nandrolone doesn’t seem to be a compound that directly causes depression/ anhedonia. As far as any long term health concern with nandrolone, I can’t speak on that. Haven’t done enough research on the matter
 
What were ur protocols when using Test w/ nandrolone?

Did u ever try controlling E2 and/ or prolactin while using nandrolone? From my understanding, nandrolone sensitizes estrogen and prolactin receptors. So even if ur levels of E2 and prolactin don’t increase from adding nandrolone, it can sensitize ur receptors of both and whatever E2/ prolactin being produced by the test can become more potent and cause issues

Obv everyone is different, but I know a ton of guys that didn’t do well on a test base, possibly due to E2 and prolactin issues, and feel amazing using a nandrolone base (mentally, physically, and sexually) with the minimum dose of test needed to keep their E2 where they need it to feel best and to keep their health parameters within range, and just for optimal health in general. Obv healthy E2 levels play a big part in that.

There’s a fb group based around using nandrolone only steroid cycles, and most of the guys feel great mentally. Some don’t, and just require small doses of either an aromatizing compound, or direct E2 supplementation to feel good mentally. But nandrolone doesn’t seem to be a compound that directly causes depression/ anhedonia. As far as any long term health concern with nandrolone, I can’t speak on that. Haven’t done enough research on the matter
100-120 mg/week of TC. ~80-120 mg/week of ND.

My previous response to you:

Take a look at the links I posted above. The effect of ND on neurotransmitters/neurotoxicity is reviewed in the literature therein. The best way I can compare the feeling on ND is that it is similar to LDN, which I tried. Look up Naltrexone if you want to understand how it works (mechanism of action). Does everyone have my experience on LDN, absolutely not.

Amazing how few times these articles get clicked on at T-Nation. I don't know about here. Few seem to want to read the literature and I sympathize. Few have the training or patience.

Good luck.
 
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100-120 mg/week of TC. ~80-120 mg/week of ND.

My previous response to you:

Take a look at the links I posted above. The effect of ND on neurotransmitters/neurotoxicity is reviewed in the literature therein. The best way I can compare the feeling on ND is that it is similar to LDN, which I tried. Look up Naltrexone if you want to understand how it works (mechanism of action). Does everyone have my experience on LDN, absolutely not.

Amazing how few times these articles get clicked on at T-Nation. I don't know about here. Few seem to want to read the literature and I sympathize. Few have the training or patience.

Good luck.

IMO every study done on hormones are either flawed or corrupt, or both, so studies to me are just people’s extrapolations and opinions on them, so it’s hard for me to put too much weight into them. But obv they’re still important and quality data can be gained from them at times, so I’ll definitely check out the links u posted
 
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Thanks for sharing your detailed writeup. Fascinating and looks very similar to all the posts I've done here and at T-Nation regarding Hct and erythrocytosis from TRT. Very nice!
Thank you for linking to other other discussions. I am reading them. I do give credit for inspiration, so if I steal anything, I might who knows, I'll add you in my notes.
The biggest boost on this, after I read a bunch of literature, was happening across the info on Rusfertide. That pretty much convinced me that if I took 120mg of iron for a few days, my HGB wouldn't actually go through the roof. Once that gets approved I have to think that our troubles are over, after all these years of donating. It will probably cost a fortune though, and naturally won't be covered by insurance being offlabel. My older hematologist who is in his 60's, great guy, says my TRT driven erythrocytosis is "Polycythemia." Like a lot of docs his age. In my case I'm just going to ask him to write me a scrip for this stuff for my "Polycythemia." If he wants to call it that I'll go with it and maybe insurance will be happy.

EDIT I took a quick scroll stroll through the other thread where you address that old "NO takes care of everything" some guys spout with their dismissive hand wave. I wish I had seen that thread before I started writing my stuff. Jeez. You have a slightly different emphasis but you pull together a lot of great material on this HCT stuff.
I constantly restrain myself from adding to my page since I think most guys in our community have a short attention span and their eyes glaze over.
 
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Echo came back as normal apart from grade 1 LV relaxation, ejection fraction 60% so asymptomatic

I'll discuss this with my cardiologist but he's very anti AAS in general so he'll just tell me to stop TRT

I cant find anything specifically pointing to ND as causing LV relaxation but who knows. I don't know if this is a concern but it's certainly concerning not to get a clean bill of health like I did 10 years ago when I had one last

"
Left Ventricle:
The left ventricular chamber size is normal. There is normal left
ventricular systolic function. Global left ventricular wall motion and
contractility are within normal limits. The EF is estimated at 55-60%.
Abnormal left ventricular diastolic filling is observed, consistent with
impaired LV relaxation(Stage I). "
 
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Assuming I keep running ND is 50mg a week going to have the desired therapeutic affect on collagen synthesis? 100mg doesn't seem to have done shit for my knees or shoulder post surgery TBH so I'm wondering if it's even worth including

The study that showed its 100x more toxic to artery endothelium walls than test is concerning, but the studies where they gave rats the equivalent of 1 gram a week and made them swim don't seem to really carry over to humans imo

The human studies where they gave young males ND for 6 weeks also seem ridiculous and pointless
 
The more I read, it appears that LV relaxation is potentially caused by fibrosis, which ties in with the ND causing cardiac fibrosis theory

I'm hoping it can be reversed with high dose niacin, increasing my ACE inhibitor dose to 20mg lisinopril (will ask about ramipril as it seems better in reversing fibrosis in studies) and doing hard HIIT 5 days a week along with fish oil and a keto diet

I'll just be doing 200mg test from now on with no more ND

Does the 55-60% Ejection Fraction seem low? I don't have data on my previous Echo sadly so can't compare with that
 
100-120 mg/week of TC. ~80-120 mg/week of ND.

My previous response to you:

Take a look at the links I posted above. The effect of ND on neurotransmitters/neurotoxicity is reviewed in the literature therein. The best way I can compare the feeling on ND is that it is similar to LDN, which I tried. Look up Naltrexone if you want to understand how it works (mechanism of action). Does everyone have my experience on LDN, absolutely not.

Amazing how few times these articles get clicked on at T-Nation. I don't know about here. Few seem to want to read the literature and I sympathize. Few have the training or patience.

Good luck.
How did you feel on LDN. I tried it 3 months for chronic pain. Only thing I really noticed was I had tons of trouble waking up. And had vertigo spells like crazy.
 
The more I read, it appears that LV relaxation is potentially caused by fibrosis, which ties in with the ND causing cardiac fibrosis theory

I'm hoping it can be reversed with high dose niacin, increasing my ACE inhibitor dose to 20mg lisinopril (will ask about ramipril as it seems better in reversing fibrosis in studies) and doing hard HIIT 5 days a week along with fish oil and a keto diet

I'll just be doing 200mg test from now on with no more ND

Does the 55-60% Ejection Fraction seem low? I don't have data on my previous Echo sadly so can't compare with that

55-60% ejection fraction is normal. Is it rest or during high exercise ?
 
How did you feel on LDN. I tried it 3 months for chronic pain. Only thing I really noticed was I had tons of trouble waking up. And had vertigo spells like crazy.
Totally horrible. Complete anhedonia at 1.5 to 4.5 mg/day for 3 week trial. Immediate effect. I don't get all the hype.
 
Echo came back as normal apart from grade 1 LV relaxation, ejection fraction 60% so asymptomatic

I'll discuss this with my cardiologist but he's very anti AAS in general so he'll just tell me to stop TRT

I cant find anything specifically pointing to ND as causing LV relaxation but who knows. I don't know if this is a concern but it's certainly concerning not to get a clean bill of health like I did 10 years ago when I had one last

"
Left Ventricle:
The left ventricular chamber size is normal. There is normal left
ventricular systolic function. Global left ventricular wall motion and
contractility are within normal limits. The EF is estimated at 55-60%.
Abnormal left ventricular diastolic filling is observed, consistent with
impaired LV relaxation(Stage I). "
Same here. I must be the world's unluckiest anabolic therapy user. My brief foray into anabolic therapy looks modest but our bodies can respond differently to doses that seem reasonable. If my heart wants 400 ng/dl and I am running 1200 peak and 500 trough I am probably asking for trouble. And I found it.
 
Same here. I must be the world's unluckiest anabolic therapy user. My brief foray into anabolic therapy looks modest but our bodies can respond differently to doses that seem reasonable. If my heart wants 400 ng/dl and I am running 1200 peak and 500 trough I am probably asking for trouble. And I found it.
Are you saying this happened
with testosterone only ?
 
55-60% ejection fraction is normal. Is it rest or during high exercise ?
At rest, I have a stress test to do but can't do it until my bicep repair surgery heals (since they want you to hold onto the treadmill during the test)

Good to know it's normal, my LV is just slightly over the margin for normal sizes but not enough to be significant. I had legitimate LVH a decade ago after running higher dose aas and hgh, when I was 260+ but that regressed when I stopped using it

I'm curious about hghs potential benefits on the heart in lower doses, but the studies that show big benefits all use GH deficient adults not those with normal/low levels (my IGF1 has always been very low)
 
nothing to worry if your RWM (regional wall motion) is good. My rest EF is the same as you. But at full exercise capacity, my LVEH increases to 65%.

A way to maintain the LVEF capacity: beta blocker and weight loss.
 
I dropped from 245 to 225 pre bicep surgery , I'm planning on dropping to 200ish (hopefully @10% bodyfat) once I'm done with rehab - cutting while recovering from surgery doesn't seem a great idea as I want a full fast recovery so I'm eating slightly over maintenance calories to get in a ton of protein and good fat

Beta blockers- asking my cardiologist about this, my resting heart rate is too high imo as it's often in the mid 80s even sitting down and a beta blocker would help there. Thanks!
 
Beyond Testosterone Book by Nelson Vergel
Resting EF or Exercise EF is not the full story. Check out these link for more info:

Familiarize yourself with this topic....heart failure with preserved ejection fraction (HFpEF)

 
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