Thoughts on Nolva for stand-alone estrogen control on TRT?

[Swifto]

Tamoxifen however has been studied for a extend period of time while raloxifene isn't but shows promising effects indeed.

I know. I alluded to this in both post #2 and #8.

 

[Delt123]

I know. I alluded to this in both post #2 and #8.

Didn't check that, my bad!

 

[fitzchivalry]

Does raloxifene cause depression as Nolvadex does to some?

 

[Lilleo187]

Does raloxifene cause depression as Nolvadex does to some?

No theres no sides with ralox

 

[Kaladryn]

No theres no sides with ralox

In every way, except bone loss, it has the exact same side effects from what I've read.

 

[Kaladryn]

Does raloxifene cause depression as Nolvadex does to some?

People often get depression/lack of motivation from anything that takes E2 too low or blocks it too much, some people seem completely unaffected (probably sociopaths).

 

[Lilleo187]

In every way, except bone loss, it has the exact same side effects from what I've read.

Ive ran it for 90 days without any. It was pharma Evista.

 

[Swifto]

In every way, except bone loss, it has the exact same side effects from what I've read.

Raloxifene has less estrogen-like effects than Tamoxifen in tissues. In comparable studies there were less thromboembolic events and fewer cataracts in the raloxifene groups, as shown in this study.

 

[Swifto]

No theres no sides with ralox

Ive ran it for 90 days without any. It was pharma Evista.

Just because you haven't experienced negative side effects, it doesn't mean someone else won't.

Your ignorance is ridiculous.

 

[Lilleo187]

Just because you haven't experienced negative side effects, it doesn't mean someone else won't.

Your ignorance is ridiculous.

Yea theres minor possoble sides. Most people ive talk to that ran it never had any issues.

 

[Kaladryn]

Raloxifene has less estrogen-like effects than Tamoxifen in tissues. In comparable studies there were less thromboembolic events and fewer cataracts in the raloxifene groups, as shown in this study.

Most of those side effects are from people who have E2 levels so low that the SERM is actually replacing some E2 in the receptors it activates, resulting in less "low E2" related side effects. It still doesn't look at safe as well managed AI from the studies that are out there.

Yea theres minor possoble sides. Most people ive talk to that ran it never had any issues.

I've never "noticed" side effects from nolva for the most part, but I still believe the scientific literature and studies that show what effect it has on the body. All the SERMs look pretty nasty for long term use, compared to the AIs.

 

[Knight9]

that is not a good idea at all... you are simply refering to tamox blocking the E2 binding that results in noticable size effects which is about appearance/feeling not health!

and how is tamox going to block prolonged elevated E2 levels on the liver?

I would almost always suggest an AI to keep E2 levels in range ( not bottomed out which causes issues) Tamox can be used for acute sympomatic flairs as it works on selective target tissues but not long term.

SERMS like clomid can be used long term at a low dose when off AAS although id prefer enclo mostly due to the estro effects of zuclo isomer

If you think prolactin gyno doesn't exist, you don't understand how prolactin works. Your "pretty knowledgable guys, like one's that write scientific papers" are just spreading the typical misinformed broscience that has been going around about 19-nor based gyno for decades.

Now you could debate if the prolactin effect is from the prolactin receptor itself or from some kind co-binding factor involving estradiol and maybe progesterone, THAT part is debatable.

Why throw around so may guesses and blind secondhand info? It misinforms people.



There is no doubt that tamoxifen will raise your HDL, as will anything that increase estrogen and it is great for symptoms of high E2, but that doesn't have anything to do with it's long term application in TRT.

To add a bit to this on the lipid discussion. If one has dire interests on their application approaches to lower Lp(a), nolvadex has been suggested to be a therapeutic in this regards unlike aromatase inhibitors that increase Lp(a). The caveat is that nolvadex can increase triglycerides.

Well, I quoted you guys specifically for a reason. We have a lot going on here on this board and being talked about on various youtube channels regarding estrogen.

The real problem is that we have not established a 'probable acceptable' range when on trt, aggressive trt, or a cycle.
Is an e2 of 50-70 ok when on 300-600mg test?
What about 800-1000mg?
What kind of estrogen protocols would you take if you were using something like Trestolone/Ment?

This 15-21 e2 levels doesnt work with guys that are using exogneous test..



I have really started to think that whether you are taking 200mg, 300mg, or 600mg, the estrogen conversion from test might be exactly what it should be and not warrant an ai.

My friend is currently considering taking raloxifene to counter his upcoming trestolone cycle and I can't even begin where to suggest he starts.

Lower estrogen levels seem to be more of a problem than high estrogen lately and I am starting to believe that levels between 40 and 50 and even up to 70 are ok. I have heard several doctors say 50 is fine and I believe Serrano or McClain said up to 70 is acceptable.


I personally convert a fair amount of e2 from my trt and I switched from arimidex to aromasin about a year ago. Overall, I was doing mostly fine until recently when I feel my joints hurt and started to subscribe to the theory that my e2 levels don't need to be lower than 30-45.

.....and then we need to have the discussion about how e2 (sensitive) is the actual test we need to be ordering/taking as males..

Sorry to ramble but let's hear your thoughts. Apparently I missed a gem of a thread - til now.

 

[Fa Seeshus]

If you are getting bone loss it can show through hypercalcemia on your blood work. I got that from running exemestane too high. Did not get any hypercalcemia on Rx ralox 60mg. The ralox can effect your shbg and free test, put adding proviron or a low dose of masteron would fix that. Or maybe even just some boron.

 

[Kaladryn]

Well, I quoted you guys specifically for a reason. We have a lot going on here on this board and being talked about on various youtube channels regarding estrogen.

The real problem is that we have not established a 'probable acceptable' range when on trt, aggressive trt, or a cycle.
Is an e2 of 50-70 ok when on 300-600mg test?
What about 800-1000mg?
What kind of estrogen protocols would you take if you were using something like Trestolone/Ment?

This 15-21 e2 levels doesnt work with guys that are using exogneous test..



I have really started to think that whether you are taking 200mg, 300mg, or 600mg, the estrogen conversion from test might be exactly what it should be and not warrant an ai.

My friend is currently considering taking raloxifene to counter his upcoming trestolone cycle and I can't even begin where to suggest he starts.

Lower estrogen levels seem to be more of a problem than high estrogen lately and I am starting to believe that levels between 40 and 50 and even up to 70 are ok. I have heard several doctors say 50 is fine and I believe Serrano or McClain said up to 70 is acceptable.


I personally convert a fair amount of e2 from my trt and I switched from arimidex to aromasin about a year ago. Overall, I was doing mostly fine until recently when I feel my joints hurt and started to subscribe to the theory that my e2 levels don't need to be lower than 30-45.

.....and then we need to have the discussion about how e2 (sensitive) is the actual test we need to be ordering/taking as males..

Sorry to ramble but let's hear your thoughts. Apparently I missed a gem of a thread - til now.

My experience shows that Aromasin has a nasty side effect of becoming slightly more effective over time until it is blocking too much E2, requiring ongoing bloodwork and dosage adjustment. Adex gives me gastrointestinal sides (more common than many people realize).

 

[Stewie]

My thoughts are, you had no need for inhibition of aromatase during your eugonadal years. Incidentally, we had no idea of what our sex hormone levels were during this period of time.

Over the last couple of years, I've unsubscribed to the metrics and the 'precise ratio' of testosterone:estradiol. I've also stepped-aside of the 'higher' physiological levels of testosterone is where "you need to be". <--- that will be taken out of context by people that don't comprehend genetic setpoints. Do I know what my hereditary (chromosomal locus of sex hormones) genetic setpoints were prior to being hypogondal, no I don't.

What I do know is my children's sex hormone levels. What I did when my children turned 18, 21 and 24 twice a year was pulled their NMR [I have genetically elevated Lp(a)], CMP, LH, FSH, Full thyroid panel, Testosterone, Alpha-1-antitrypsin, (my mother and grandfather both had emphysema, [I only pulled this once]), progesterone, prolactin, SHBG, estradiol and total estrogens on all three children. There's a few other basic lab's I pulled. I didn't do this for my gratification or without the consent of my children, which they agreed with very much knowing our family history of diabetes, heart disease, and emphysema. I've asked that they keep these records tucked away for in the future as most of us if we live long enough will end up in some situation where we're going to need some sort of hormone replacement. This will give them a better idea if they choose to shoot for numbers they can look back on these and try to get as close to these numbers as possible for their better sense of well-being and health.

So I averaged my sons and my daughters sex hormone levels, particularly testosterone and estrogen. Given the numbers for testosterone for both my daughters and my son, none were in the higher range of testosterone, morso mid-range. So what this tells me is I would probably be better suited mid-range than the higher percentile. Is this methodology correct to determine what my genetic setpoints are. No, because they have their mothers genes to take into account. So I have half of an equation to work off of.

As for where I feel best with a particular estradiol level? I dunno somewhere between 40 and 70? I really don't hyperfixate on numbers as much as I used to.

I know this doesn't answer your question directly, knight. Although I do feel aromatase inhibitors are way over prescribed and way overused.

That's my take