How Anti-Es Affect Your Cholesterol/Lipid Profile

This was posted by crankin'stein and it looked like it would be worth sharing.

ORIGINALLY POSTED BY SUPERCHICKEN

theres been a lot of talk on other boards about this lately, and a lot of bad information thrown out as well. i wanted to share the good info.

somone keeps posting how letrozole is the strongest and doesnt negatively affect cholesterol. this is not true. letrozole is NOT the strongest and it DOES negative affect cholesterol/lipid profile in a bad way.

aromasin(exemestane) is the best. this is why

both arimidex/ldex/anastrozole and femara/letrozole hurt your cholesterol. the way these 2 anti e's work is they inhibit the aromatase enzyme. by inhibiting the enzyme which converts testosterone to estrogen, you reduce or even come close to eliminating estrogen production. we need some estrogen to be healthy. the major drawback to this is without estrogen, your lipid profile gets fucked.

exemestane works differently. it does not stop the body from producing estrogen. rather, it makes it so the estrogen is unable to bind to receptors by deactivating the binding enzyme. if the estrogen cannot bind, you simply will not get bloated or get gyno. the estrogen is crippled due to exemestane. however, since the estrogen is still floating around, it will not negatively affect your lipid/cholesterol profile.

anastrozole doesnt cause a rebound effect, and neither does exemestane, but letrozole does. this means after you stop the letrozole, your estrogen rebounds and goes pretty high for a while, eventually it normalizes. you can avoid this by tapering your letro dose down before stopping it, but that is a pain in the ass. higher than normal can mess many things up post cycle when you stop. since the hpta has a feedback loop is primarily controlled by estrogen, high estrogen will tell your hpta to produce less testosterone, because it thinks the high estrogen is caused by too much testosterone. this is fact. now post cycle, dont we want to raise our test levels, not lower them? of course! so rebounds are bad. if you use letro taper the dose off to zero over a couple weeks.

fyi- nolvadex(tamoxifen) is a SERM(Selective Estrogen Receptor Modulator). this means on certain tissue it can act antagonisticaly or agonistically. in the case of lipid profiles, it acts agonistically. so, running tamoxifen with your anti e's will IMPROVE your cholesterol profile even if not on cycle or using any gear or other anti e's. its just plain good for cholesterol.

one thing to keep in mind though when runing tamoxifen with letro. letro reduces blood levels of tamoxifen by over 50%. a study showed 2.5mg letro ed made nolva levels drop to 40% of what they were before adding letro. this does not mean you cant use tamoxifen with letro, it just means you need to use more, about double. 20mg of nolva will act like 8mg if running letro. so make sure you are aware of this because you will need to buy more nolva to compensate. this does not happen when mixing tamoxifen with anastrozole or exemestane, it only hppens with letro.

also, many people and myself experince a reduction of libido on letro. this doesnt happen w/ ldex or exmestane as far as i know, and in my own experience, and ive run all 3 quite a bit.

the best combo IS exemestane and tamoxifen together. your cholesterol will be as good as can be considering your on a cycle of steroids. the dose of aromasin will vary depending on the users needs and how much aromatizing gear is being taken. usually 10-25mg ed works well. run 10mg ed nolva to improve your cholesterol.

second best combo i feel is anastrozole(ldex) and tamoxifen. ldex dose ranges from usually .15mg ed to 1mg ed. run 10mg nolva ed to improve cholesterol.

thierd best is letro and nolvadex. letro doses usually range from 1-2.5mg ed. run 20mg ed nolva to improve cholesterol w/ letro.

you do not need to run nolva with any of these 3, i do recomend it though as it will improve cholesterol compared to using the anti e's alone without nolva.

so in order of strength, on a dose per dose basis(not mg per mg) aromasin is def the strognest, next is letro, and then ldex.

ive been running aromasin now for about 4 months, i wont switch back to ldex or letro. it works much better and its much healthier for cholesterol profiles.

i think we all need to stop only worrying about side effects that we can see visually. cholesterol KILLS many people around the world everyday(well not directly kills but leads to it). steroids are hrting us badly in this sense. steroids do mess our cholesterol up pretty badly, and we will pay for it later in life. now not many of us are going to stop using gear because of that, but we should at least take the proper other drugs to help minimize.

aromasin is only a little bit more expensive than ldex or letro, and its actually about the same price as many places sell ldex or letro for. but its more powerful and healthier. people spend money all the time on steroids which dont have as many side effects as some of the harsher, cheaper steroids. a few extra bucks for the proper anti e's is def money well spent.

xcel

I'm sorry, but there are many flaws in this article.
Exemestane does NOT work how described above. It irreversibly binds aromatase, being a type I AI, whereas anastrazole and letrozole competitively bind aromatase, since they are type II AIs. Exemestane does not work at the level of the receptor....it merely binds (irreversibly) and renders each aromatase enzyme it binds incapable of ever again causing aromatization. For this reason, exemestane DOES have the potential to affect lipid profiles, although, for some reason, few studies have shown this to actually happen....yet some have.
Letrozole has no more (even less actually) potentially for estrogen rebound than anastrazole.
The libido issue is no more a problem for anastrazole as it is for letrozole.

I do agree that an AI, which reduces HDL, should always be run with tamoxifen, which increases HDL, since it is an estrogen agonist in both bone and liver.

einstein1905 said:

I do agree that an AI, which reduces HDL, should always be run with tamoxifen, which increases HDL, since it is an estrogen agonist in both bone and liver.

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What's your take on AI effects on IGF-1?

Since letrozole increases IGF-1 and Nolva reduces IGF-1, these will cancel each other regarding IGF-1?

I'm not saying this is bad as there's no net gain OR loss.

xcel

xcelbeyond said:

What's your take on AI effects on IGF-1?

Since letrozole increases IGF-1 and Nolva reduces IGF-1, these will cancel each other regarding IGF-1?

I'm not saying this is bad as there's no net gain OR loss.

xcel

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The majority of the studies out there show that both type II AIs, anastrazole and letro, increase IGF-1, but there have also been a study or two to refute this. Somewhat of the same deal for tamoxifen: There is about a 50:50 split in studies where IGF-1 levels are examined in response to tamoxifen administration. The decreases seen in some studies of IGF-1 are about the same magnitude of the increases shown in other studies.
It'd be really hard to conclude tamoxifen's effects on IGF-1 at this point, with so much contradictory data. If it does have any adverse effect on IGF-1, it appears only to be in the ballpark of 20% or so, which would/should be compensated for by the increase of IGF-1 levels that come with AIs.
I can say, pretty comfortably, that the combination of an AI with nolva should have negligible effects on IGF-1, if any at all.

On a tangent, The IGF-1 to which we're referring is only hepatically-derived IGF-1 and not the splice variant of IGF-1 that is expressed in skeletal muscle. It's still debatable whether or not systemic, hepatically-derived IGF-1 plays any significant role in skeletal muscle hypertrophy. When injected IM, it induces hypertrophy in the muscle into which it was injected....also, when IGF-1 (the hepatic isoform) has been expressed in skeletal muscle (rats), there is significant hypertrophy in the muscle in which it was overexpressed and some effect on nearby muscles, but there has shown to be NO increase in plasma IGF-1 levels. This implies that IGF-1 does not leave the muscle,which is its site of origi, very effectively. This would also suggest the opposite is true; that it won't enter muscle efficiently.

I've had definite site-specific effects using LR3...that's indebatable, but I also have noticed an increased hardness all over as well as reduced bf%.

I guess that little tangent, although related, may not have been necessary.

This also brings me to GH, which increases hepatic IGF-1 production. However, I'm of the opinion that GH binding its receptors on skeletal muscle induces expression of the skeletal muscle isoform of IGF-1 (I believe IGF-1Ea). I have my doubts on just how important hepatically-derived IGF-1 is on muscle, although it certainly has its own respective effects on connective tissue and many other tissue types.

I only site-inject LR3 IM into the muscles just worked. IGF receptors are upregulated in response to resistance training, so jst the increased ratio of IGF-1 to its receptor allows for a much greater potential of succesful bindings to occur in the muscles just worked. This is also an insurance plan in case IGF-1 really does not have the ability to efficiently leave or enter muscle.

That all being said, I gues I'm just trying to emphasize that hepatic IGF-1 expression may not be the most important thing to focus on. It's really not clear yet.

xcelbeyond, what do you think about running anti-e's to increase natural test levels?

eatcrow said:

xcelbeyond, what do you think about running anti-e's to increase natural test levels?

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I saw a study where anastrozole purportedly increases natural test levels - so I thought it would be could to supplement with it during PCT. That is until I discovered that ana messes your lipid profile (which a lot of different gear does also) and I feel you should be recovering in that aspect, probably moreso than test recovery.

xcelbeyond said:

I saw a study where anastrozole purportedly increases natural test levels - so I thought it would be could to supplement with it during PCT. That is until I discovered that ana messes your lipid profile (which a lot of different gear does also) and I feel you should be recovering in that aspect, probably moreso than test recovery.

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I'm thinking about trying nolva on its own to get to the high-ends of my natural test levels without the use of an anobolic steroid.

I'd like to try Nolva with Femera for this purpose alone but I'm currently using Nolvadex on its own right now. Is this a good idea?

eatcrow said:

I'm thinking about trying nolva on its own to get to the high-ends of my natural test levels without the use of an anobolic steroid.

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Jusy my opinion but I think that you're only fooling yourself if you think you can increase "natural" test levels when you're supplementing with endogenous test (AAS). You basically shut down that function when you're on a cycle.

xcelbeyond said:

Jusy my opinion but I think that you're only fooling yourself if you think you can increase "natural" test levels when you're supplementing with endogenous test (AAS).

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I meant without using an AAS

I spoke to someone who tried it specifically to increase his test levels. He said it increased from the mid to low 200 ng/dl to the mid 900s.

Sorry - I read your post too quickly and thought you stated "with"

I'd be VERY interested to see your results if you get blood tests to determine effectiveness. Do you know or have been tested recently to establish a baseline?

xcelbeyond said:

Sorry - I read your post too quickly and thought you stated "with"

I'd be VERY interested to see your results if you get blood tests to determine effectiveness. Do you know or have been tested recently to establish a baseline?

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No. I dont know where I can get it done privateley. I've asked around but no one I've spoken to knows.

I wont use the nolva until I get tested or I'll preserve my blood somewhere (if thats realistic) then use the Nolva.

I have an Idea... How bout synthtek makes a product that will protect and Improve lipid profiles while on cycle or off for that matter.. If thaey acn amke a liver protector that is the most potent detoxifier and protector then I think it would only be natural that they would have a product to protect our lipid profiles...Synthtek?? can you do this??? Big A, MikeS whatta ya think??? They could get it done, there are a ton of things out thnere that work lets get them to do it...