I don’t see many people making mention of aromasin on this board. Seems that arimadex is the standard.
Is this bc people feel aromasin is that inferior to adex in terms of controlling estrogen?
I’m just curious bc I’ve read that aromasin is much more forgiving on your lipid profile and actually increases IGF.
For longer cycles, or especially ones including orals…it seems like one would opt for the aromasin (because of its supposed less harsh nature) if it is adequate for controlling E2.
Just a question that’s been bouncing around in my head lately.
[quote]Mr. Walkway wrote:
aromasin has a really short half life and has to be consumed with fat
so it’s less convenient. [/quote]
Is the half-life short enough to make that much of a difference? I was under the impression that a short half-life wouldn’t really matter here, since it’s a suicide inhibitor and all it has to do is bind to the enzyme, not stick around.
[quote]Mr. Walkway wrote:
aromasin has a really short half life and has to be consumed with fat
so it’s less convenient. [/quote]
Is the half-life short enough to make that much of a difference? I was under the impression that a short half-life wouldn’t really matter here, since it’s a suicide inhibitor and all it has to do is bind to the enzyme, not stick around.[/quote]
yes because it peaks rather quickly, after which estrogen begins to rise again.
[quote]Mr. Walkway wrote:
aromasin has a really short half life and has to be consumed with fat
so it’s less convenient. [/quote]
When did the FDA demand we use exemestane with fats? Tablespoon of extra-virgin olive oil with 12.5 mg everyday is what I do. (starting 10 minutes ago) … and three whole eggs.
With this new (new to me) information on its short half life is 12.5 ed with 500mg/t weekly not doing what I thought it was doing? I’ve had no labs since February.
lef.org prices just went up as they usually do this time of year.
[quote]Mr. Walkway wrote:
aromasin has a really short half life and has to be consumed with fat
so it’s less convenient. [/quote]
Is the half-life short enough to make that much of a difference? I was under the impression that a short half-life wouldn’t really matter here, since it’s a suicide inhibitor and all it has to do is bind to the enzyme, not stick around.[/quote]
yes because it peaks rather quickly, after which estrogen begins to rise again.
I don’t know what you mean by suicide inhibitor?[/quote]
Adex and Asin are in different classes of AIs (Letro is same class as Adex), but you probably knew that. What’s important is that the mechanisms of action of each are different. Adex and Letro reversibly bind to aromatase, so they bind and after awhile they dissociate. As such, half-life effects are definitely relevant for these drugs. But Asin is special. It’s a suicide inhibitor, which means it binds to aromatase and covalently bonds to its active site, permanently inactivating the enzyme. The only way for the body to overcome this is to make more aromatase, which is a slow (several days) process. The only way that I would think half-life could be relevant in this case would be if the metabolic half-life was so short that most of the drug is degraded before doing its job, but then I don’t think it would be approved for therapeutic reasons if that were the case. This mechanism difference is, AFAIK, the reason why some dosing protocols for Asin use E3D and why Asin doesn’t have to be tapered like Adex.
I definitely didn’t know about the take with fat thing, though, and that seems important. Would be awesome if you could explain that in a bit more detail.
aromasin should be dosed ED at least… 2x ED is optimal… the point about it permanently deactivating aromatase is moot because the body is constantly making new aromatase… so sure it may take days to make new aromatase, but the body has been working at making new stuff for days…
[quote]Mr. Walkway wrote:
fat just helps with absorption…
aromasin should be dosed ED at least… 2x ED is optimal… the point about it permanently deactivating aromatase is moot because the body is constantly making new aromatase… so sure it may take days to make new aromatase, but the body has been working at making new stuff for days…
sooo…assume a constant supply[/quote]
The body may have been making new aromatase for days, but how much you get depends on the rate of protein synthesis. Your body wouldn’t want to synthesize aromatase at more than a very low rate, as doing so would mess up your hormone balance beautifully. As hormones can cause great physiological changes, even in relatively small amounts, the enzymes that make them are going to have to be present in more minute quantities. I would speculate that aromatase is a stable enough protein, too, which would necessitate low levels of transcription by default. That said, an increase in aromatase transcription in response to low estro levels would almost certainly occur, so I wouldn’t disagree with you that dosing more frequently is probably better and at worst, can’t hurt.
WW, I’m curious to know whether you think Aromasin has a place for AAS users?
WW, I’m curious to know whether you think Aromasin has a place for AAS users?[/quote]
I think it does… but imo adex and letro are better lol[/quote]
I could see that. I often see Asin being recommended for PCT since type I AIs apparently don’t have the same interaction with Nolva, and I was thinking of using it for that purpose. I also really like the idea of not having to taper the Asin, so it’ll be pretty idiot-proof for a first cycle. The effects on SHBG and IGF-1 are nice too. I’m thinking Adex on cycle and Asin during PCT. Would that be a reasonable way to do it?
WW, I’m curious to know whether you think Aromasin has a place for AAS users?[/quote]
I think it does… but imo adex and letro are better lol[/quote]
I could see that. I often see Asin being recommended for PCT since type I AIs apparently don’t have the same interaction with Nolva, and I was thinking of using it for that purpose. I also really like the idea of not having to taper the Asin, so it’ll be pretty idiot-proof for a first cycle. The effects on SHBG and IGF-1 are nice too. I’m thinking Adex on cycle and Asin during PCT. Would that be a reasonable way to do it?[/quote]
Mr. Walkaway’s finding again gives us incentive to update our knowledge base and not feel our initial indoctrinating is all encompassing. I didn’t just read an hour for nothing so I’ll post some of what I found:
…study which showed an increase in the absorption of exemestane of 40% when taken with fats.
…it takes time for the body to produce new aromatase- so its effective time is much longer than the half life indicates.
…it seems to be forgiving in the area of eliminating all estrogen - even at 50mg/day with no exogenous test - the e levels were low but still in reference range. (we need some estrogen)
…no changes in circulating serum triglycerides, cholesterol, or LDL or HDL cholesterol concentrations with either a 25mg or 50mg daily dose of exemestane.
Exemestane (Aromasin) is a potent and selective irreversible aromatase inhibitor. To characterize its suppression of estrogen and its pharmacokinetic (PK) properties in males, healthy eugonadal subjects (14-26 yr of age) were recruited. In a cross-over study, 12 were randomly assigned to 25 and 50 mg exemestane daily, orally, for 10 d with a 14-d washout period. Blood was withdrawn before and 24 h after the last dose of each treatment period. A PK study was performed (n = 10) using a 25-mg dose. Exemestane suppressed plasma estradiol comparably with either dose [25 mg, 38% (P 0.002); 50 mg, 32% (P 0.008)], with a reciprocal increase in testosterone concentrations (60% and 56%; P 0.003 for both). Plasma lipids and IGF-I concentrations were unaffected by treatment. The PK properties of the 25-mg dose showed the highest exemestane concentrations 1 h after administration, indicating rapid absorption. The terminal half-life was 8.9 h. Maximal estradiol suppression of 62 14% was observed at 12 h. The drug was well tolerated. In conclusion, exemestane is a potent aromatase inhibitor in men and an alternative to the choice of available inhibitors.
… also BIG difference between aromasin / exemestane and arimidex / anastrozol:
There was an increase in circulating testosterone concentrations after both 25 mg (60 + 58%; P = 0.001) and 50 mg (56 48%; P = 0.003) exemestane. Androstenedione concentrations were increased as well after 25 mg (32 �± 36%; P = 0.004) and 50 mg (47 59%; P = 0.052) exemestane, respectively (Fig. 1Go and Table 2Go).
SHBG concentrations were decreased by 217% (P = 0.0003) and 19 39% (P = 0.18) at 25 and 50 mg exemestane, respectively.
Free testosterone concentrations were increased by 117 74% (P = 0.0001) and 154 95% (P < 0.0001) at both doses, due to the decrease in SHBG and the increase in total testosterone.
I just got some aromasin and have started using it. I am off cycle and am so far 4 days into using 5mg/day.
I have come off of letro. I had a very difficult time finding my sweet spot, as I either crashed e2 too far or had it come up too much. I used between .18-.36mg of letro per day. .36mg per day being simply 2.5mg/7days which is what Bill Roberts said he uses.
I have used letro in liquid form, but my liquid degraded I am pretty sure. I also have letro in capsules, which I opened up and roughly divided up into 7 parts. I then took the appropriate amount of powder each day, but I did not have much success with that.
Does anyone have good experience with aromasin, especially off cycle, and how long should I wait before making adjustments?
Currently I plan to wait for 7 days at least before I up the dose, because I have noticed some bloating and a lowering of sex drive which I notice when my e2 gets too high.
