I have been looking for more information about alcohol consumption, and increased aromatase activity. I’m one of those guys that like to come home and have a couple of drinks, to wind down after work, and maybe a few during football on Sunday. I don’t go to crazy but some times two can be three or four, especially on Sunday during the game. I’m getting a little older, almost 60 and on TRT. I was wondering if the “social” drinking is causing my E2 levels to increase notably. As you are probably aware, there has been a push to get of of AI’s and I guess let you body deal with the increase in E2 on it’s own. I tried that and my E2 went up to about 70. I was injecting 50mg E3D, sub-Q and I decided to try lowering my T dose to 40mg E3D and I’m still having a problem with high E2. Then I remembered hearing something about alcohol consumption increasing aromatase activity. So my question is simple. If I give up the hallowed cocktail hour would my E2 drop enough to continue TRT without an AI? I realize there isn’t any way to be certain but can alcohol consumption be enough of an aromatase stimulus to make a big difference in E2 levels considering my drinking frequency.
Please share your thoughts and thank you!
Alcohol can increase aromatase activity, but I’m not knowledgeable enough to say that it’s a DIRECT 1 to 1 influence.
Alcohol inhibits metabolism, which leads to increased body fat, and not to mention fat increase in the organs (dangerous). It affects insulin sensitivity as well. All of these thing add up to increased fat area, which means more aromatase.
Alcohol is poison to your body and if you are drinking daily, you’re negating the benefit that healthy testosterone levels can have on your body. I’m not saying that you have to quit completely, unless you are one of those guys that can’t control the need to scratch the itch so to speak.
If you are disciplined enough to put it down during the week, and pick a night or two on the weekend where you allow yourself to have 1 or 2 (not get blind ass drunk), change dietary habits and choose a healthier cleaner eating regimen, and start a regular exercise routine (if you don’t already), then you could probably be ok.
The bottom line is that E2 is aromatased in fat tissues. If you have more fat, you have more aromatase. Alcohol is contributing to that, among other very damaging factors. Concentrate on limiting yourself, cleaning up diet, and losing the excess and your hormones will stabilize like you wouldn’t believe.
Thank you for taking the time to respond, all good stuff! If I understood you correctly, alcohol itself doesn’t really have an effect on estrogen, or testosterone. it’s the increase in fat from alcohol consumption that get things off track. OK, cool. Here is another question, how does alcohol make someone fat, when each drink is only about 100 calories (1.25 oz sprites, 6 oz wine) and zero fat content? I know your right, I just don’t understand where the fat comes from, when a person drinks alcohol.
It’s not the calories in alcohol, it’s the fact that when you consume it, ALL other digestive process are put on hold and priority is given to the alcohol. Your body wants to metabolize it and get it out as quickly as possible. The effects on the liver are ENORMOUS. This leads to insulin resistance (I’ll explain in a more detailed post), which in turn leads to excessive fat storage providing you eat a normal amount of calories otherwise. Not to mention the effect on adrenal function, which causes huge hormonal imbalances, which also leads to weight gain.
You can see skinny alcoholics running around all day, but the difference is that they don’t eat very much at all (so they don’t gain much in visible body fat), but if you did a scan you would see that their organs are loaded with fat.
That’s not quite what I said…I said that I am not knowledgeable enough to tell you if there is also a DIRECT 1 to 1 effect relating alcohol and immediate circulating estrogen levels. All I can really elaborate on is the indirect effects.
When you drink alcohol, insulin levels are increased. If you drink chronically (every day), then you are keeping these levels elevated all the time, which desensitizes receptors. This is how insulin resistance is created. Insulin resistance will effect how your body metabolizes food (fat gain is inevitable if you eat anywhere close to maintenance caloric intake), and lead to diabetes over time. There’s no good outcome to daily alcohol consumption.
Amazing I had NO idea. I just thought I was chilling out. Fortunately, I don’t have an physical dependency on alcohol, for me it’s a choice. Believe it or not, I’m actually a bit of a gym rat. Supplements, diet the whole deal. But, I screwed up my knee and I hasn’t been able to work out for a couple months so I “took advantage” of the off time.
Thanks for the biology lesson I appreciate it and I’ll probably make some better decisions noe that I know it’s not as harmless as I though at the “moderate” level.
mmmmm, if you’re drinking daily… as in multiple drinks per day (even one drink daily seems excessive to me, but many follow such practice and live long, healthy lives) then you probably should quit for a while. Then again, some think of ethanol as a cultural normality, perceiving a glass of wine to be the equivalent of a tea/social beverage whilst I think of ethanol as a recreational drug (I believe many have the aforementioned opinion due to the societally engrained acceptance/normality of ethanol… primarily due to heavy marketing from the alcohol industry. It’s interesting that booze hasn’t garnered a similar reputation to tobacco, considering the two are arguably just as terrible for you… and highly addictive).
Regardless I view alcohol to be a recreational drug, on par with benzodiazepines, GHB, MDMA (I’d stipulate cocaine is more dangerous acutely) and other depressants (MDMA isn’t a depressant, but the perceived level of harm from acute use vs getting plastered)… the only reason one will think “bro, you took a xanny, that’s beyond fucked” is because Xanax is a scheduled substance and thus abuse carries a stigma… Both are HIGHLY addictive with a high potential for abuse, although in terms of physical harm, acutely alcohol is far worse. What I decide to take has nothing to do with societal perception or opinion, rather I base my views off literature and not the stupidity of a populace who doesn’t know any better (no offence to anyone who views alcohol as okay), but when someone says (classmate made a presentation on why pill testing at festivals shouldn’t be allowed) “pills can kill when taken recreationally, even if the substance is what is indicated, thus it isn’t safe…” I think (and this is a bit harsh) “fuck off… I know for a fact that you presenting… YES YOU, frequent the same parties I go to and drink LITERALLY a bottle of vodka… and that’s better than my half cannabis cigarette?”
I don’t take hard drugs, however it effects many whom I know, who at music festivals when presented with sniffer dogs and police presence down everything they have (typically large dosages of unverified MDMA) as mere possession here is grounds for criminal prosecution, as the police force and courts clearly have nothing better to do than enforce prohibitionist era logic and ruin young lives (not as if the rates of drug use amongst teenagers are low either, I believe here about 20% of teens use MDMA, 50%+ have tried cannabis etc, we have very high rates of use here)
Also, hops in yeast are highly estrogenic. I haven’t had a singular alcoholic beverage in like 8 weeks, that’s simply because I don’t drink during the school year (I go out during holidays). However my irritating tangent remains, for a one off scenario, I would legitimately stipulate that taking a majority of illicit recreational drugs at reasonable dosages is safer (physically…) than getting drunk.
You’re very welcome sir and it’s my pleasure to help anywhere I can.
I see that @unreal24278 is replying now. This kid will blow you and me both away with how knowledgeable he is. He’ll give you the full rundown I’m sure, as well as correct any potential misunderstandings that could be inferred from my simplified explanation.
Oh… hepatic dysfunction induced by ethanol will interfere with oestrogen metabolism/clearance too.
Alcohol is a dirty, dirty drug. The sheer amount of cells/receptors and pathways it acts upon is unparalleled by most, if not all pharmaceuticals. The precise mechanism by how ethanol exerts all it’s effects STILL remains undeciphered. However we know one thing… acetaldehyde is super, SUPER bad for you at high concentrations… It’s poison… literally
If you have to drink, do so within a moderated context (this means if you drink for the taste, limit t 1-2 times weekly… If you binge drink, make it a rarity, not a weekend thing
Firstly, alcohol can induce hypothalamic inflammation which can theoretically induce insulin dysregulation (reduced response to, metabolic irregularities etc). Should also be noted alcohol can inhibit autophosphorylation within insulin receptors, impairing glucose regulation/homeostasis (complicated process, don’t wish to go through it all)… however once alcohol/metabolites have cleared the system this isn’t that much of an issue I guess. The release of pro inflammatory cytokines following ethanol consumption may induce a systemic pro inflammatory state following repeated consumption, of which is a potential issue… There’s even MORE pathways… but these are the predominant I can think of…
Also the high glycemic index of alcohol/high caloric values with little legitimate nutiritional value don’t help either
It sounds like this twice weekly protocol is no longer going to be optimal, you need smaller more frequent dosing to minimize this E2 conversion issue. You don’t need an AI, you need to optimize your protocol, the AI will not address the slower metabolism caused by the alcohol.
I had a 72 E2 Sensitive FT 20 TT 1300 and that was at 70mg E3D. Then I lowed to 50 mg E3D I was still getting high E2 symptoms, so I lowered to 40mg E3D my current level, but I haven’t had labs on this level I just started 2 weeks ago. I was trying to lower until I could go to zero AI. So far I haven’t been able to get to zero AI.
The more frequent the better, your choice will reflect the outcome. When I was on 50mg twice weekly, my E2 was 70, but on a daily protocol E2 was 26 and 32. I have the advantage because I feel optimal at 400 ng/dL, FT 15 pg/mL (6.8-21.5) and SHBG is low.