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  1. #1
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    Baffled....






    I'm finishing up the tail end of a cycle and I'm curious about a couple of things. Previously I usually just ran Dbol for the first 5 weeks and test for 8-12 weeks. The last cycle I did I ran the dbol at 30mg for 5 and the test for 12 at 500mg and barely drank on it and ate very cleanly and had hellish bloodpressure, migraines, nosebleeds, and I had a lot of body fat gained with the cycle that stayed around when I got sick several times over this spring that tore a lot of my gains away but left the fat. This cycle I ran the Dbol for only 4 weeks at 25mg, ran Deca at 375mg for the first 6 weeks along with Test E throughout at 600mg, and I added in Tren Ace and Tren E when I took my last shot of Deca and have been running it the rest of the way through. I used the two together then just ran the E after a week and am now running the Ace again to finish out with a short ester. I have to admit since I started back up in retail ( I was laid off the last cycle), my diet has been a lot more hap hazzard and probably includes at least a double cheeseburger each day. Being it summer and beach time, I've definitely drank a lot more alcohol than I have on previous cycles, a lot, yet I've had my cleanest gains ever. I went from 182lbs and 19.7% Bodyfat, to 200lbs and 14.9% bodyfat. I went as high as 208lbs but started arimidex two weeks ago and lost about 8lbs in water and a little fat as well. My blood pressure has been a lot lower, no headaches or nosebleeds either. I'm curious if the drinking more often helped or just something as simple as lowering the dbol dosage and not running it as long is it. Since I was running Tren I've been very concious of my water intake as well.
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    That you drink at all on cycle baffles me.
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    I know I shouldn't at all but I wondered if by having a few drinks when I was out helped with keeping the blood pressure down this time around.
    "I may not be the best looking guy in the bar, but I'm the only one talking to you" - J King

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    I have bad reactions to dbl, or any oral for that matter. Your liver values are probably high so you're overworking your liver which can lead to sickness, fat,insulin instability, lathargy etc. I'd say skip the orals, except for primo or anavar. I'd also extend my cycle to sixteen weeks with a mixture of deca/test 50% each. Or, test/eq, run around G a week. I've done blood work on several different cycles, this one seems to have the greatest gain to health ratio. Dropping the orals is probably the best change however.

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    Quote Originally Posted by luke69duke69
    I know I shouldn't at all but I wondered if by having a few drinks when I was out helped with keeping the blood pressure down this time around.
    There are better ways to keep blood pressure down.

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    Yep the HBP is coming from the dbol. If you are having those problems, it is probably dangerously high. I would check it and stop the dbol immediately.




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    I did stop the dbol. Earlier this time. I dropped it after 3 weeks. I just checked my BP yesterday and it was 130 over 80 and I'm in week 11 of a 12 weeker. So my BP is a little high, but not rediculous. It always goes back down to about 110 over 70 or 60ish.
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    Two guesses, could be that its a bit of both.

    1. Being laid off is known to be excessively stressful. That happened last cycle, when you were generating oxidative stress metabolites like crazy, while pushing up inflammation reaction and decreasing its control, despite diet. By the way, if you diet doesn't feature certain lipids and antioxidants, it don't really matter if you eat :clean: or not.

    2. You were using a mixture of steroid analogs that altered receptor binding site activation by dbol, first and test E second, by the addition deca and tren, known tight binders at the OTHER nuclear receptors (other than just AR) that cause inflammation response.

    Interesting case. Alcohol has nothing to do with the observed effect, by the way. It does, however, have much to do with the subsequent liver damage.

    A fool and his liver are soon parted.

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    Alcohol inhibits ADH, so it is very likley it has made the nosebleeds and migraines worse .
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    I belive you meant to say: ethanol activates ADH enzyme activity.

    ADH, alcohol dehydrogenase, is an enzyme that catalyzes the oxidation of ethanol to acetaldehyde, the first step in the metabolism of alcohol by the liver.

    "Alcohol dehydrogenases are a group of dehydrogenase enzymes that occur in many organisms and facilitate the conversion between alcohols and aldehydes or ketones. In humans and many other animals, they serve to break down alcohols which could otherwise be toxic; in yeast and many bacteria they catalyze the opposite reaction as part of fermentation.

    The EC number of alcohol dehydrogenases is EC 1.1.1.1; their CAS number is 9031-72-5.
    In humans

    In humans, the enzyme is contained in the lining of the stomach and in the liver. It catalyzes the oxidation of ethanol to acetaldehyde:

    CH3CH2OH + NAD+ → CH3CHO + NADH + H+

    This allows the consumption of alcoholic beverages, but its original purpose is probably the breakdown of alcohols naturally contained in foods or produced by bacteria in the digestive tract. "

    Thats from the Wikipedia webpage, by the way.

    This, sir, is what you implied: that ethanol induces activation of an interesting nuclear receptor activator: SREBP, sterol regulatory element binding protein.

    It just so happens that this same binding protein catalyzes the release of a factor responsible for blood thining, and that also regulates the expression of desaturase enzymes responsible for converting saturated fatty acids to unsaturated fatty acids (delta desaturase)

    " Alcoholic fatty liver is the earliest and most common response of the liver to alcohol and may be a precursor of more severe forms of liver injury. The mechanism by which ethanol causes fatty liver and liver injury is complex. We found that in both rat H4IIEC3 and McA-RH7777 hepatoma cell lines, ethanol induced transcription of a sterol regulatory element-binding protein."

    Source: J. Biol. Chem. 277(32): 29342-29347 (2002).

    It wasn't until subsequent finding published in 2004 and 2005, that the connection with SRC-1 (the initiation of SREPB) was tied to altered expression of these saturases, a condition also observed in insulin resistance.

    I happen to talk about this connection at some length in a particular thread at Mind and Muscle earlier this year.

    In that thread, in which I tied together SRC-1 and its activation of archidonate synthesis and subsequent induction of prostanoid inflammation.

    Hence, we have the linkage between nosebleeds, migraine headaches, and alcohol consumption...when coupled with steroids, that also activate SRC-1.

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    No I did not mean to say that. ADH is inhibited by alcohol thus the constant pissing and hangover the next day. Dehydration can add to the nosebleeding problem but is not necessarily the only cause of it.
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    I actually was saying this time around that I would go out and have a few drinks whereas the cycle previous I did not and the previous cycle was the one with a 170/110 bp whereas this cycle as of last week was 130/80. The dehydration really wasn't that bad because I would drink at least a quart of water before bed and in the course of a day would drink about a gallon and a half of water per day. I didn't get a single nose bleed this time around but last time got them constantly. The last cycle was less compounds too. would the fact that I ran arimidex have helped with the blood pressure being lower this time around?
    "I may not be the best looking guy in the bar, but I'm the only one talking to you" - J King

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    Yes sir, you are astute.

    Aramidex does indeed inhibit water retention (sodium imbalance in the kidney tubule) that causes high blood pressure, that can cause headaches.

    However, and more to the point of pain and inflammation, this landmark paper indicates that unlike tamoxifen and its analogs, aramidex does NOT cause the release of arachidonatic acid and prostaglandins that are involved in inflammation response (PGI2), and other COX2 pathway metabolites.

    Whoever among you is the most astute on the science behind use of the AIs should really read this paper and think on the consequences of tamoxifen de-esterification of phospholipids in cellular membranes.

    That is chemical karma of the most profound sort. Very bad.

    So, the answer to your initital question of what saved your ass, despite the bad choices you made in diet and alcohol this cycle versus last cycle:

    T'was the Aramidex that done it.

    If you think alcohol is a permissible, even thinkable choice of action while on cycle using these steroid analogs...I would strongly suggest you reconsider your rationale, Luke. Else, I will spell it out in liver-twitching detail.

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    Arimidex, you mean?
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    Thanks for the input trouble. I'll be sticking to water and fruit juice the tail end of this one and leaving the alcohol out knowing it wasn't the few drinks that were keeping the BP down.
    "I may not be the best looking guy in the bar, but I'm the only one talking to you" - J King

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    Quote Originally Posted by musclepump
    Arimidex, you mean?
    LOL, sorry. Nothing like consistantly mispelling the drug tradename. Thanks for the correction.

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