![]() |
| LinkBack | Thread Tools | Search this Thread |
|
# 1
07-10-2010
# 2
07-11-2010
|
I have never been a heavy drinker but I do like the occasional toke. I was just curious as to all of your opinions on the use of Marijuana on cycle? And just its use in general?
|
First, marijuana is highly estrogenic. Marijuana causes apathy, and most people get the junk-food munchies.
I definitely wouldn't use it on cycle.
In general, that's up to you; but it certainly wouldn't help you in any way that's realted to your general health/bodybuilding.
# 3
07-11-2010
|
I have never been a heavy drinker but I do like the occasional toke. I was just curious as to all of your opinions on the use of Marijuana on cycle? And just its use in general?
|
Its up to you, just stay responsible.
# 6
07-12-2010
# 7
07-12-2010
|
This is going to be a highly opinionated question. I say smokem' if you gotem'. Marijuana can cause an increase in appetite (just force yourself to stay on your macro plan), relaxation to combat soreness.
Its up to you, just stay responsible. |
i personally think marijuana has a bad rap, its used for medicinal purposes, has no side effects cept drowsiness n hunger, you cant overdose, you cant die from it, and most importantly is non-addictive(contrarly to all other classA,B,C drugs....1=3smokes, I used to smoke 1/day, not a pack of cigs like some people....its only illegal because of the tobacco and drug industries forced it upon the govt in 1929 in the US....explain how its a classB drug and all the date rape stuff like ghb n ex is classC (w anabolic steroids), even ritalin is in the same class as pot yet in my personal opinion (im a child psych mind you), is far worse as drugs go, long term use can lead to an array of psychotic problems (one of the reasons its frowned upon now, without mentioning short term issues which are bad as well)
# 8
07-12-2010
|
im in week 5 on turinabol lv. i just quit my heavy pot habit about a week ago. imo, pot must have slowed tbols conversion, because i wasnt seeing much from 90mg(60/60/90/90/120/120). as soon as i quit and bumped up to 120mg.....DAYUM. i just blew up, but now its the end of the cylce..so woopty-do. on inject cycles, it never bothered me. atually helped me sleep better, and easily force in extra food. so here is just an anecdote in relation to pot/tbol-lv. ive never experienced any estro increase from it as far as i could tell. actually, it could be argued that pot is "anabolic". in that, it mellows you out(possibly reducing cortisol), and increasing appetite.
|
T-bol doesn't kick in until about half way through the cycle, so this may be why you noticed a difference; and seeing that you're using 120 mg, that could have something to do with it too.
BTW 120 mg is a little high IMO, unless you weigh 300 lbs.
# 9
07-12-2010
|
I assure you it's estrogenic, and in no way is marijuana "anabolic".
T-bol doesn't kick in until about half way through the cycle, so this may be why you noticed a difference; and seeing that you're using 120 mg, that could have something to do with it too. BTW 120 mg is a little high IMO, unless you weigh 300 lbs. |
# 11
07-12-2010
The heart rate, normally 70 to 80 beats per minute, may increase by 20 to 50 beats per minute or, in some cases, even double. This effect can be greater if other drugs are taken with marijuana.
As THC enters the brain, it causes a user to feel euphoric - or "high" - by acting in the brain's reward system, areas of the brain that respond to stimuli such as food and drink as well as most drugs of abuse. THC activates the reward system in the same way that nearly all drugs of abuse do, by stimulating brain cells to release the chemical dopamine.
As a chemical messenger, dopamine is similar to adrenaline. Dopamine affects brain processes that control movement, emotional response, and ability to experience pleasure and pain.
So if you where in pain because you over did it, you may not even know it until after the fact. In which case could be too late. If you are serious about W.O. it would not be advisable.
robert
# 12
07-12-2010
|
I assure you it's estrogenic, and in no way is marijuana "anabolic".
T-bol doesn't kick in until about half way through the cycle, so this may be why you noticed a difference; and seeing that you're using 120 mg, that could have something to do with it too. BTW 120 mg is a little high IMO, unless you weigh 300 lbs. |
# 14
07-12-2010
|
Most of the time with liver sides, you don't necessarily "feel" them until the danger is imminent. Be careful with that dosage.
|
btw, just to get you guys a bit more riled up, the first 3 weeks i was stackinn this with superdrone @ 10mg.
# 15
07-12-2010
# 16
07-12-2010
|
ya well, we're past half-way dude. mid-week 5 it kicked in. estro?...guess it does have this effect in my body. anabolic....of course it isnt, hence the "qoutation marks". didnt mean it literally. 120mg....im not "feeling"any side effects. so, IMO, 120mg is acceptable for someone under 300lbs.
|
# 17
07-12-2010
|
No offense, this may not be your first "rodeo", but are you sure you're not high right now??? (1. You took T-bol alongside S-drol (2. You're running T-bol for 6 weeks. (3. You're running it a dosage that someone who's 300 lbs. would run it at. The fact that you didn't notice anything until week 5 while stacking the 2 strongest DS's on the market, throws up a red flag to me: not to worry you, but your liver may be in trouble now. Seriously.
|
# 18
07-12-2010
|
i personally think marijuana has a bad rap, its used for medicinal purposes, has no side effects cept drowsiness n hunger, you cant overdose, you cant die from it, and most importantly is non-addictive(contrarly to all other classA,B,C drugs....1=3smokes, I used to smoke 1/day, not a pack of cigs like some people....its only illegal because of the tobacco and drug industries forced it upon the govt in 1929 in the US....explain how its a classB drug and all the date rape stuff like ghb n ex is classC (w anabolic steroids), even ritalin is in the same class as pot yet in my personal opinion (im a child psych mind you), is far worse as drugs go, long term use can lead to an array of psychotic problems (one of the reasons its frowned upon now, without mentioning short term issues which are bad as well)
|
# 20
07-12-2010
|
I assure you it's estrogenic, and in no way is marijuana "anabolic".
|
A FOAF who is not me used to smoke all the time in college. Said FOAF was biggest and strongest when he smoked in fact (probably just coincidental-FOAF worked out and FOAF smoked a lot and also started cycling roids). My FOAF smoked a LOT, multiple times a day, probably an oz/wk. Just never before working out or my FOAF's muscles would feel like jelly. FOAF really doesn't think that MJ has a very detrimental effect on anabolism or excessive estrogenic activity that would make it a bad idea on a cycle. And depending on what you are running, a small amount of exogenous estrogenic activity might even be desirable. FOAF found cannabis most useful on cycle when trying to bulk and cram down absurd amounts of calories (like 5,000-6,000 kcal/day on some M1T cycles). FOAF also just liked to smoke cannabis for the hell of it at the time.
One of the biggest guys I ever knew in college (huge and strong as hell) used to work out and then go back home and smoke a blunt and eat a ton of food. I know this b/c (A) he told me, and (b) FOAF smoked with him regularly. He just got better gains that way he said, and his physique and strength were proof of that. He did maybe 1 cycle of test in college, but other than that, I don't think he used much in the way of steroids. I probably used as much or more steroids than he did at the time, and he and FOAF smoked similar amounts of herb.
Experientially, I just don't hear about people having any major estrogenic issues due to using cannabis. If it were very estrogenic, I would expect pot heads to be more emotional and girly and watch Sex in the City reruns (like a Clomid PCT), but most of the smokers that FOAF knew were nothing of the sort.
This is clearly a hotly debated area, but IMHO, MJ is not very detrimental to anabolism, esp. when using steroids at the equivalent of supraphysiological levels. And this applies to most steroids and cycles; if steroids only shut you down (test and LH) and didn't compensate for it with dramatically increased androgenic and anabolic activity, then there would be little reason to take them in the first place.
I guess everyone just has to decide for themselves. Healthwise, I think that cannabis is far safer than steroids (which aren't that dangerous themselves, though they can be whereas cannabis really cannot ever cause life-threatening toxicity). But with both of them, moderation and discipline is key.
FOAF doesn't smoke anymore, for years now, but that is a personal decision (to each his own).
-------------------------------------------
Delta(9)-tetrahydrocannabinol inhibits 17beta-estr... [Anticancer Res. 2008 Jan-Feb] - PubMed result
|
Anticancer Res. 2008 Jan-Feb;28(1A):85-9. Delta(9)-tetrahydrocannabinol inhibits 17beta-estradiol-induced proliferation and fails to activate androgen and estrogen receptors in MCF7 human breast cancer cells. von Bueren AO, Schlumpf M, Lichtensteiger W. Institute of Pharmacology and Toxicology, University of Zurich, Switzerland. Andre.vonBueren@kispi.uzh.ch Abstract BACKGROUND: Delta(9)-tetrahydrocannabinol (THC) exerts palliative effects in cancer patients, but produces adverse effects on the endocrine and reproductive systems. Experimental evidence concerning such effects is controversial. Whether THC exhibits estrogenic or androgenic activity in vitro was investigated. MATERIALS AND METHODS: Estrogenic effects of THC were analyzed in vitro by measuring the proliferation of estrogen-sensitive MCF7 cells. Androgenic activity was investigated by the A-Screen assay that measures androgen-dependent inhibition of proliferation of the androgen receptor (AR)-positive human mammary carcinoma cell line, MCF7-AR1. RESULTS: In contrast to 17beta-estradiol, included as positive control with an EC50 value (concentration required for 50% of maximal 17beta-estradiol-induced proliferation) of 1.00 x 10(-12) M, THC failed to induce cell proliferation in the MCF7 cell line at concentrations between 10(-13) and 10(-4) M. THC inhibited 17beta-estradiol-induced proliferation in wild-type MCF7 and MCF7-AR1 cells, with an IC50 value of 2.6 x 10(-5) M and 9 x 10(-6) M, respectively. CONCLUSION: THC failed to act as an estrogen, but antagonized 17beta-estradiol-induced proliferation. This effect was independent of the AR expression level. PMID: 18383828 [PubMed - indexed for MEDLINE] |
Marijuana: interaction with the estrogen receptor. [J Pharmacol Exp Ther. 1983] - PubMed result
|
J Pharmacol Exp Ther. 1983 Feb;224(2):404-7. Marijuana: interaction with the estrogen receptor. Sauer MA, Rifka SM, Hawks RL, Cutler GB Jr, Loriaux DL. Abstract Crude marijuana extract competed with estradiol for binding to the estrogen receptor of rat uterine cytosol. Condensed marijuana smoke also competed with estradiol for its receptor. Pure delta 9-tetrahydrocannabinol, however, did not interact with the estrogen receptor. Ten delta 9-tetrahydrocannabinol metabolites also failed to compete with estradiol for its receptor. Of several other common cannabinoids tested, only cannabidiol showed any estrogen receptor binding. This was evident only at very high concentrations of cannabidiol. Apigenin, the aglycone of a flavinoid phytoestrogen found in cannabis, displayed high affinity for the estrogen receptor. To assess the biological significance of these receptor data, estrogen activity was measured in vivo with the uterine growth bioassay, using immature rats. Cannabis extract in large doses exhibited neither estrogenic nor antiestrogenic effects. Thus, although estrogen receptor binding activity was observed in crude marijuana extract, marijuana smoke condensate and several known components of cannabis, direct estrogenic activity of cannabis extract could not be demonstrated in vivo. PMID: 6296360 [PubMed - indexed for MEDLINE] |
Antiestrogenic effects of marijuana smoke condensa... [Arch Pharm Res. 2005] - PubMed result
|
Arch Pharm Res. 2005 Dec;28(12):1365-75. Antiestrogenic effects of marijuana smoke condensate and cannabinoid compounds. Lee SY, Oh SM, Lee SK, Chung KH. National Institute of Scientific Investigation, Seoul, Korea. Abstract The antiestrogenic effects of marijuana smoke condensate (MSC) and three major cannabinoids, ie., delta9-tetrahydrocannabinol (THC), cannabidiol (CBD), and cannabinol (CBN), were evaluated using in vitro bioassays, viz., the human breast cancer cell proliferation assay, the recombinant human estrogen receptor (ER) competitive binding assay, and the reporter gene assay. The inhibitory effects on estrogen were also examined using the ethoxyresorufin-O-deethylase (EROD) assay, the aromatase assay, and the 17beta-estradiol (E2) metabolism assay. The results showed that MSC induced the antiestrogenic effect via the ER-mediated pathway, while THC, CBD, and CBN did not have any antiestrogenic activity. This suggests that the combined effects of the marijuana smoke components are responsible for the antiestrogenicity of marijuana use. In addition, MSC induced the CYP1A activity and the E2 metabolism, but inhibited the aromatase activity, suggesting that the antiestrogenic activity of MSC is also related to the indirect ER-dependent pathway, as a result of the depletion of the in situ E2 level available to bind to the ER. In conclusion, pyrogenic products including polycyclic aromatic hydrocarbons (PAHs) in the non-polar fraction, which is the most biologically active fraction among the seven fractions of MSC, might be responsible for the antiestrogenic effect. PMID: 16392670 [PubMed - indexed for MEDLINE] |
Now...the most damning evidence for the absence of significant, negative estrogenic effects of THC/Pot use:
Potheads Make the Best Athletes (Top 10 Pothead Athletes of All Time) Elephantbeans
![]() |
| Thread Tools | Search this Thread |
Posting Rules
|
|






