mega H
- Thread starter nobady
- Start date
stxnas
Well-known member
Before you get flamed I'm going to tell you what everybody else is going to tell you...but in a much nicer way...hit the search button bro...this stuff is the same thing as Halodrol aka H50. Check out these links for a good start and for your PCT check out the PCT section of the board (I can't remember if any of the logs included their PCTs, but I would think they would).
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Good Luck Bro.
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Good Luck Bro.
bubsnt3
Member
with/without food; doesn't matter
dose: I would go with 3 a day
split or all at once: I would go with split beings it has a 8 hour half-life.
P.S. halodrol is dosed at 50mg(2 pills) but if I am going to shut my test down I want to make sure that I get results that are worth it so I would go with 3, there is a couple threads on here about people taking 1 and a half halodrol pills(75mg) and getting better results then they were on 2. Oral Turinabol has an anabolic rating of only 56. FYI
dose: I would go with 3 a day
split or all at once: I would go with split beings it has a 8 hour half-life.
P.S. halodrol is dosed at 50mg(2 pills) but if I am going to shut my test down I want to make sure that I get results that are worth it so I would go with 3, there is a couple threads on here about people taking 1 and a half halodrol pills(75mg) and getting better results then they were on 2. Oral Turinabol has an anabolic rating of only 56. FYI
stxnas
Well-known member
bubsnt3 said:
From what I understand this stuff is fat soluble so taking it with about 10g of EFAs (ie flax seed oil) would help with absorption. Grapefruit juice is said to aid in this as well.
More/extra pills don't always equal more/better results, but usually will result in (more) sides.
Please just do some searching and reading and come up with your own opinons. Once you have some of your own thoughts you can run them by the board members and ask specific questions and you will get far more responses than you will from your original post.
bubsnt3
Member
If it is fat soluable you would not want to eat it with fat beings it would absorb into the fat and then be ingested by the body, you want it to be dispersed quickly(actually fat soluable has more to do with where it is stored and not with how it is ingested). It is true however that you want to take the lowest dose possible to produce the desired gains, I was just stating for me 3 a day of OT is not a very high amount here is a qoute about it "I generally think that it is not very strong (as compared to many other orals) and wouldn´t drop below the 40mg mark if I were to use it personally." Anyways start with 2 and after a week if you aren't happy up it.
stxnas
Well-known member
nobady said:
In general most are taking H in doses of 50mg per day. Some people do move up to more, but being that it's your first time trying it I would start out low, assess the sides/results and then possibly bump it up from there. Everybody responds differently to various compounds and the only way to truly find out is to try it out. I have seen guys on this board that only use 10mg of Superdrol and get great gains to where others ramp up or even start out at 30mg. Play it safe and start out lower for at least the first couple of days to get an assessment for at least the sides. Then bump it up if you feel the need to. Keep in mind this is a methylated substance and has the potential to cause havoc with your liver/lipid profiles.
jrkarp
Registered User
The absorption with fat thing has nothing to do with the 17a alkylation. Alkylation has to do with what happens at the liver, taking the steroid with fat has to do with what happens in the stomach.
Taking an oral steroid with fat will (theoretically) cause the steroid to dissolve in the fat and since fat is easily absorbed from the gut, more of the steroid will enter the blood stream.
Personally, I think that while the theory is great, it's unnecessary. I doubt it would make enough of a difference to notice.
Taking an oral steroid with fat will (theoretically) cause the steroid to dissolve in the fat and since fat is easily absorbed from the gut, more of the steroid will enter the blood stream.
Personally, I think that while the theory is great, it's unnecessary. I doubt it would make enough of a difference to notice.
Mass_69
Well-known member
J,jrkarp said:
I understand the differences in the mechanisms, but my point is with the 17aa and missing the breakdown in the liver, you will absorb almost 100% of the steroid, anyway. That's the reason for using the 17a methyl.
There's no point in taking it w/fat other than ingesting calories.
Taking a non-17aa oral steroid with fat is another story, and probably a necessity, regardless of any THP ethers..
jrkarp
Registered User
I understand your point, but you're missing mine.
The steroid has to get from the gut to the bloodstream to the liver for the alkylation to have an effect.
The theory of taking steroids with fat is to help it get from the gut to the bloodstream.
Absorption does not take place in the liver, it takes place in the gastrointestinal system.
The steroid has to get from the gut to the bloodstream to the liver for the alkylation to have an effect.
The theory of taking steroids with fat is to help it get from the gut to the bloodstream.
Absorption does not take place in the liver, it takes place in the gastrointestinal system.
Mass_69
Well-known member
Well, I didn't want this thread to turn into a discussion of the digestive system, but here goes.jrkarp said:
Foods like salt, sugars, and alcohol (17a-methyl?) can be absorbed in the stomach. Food that was not absorbed in the stomach is turned into liquid, and sent to the small intestine to be aborbed into the blood, where is is met by enzymes from the pancrease & liver to aid in further digestion. The 17a-methyl group protects the steroid from being broken down and excreted, as the body sees it as a foreign substance with no nutritional value.
Most fats are broken down and absorbed in the intestines (with help from liver bile), and not the stomach. You should see your liver enzyme levels after a high-fat meal (Anyone see Super-Size Me?)
So, my original point was, Mega-H/Halodrol/H50 is a 17aa steroid, and needs no assistance from fat solubility for optimal absorption. I never said methylated steroids are absorbed by the liver, but methylation prevents the liver from excreting it before it is absorbed.
McBurly
Active member
Mass_69 said:
Alcohol is something with a -OH group on it.... methyl = CH3
from my basic understanding of the digestive system Halodrol is not absorbed in the stomache, this occurs in the intestines
steroids(sex hormones) = cholesterol w/ a few changes so they are all considered fat soluble
also, you guys are confusing me with your reasons for backing up each point :think:
Mass_69
Well-known member
That's why I put a "?" next to that, because I don't know enough in that subject, myself. I guess methyl alcohol would be methanol (CH3OH), so that doesn't apply in this case.McBurly said:
Anyhoot, whether the oral steroid has a methyl group added, an ether, an ester, or fats taken with it, the bulk of the digestion will be in the intestines. And either way you slice it, it will meet the liver. 17aa methylation is a proven method at improving absorption (hence my original point of not needing fats w/Halodrol).
I already mentioned that all steroids are fat soluble.
Hey, I'm all for intelligent discussion, that's what I love about this site. I would hope this discussion would help rather than confuse. I'm learning myself. Either way, I still stand by my original statement:McBurly said:
Mass_69 said:
jrkarp
Registered User
Mass_69 said:
My understanding has always been that 17a alkylation helped the steroid resist breakdown in the liver, not that it improved absorption from the GI system.
I'm not saying you're wrong, I'm just saying that I've never heard that. Can you please provide references for this?
Mass_69
Well-known member
Well, I'm kinda bulking right now, and seeing mostly strength increases, and a little size. I got a little bit of a late start. Haven't added fat so far, which is always a plus for me!McBurly said:
How bout you?
jrkarp said:
I don't have a specific reference at the moment in regards to absorption & 17aa steroids. I do have links to the digestive system. Invalid Link Removed - Some good links off of this page.
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Think of the liver as the gatekeeper of how your food is digested and used. It regulates fuel management (usage of protein, carbs, & fat) and metabolism, and nitrogen & waste excretion. I don't know what role the liver plays in the small amount of foods digested in the stomach (sugars, salt, water, etc.), but I believe that all food intake eventually meets up with the liver in one way or another. The 17aa prevents the liver from breaking the steroid down for excreting, which in turn would keep it in tact for absorption. The liver sees an oral steroid as a "foreign" object with no nutritional value, and would do it's best to excrete it rather than absorb it. So if the liver doesn't rid/excrete the 17aa steroid, it can then still be absorbed through the intestines. This is why 17aa steroids are considered "orally active," hence taking it with fat isn't needed.
The idea of taking a non-17aa oral steroid with fat works by the same concept, but not the same mechanism. The main goal is to avoid breakdown & excretion by the liver. Once the steroid is "disolved" into the fat, it will then be mostly digested via liver bile in the small intestines, rather than excreted. See where I'm going?
Maybe someone such as Bobo with a good understanding of Nutrition can elaborate or explain this better.
Sorry to hijack your thread, Nobady, but hopefully this helps with one of your original questions.
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Mass_69
Well-known member
The liver breaks down food via enzymes and bile, but this actually takes place in the small intestine for the most part, and not necessarily in the liver. This means it makes it passed the liver's "first pass," and is able to be absorbed into the blood from the small intestine.jrkarp said:
By the time it gets back to the liver via the blood (what did not make its way the the androgen receptors), it then gets changed into 16-keto steroids (I believe), and is excreted from the body via pee-pee & poo-poo :dump:. Even though the liver isn't part of the GI, digestion does not happen without it.
I'm no Gastroenterologist, but this is my understanding of how this all works.
Sheesh Karp, quit being a ****! :icon_lol:
DR.D
Well-known member
17aa hormones resist oxidative destruction of the 17b-OH to the 17-keto form first in the gut and then again in the liver. Absorption is really not the issue and a fatty meal is not needed for 17aa's. They are only absorbed better in the sense that they all make it to the liver intact where only part of the non-17aa would be.
bubsnt3
Member
OT: Dr. D and other intellectuals I was wondering how much of a difference there is between oral tuinabol and halodrol. I need a very low androgenic compound that I can still make decent gains on and from what I understand OT would be the way to go. The 2 chemical compounds look like this:
OT
4-chlorodehydromethyltestosterone)
4-chloro-17b-hydroxy-17a-methyl-androst-1,4-dien-3-one
HD:
4-chloro-17a-methyl-androst-1,4-diene-3,17b-diol
from what I understand 4-chlorodehydromethyltestosterone is not very androgenic but just change the -1,4-diene to -4-ene and it turns it into 4-chloromethyltestosterone which is alot more androgenic. If OT is 4chlorodehydromethyltestosterone, what would Halo be? How much of a difference is there and what would the effects be on AR binding and the A:A ratio? This is all over my head but BK said that this was the 3-hydoxyl variant of OT, what does that mean? Thanks in advance for your insight.
OT
4-chlorodehydromethyltestosterone) 4-chloro-17b-hydroxy-17a-methyl-androst-1,4-dien-3-one
HD:
4-chloro-17a-methyl-androst-1,4-diene-3,17b-diol
from what I understand 4-chlorodehydromethyltestosterone is not very androgenic but just change the -1,4-diene to -4-ene and it turns it into 4-chloromethyltestosterone which is alot more androgenic. If OT is 4chlorodehydromethyltestosterone, what would Halo be? How much of a difference is there and what would the effects be on AR binding and the A:A ratio? This is all over my head but BK said that this was the 3-hydoxyl variant of OT, what does that mean? Thanks in advance for your insight.
Trauma1
Legend
Mass_69 said:
Well good discussion here guys....but i'm gonna throw in my two cents as well. The "first pass effect" is when nutrients/drugs are absorbed from the lining of the small intestine and enter the portal system via the hepatic portal vein. After it enters the portal vein these nutrients/drugs are taken to the liver where the primary metabolism of the drugs take place aka "the first pass effect." It's almost like the body's safety net before sending anything into general cirrcualtion. Once this takes place the nutrients/drugs are then released into systemic cirrculation for the body to use. This first pass effect can be avoided through transdermal, intramuscular, and sublingual routes of administration which get absorbed directly into systemic cirrculation. The oral ingestion of a 17a alkylation steroid prevents the liver from breaking it down through the first pass effect so it can be released into general cirrculation virtually intact. The liver is such a vital organ and plays major roles in digestion, hematology and immune function. The major stress that's placed on the liver is its attempt to metabolize the steroid with 17 a alkylation that's designed to prevent it.
Hope this is helpful, but i'm in no way trying to give a lecture here either. Bottom line it's a good intellectual discussion and we all continue to learn everyday.
Mass_69
Well-known member
2 cents excepted (but I still can't by my Big Mac). :burg:Trauma1 said:Well good discussion here guys....but i'm gonna throw in my two cents as well. The "first pass effect" is when nutrients/drugs are absorbed from the lining of the small intestine and enter the portal system via the hepatic portal vein. After it enters the portal vein these nutrients/drugs are taken to the liver where the primary metabolism of the drugs take place aka "the first pass effect." It's almost like the body's safety net before sending anything into general cirrcualtion. Once this takes place the nutrients/drugs are then released into systemic cirrculation for the body to use. This first pass effect can be avoided through transdermal, intramuscular, and sublingual routes of administration which get absorbed directly into systemic cirrculation. The oral ingestion of a 17a alkylation steroid prevents the liver from breaking it down through the first pass effect so it can be released into general cirrculation virtually intact. The liver is such a vital organ and plays major roles in digestion, hematology and immune function. The major stress that's placed on the liver is its attempt to metabolize the steroid with 17 a alkylation that's designed to prevent it.
Hope this is helpful, but i'm in no way trying to give a lecture here either. Bottom line it's a good intellectual discussion and we all continue to learn everyday.
I think you helped to better word/explain what I had been trying to say. Good discussion, and I learned a bit more about the digestive system as I was referencing facts before posting. :thumbsup:
DR.D
Well-known member
Mass_69 said:
Yes, they will produce other metabolites in many cases, especially at the 3, 6 and 11 positions, and metabolites of those metabolites as well. Whatever it can do to rid the body of it. The main way it usually does this is by 17-conjugation but not with a 17aa because the 17-OH will remain intact. That part of the molecule will not metabolize.
DR.D
Well-known member
bubsnt3 said:
Halo is the same as OT but possesses a 3-OH instead of a 3=O function. The same way that 4AD was related to test. That means that 2 different isomers can exist. The 3a and 3b and I'm sure only one of the two is active. Because of that and because the 3-OH usually lowers activity, I'd expect Halo to be a weak watered down version of OT both as an androgen and anabolic with a similar ratio as OT though.
DR.D
Well-known member
jmh80 said:
You are correct! Grapefruit slows clearance of 17aa's by the cytochrome P-450 (CYP450) enzyme system. It has compounds that reduce microsomal CYP3A4 activity and that's the specific isozyme involved. This prolongs the effect of the 17aa by reducing it's rate of metabolism, so blood levels stay elevated longer (increased half-life).
However, the fatty meal only helps with absorption from the stomach. Lipid solubility is the physical property governing the passage of unionized molecules in the stomach. That's why a fatty meal helps with the less lipophilic non-17aa compounds. Once it gets to the gut, the steroid is unstable to alkali and intestinal bacteria also promote it's deactivation into 3-keto derivatives. This does not occur with the 17aa's because being a tertiary alcohol, the body does not have an enzyme system that can oxidize it.
bubsnt3
Member
Dr. D.. One more thing I was reading an old prohormone page and it said this that worried me:
"You may notice that the prohormones have either the addition dione or diol behind them. First of all this signifies the way by which they convert. The dione versions use the enzyme 17-beta-hydroxysteroid dehydrogenase and the diol versions use the 3-beta enzyme. In real world terms however we can see that the diol converts at a much higher rate than the dione (15.76% as opposedto 5.61%)¹ and is therefore more anabolic and has less chance of aromatisation. Estrogen formation of the diol directly is impossible, which is not so for the diones. The target hormone can always aromatize of course, but there is no risk of estrogen formation directly off a diol prohormone, which keep the estrogen balance in check and decreases the risk of estrogen-related side-effects. It simply cannot aromatize because its structure doesn't allow it."
Does that mean that this diol only converts at 15.76% or does it achieve a higher conversion because it is methylated? Does it convert 100%?(in halo's case..)
"You may notice that the prohormones have either the addition dione or diol behind them. First of all this signifies the way by which they convert. The dione versions use the enzyme 17-beta-hydroxysteroid dehydrogenase and the diol versions use the 3-beta enzyme. In real world terms however we can see that the diol converts at a much higher rate than the dione (15.76% as opposedto 5.61%)¹ and is therefore more anabolic and has less chance of aromatisation. Estrogen formation of the diol directly is impossible, which is not so for the diones. The target hormone can always aromatize of course, but there is no risk of estrogen formation directly off a diol prohormone, which keep the estrogen balance in check and decreases the risk of estrogen-related side-effects. It simply cannot aromatize because its structure doesn't allow it."
Does that mean that this diol only converts at 15.76% or does it achieve a higher conversion because it is methylated? Does it convert 100%?(in halo's case..)
bubsnt3
Member
Does it have anabolic activity in its unconverted state, with this information I would come to the conclusion that you would almost have to take doses too high to be cost effective. That would mean that people taking the standard 75-100mg doses are only getting 20mg of "active" hormone, that is one thing that I love(d) about SD is that it was sold in its active state with no conversion needed. maybe I will just stick to the SD. Also what is the androgenic value of SD I was told by BK it was quite high but when I look up masteron wich is the same except for the 17b-hydroxy dropped and the 17a-methyl group added it says the A:A ratio was 65:24 favoring anabolic. Maybe I will go with mega-zol beings it is already active also.. Thanks for all your time and input...DR.D said:
DR.D
Well-known member
bubsnt3 said:
SD is even less androgenic than Anavar! BK is full of baloney. It's only about 20% as active as methyltest as far as that goes. I can't find any refs as to the potency of H50 in unconverted form, but if I had to guess it probably has some activity of it's own. Probably lower activity though.
bubsnt3
Member
Thanks Dr. D You are AWESOME!!! I am glad I have 11 bottles of SD(REAL SD). One more Question.. If I take a compound that is 20% as androgenic as methyltest(is this the same A:A ratio as injected test?) but I raise my blood concentration to 4-5 times the amount of test that I normally have and then I am sure it probably is not bound by sbgh would that equal the same androgenic properties that I would normally have? ie. 20%x5=100% or does that have nothing to do with it; does the fact that more of it is "free" to interact with the androgen receptor raise any concerns with relation to interacting to the androgen receptor? My questions are relating to a problem I had while taking PP, I didn't ever bother to look for my hair falling out beings neither my mothers or fathers side of the family have any people going bald so I was nearing the end of my PP cycle(30mg) and I started SD with it (30mg) after 2 days my scalp started itching and then I noticed a quite noticble amount of hair coming out as I itched it, I imediately quite the PP and continued with only SD and haven't noticed anymore problems at all but I am more cautious now.DR.D said:
DR.D
Well-known member
bubsnt3 said:
Yes, you are technically correct, but there are other factors like you said (binding affinity for AR and SHBG in various tissues, half-lives, metabolites, intrinsic activity, etc..) so it's not really that black and white. I think in your case, it wasn't so much the combo that did it but the overall dose. Had you been taking 35-40mg of PP alone it may have been a problem from the start, but adding the SD just sent it over your body's genetic tolerance for hair loss.
MANimal
New member
Interesting, I didn't know that. So what exactly is the half-life and the complete termination time of the compund? So when people say "half-life", it's just the time taken for half of the amount of the compound to be terminated? Meaning the other part would still be active? Could someone elaborate .. I feel completely retarded now.bubsnt3 said:
bubsnt3
Member
You are 100% correct, the half-life is the amount of time it would take for there to be half of the product still active or half of the product disposed of which ever way you want to look at it. Most people want to keep blood concentration levels as consistant as possible so they go off of a products half-life because they don't want the blood levels to ever drop below that point. If they went off of life termination they would have none left in there blood when they took more..MANimal said:
Mass_69
Well-known member
That's right. If a hormone has a half-life of 4 hours, you want to take it about every 4 hours to keep blood levels elevating. That's why (oral steroids) usually take days-weeks to "feel," because you have to build up your blood levels over time. So "Hormone A" has a half-life of 4 hours, and you take 10mgs/dose. You take a dose in the AM, and another 4 hours later. By that time, you still have 5mgs left in your system, and you just added 10mgs more... make sense?