NorCal--
Well, I can understand the search for that sub-6% point, because I do it every summer. Keep in mind, though, I am no bodybuilder. I am a skinny guy. However, at below 6% I look the way I want to. Now, with respect to the usage of halo for that real steely look, I can tell you that I tried it once, and yes, it did the trick. I was at about 7% and did about 15-20mg a day for about a month, but I wound up not needing to be in the shape I thought that year and dropped it. As far as sides...it made me mad and strong.
I generally used winstrol at 50 or 100mg every day to get really ripped. That along with windsprints and a pretty strict diet of fish and greens. Just that combination will work without anything else at all. I have never needed T3 or any other thyroid med, and I have never tried DNP (never will).
The fact is that sprints, diet, and a good anticatabolic such as tren, ox, or winstrol will get you to whatever bodyfat percentage you need.
I consider winstrol to be at least as effective as halotestin as far as anticatabolic properties go (better, even), but it is not as good of a muscle builder. That sounds immediately contradictory, but I have a fairly good understanding of these drugs and this is what I have concluded.
I am considering alternating winstrol with oxandrolone this summer. I had initially given up on winny altogether because of the sides (it is pretty harsh), but I think I know how to keep things fairly safe.
I will probably use 40mg of each and just alternate every two days for starters.
I will run test cyp or prop at 300mg/week along with this (I am on the low dose test now).
As far as liver protection goes, I use Tylers and ALA. N-Acetyl Cystien converts to glutathione in the liver, which is a primary anti oxidant/protectant.
I would NOT recommend stacking halotestin with any other 17aa for any reason or in any dose. There is no reason to expect better results from that than just upping your dosage for one.
Think of it this way:
You have X amount of enzymes in your liver that are able to break something down. Now, you occupy so many with halo, and so many with var (who know how much). But the halo dramatically reduces your liver's ability to cope with ANYTHING else, so the added var becomes much more stressful than it normally would. Not only that, all you have accomplished is adding more steroid, which you could have done with test, primo, etc.
The idea of an oral being better for ripping out is ludicrous. Ox is good because it can be effective in low doses. THAT IS THE REASON IT IS DESIREABLE. Everything else about it is similar to other steroids. It can burn a bit of fat around the abdomen, but not much. It is relatively non toxic because of the LOW DOSE REQUIRED FOR EFFECTIVE RESULTS, and that's it. At 80mg/day, it gets toxic, just like anything else that is 17aa. Now, it is less toxic than others, because halo at 40mg a day will deplete your resources very quickly, as we have discussed.
If you are bent on using halo, here is my suggestion. Run it with 300mg/week of Test prop and 75mg EOD of tren.
Brother, with that, you are gonna be a bulldozer. Just get your bloodwork done. BP will be an issue, as will mood. But you WILL be strong, and you can dramatically reduce your calories on that stack. You could practically starve yourself and not lose muscle with that.
Animal B--
Anadrol is not as toxic as halotestin. I know that bodybuilders in general tend to regard anadrol as the most toxic of the common orals, but they are wrong.
What is used to determine this toxicity is not always liver enzyme elevations. The key points have a lot to do with the rate of glutathione depletion, the effect on neutral red, as well as the occupation of specific enzymes.
Anadrol and D-bol showed an impact on glutathione that was more substantial than winstrol, but winstrol has a different effect on other microsystems. Winstrol tends to dehydrate in specific areas, which can be stressful in a non-toxic way, but just as debilitating if not more so.
The reduction of certain defense chemistries in the liver is bad, especially if it occurs alongside dehydration and elevated temperature, and winstrol does all three of these things at once. Halotestin depletes the liver of its detoxifying elements much faster than any of the other oral steroids. So, for the first few weeks things seem pretty equal among orals. However, if you were to run each one seperately and test weekly, you would find that running halo depletes the liver of its resources the fastest, followed by anadrol and D-bol, and then winstrol, but winstrol can do damage faster if it is taken with other liver stressing agents because it reduces the liver's ability to function in ways not directly connected to enzyme activity.
The precautions should include N-acetyl Cystien and water (ALA< TYLERS< whatever), but nothing replaces bloodwork. Each of us has a different amount of specific liver enzymes, not to mention that some people just tolerate things better than others, so there can be no blanket statement given other than this:
They are all toxic, some more than others, but without proper precautions taken any of them will eventually do more harm than good.
Incidentally, there are plenty of examples in current medical literature to suggest that the oral steroids do differ in toxicity. You might find this interesting, from the journal of the Academy of Dermatology, 2000, reads:
...(discussing a 54 year old African American patient)...Her worsening pain and extension of the induration prompted a trial of stanozolol (2 mg daily), which resulted in marked alleviation of symptoms within 2 weeks of its initiation. Unfortunately, within 2 months her liver enzyme levels rose from normal baseline levels (alanine aminotransferase, 38 U/L; aspartate aminotransferase, 38 U/L) to 257 U/L (alanine aminotransferase) and 562 U/L (aspartate aminotransferase). Although the patient did not exhibit signs or symptoms of hepatotoxicity, the stanozolol was immediately discontinued, with full resolution of the enzyme abnormalities. A newer anabolic steroid was then started, oxandrolone (10 mg twice daily), because it had been reported to be less hepatotoxic.5 Within 2 weeks, she experienced a reduction in pain (from a score of 7/10 to 3/10) as well as subjective softening of the skin. After 3 months of oxandrolone therapy, her symptoms had continued to abate, and she decided to discontinue the medication. No abnormalities in liver enzymes were noted. Incidentally, several months later she was diagnosed as having an idiopathic cardiomyopathy (a literature search failed to find any reports of oxandrolone-induced cardiomyopathy).
Prolonged venous hypertension is postulated to facilitate the leakage of macromolecules, such as fibrinogen, into the dermis, where fibrin polymerization around capillaries can lead to a decrease in oxygen and nutrient delivery to the dermis. The use of fibrinolytic agents, such as stanozolol, is thought to alleviate lipodermatosclerosis through modulation of fibrin production. The newer anabolic steroid oxandrolone also has known fibrinolytic activity,5 but unlike the majority of oral anabolic steroids it undergoes limited hepatic metabolism and is associated with a lower incidence of hepatotoxicity. In our opinion, oxandrolone represents a therapeutic option for those patients with stanozolol-responsive lipodermatosclerosis in whom hepatic toxicity develops.
16/8/106517
doi:10.1067/mjd.2000.106517
Samantha Segal, MDa
Department of Dermatology, Dartmouth-Hitchcock Medical Center, Lebanon, New Hampshirea
Jane Cooper, MDb
Department of Internal Medicine, Waterbury Hospital, Waterbury, Connecticutb
Jean Bolognia, MDc
Department of Dermatology, Yale University School of Medicine, New Haven, Connecticut
And so you see, there is a HUGE difference in relative toxicity for some people.
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