T Nation

TRT Blast Strategy

I am wondering what some of the veterans here think of this strategy of blasting and TRT. I have done higher test blasts (600 mg/wk), and a cycle of 325 mg test per week with a bit of var at the end (50 mg/day for 6 weeks). To be honest, I am a bit underwhelmed with this strategy. Maybe I am developed enough that gains are a bit harder. My stats are approximately 5’10", 210 lbs, ~16% BF. My best lifts for SBD are 507 w/ wraps, 375, and 575 lbs.

I am thinking of running an experiment in which I keep my test at TRT levels (200 mg/wk), and adding a strong oral (Anadrol or Dbol). My thoughts are these are a lot more anabolic than Test, and also less androgenic per mg. In the case of Anadrol, it is about 3X as anabolic and about half as androgenic as Test (at least on paper, which I know is flawed).

I am thinking with Test at TRT levels the high E2 symptoms of these drugs shouldn’t be too bad.

I am thinking my experiment will be occurring a few months out, but I am thinking TRT + 75 mg of Anadrol a day for 6 weeks. That ends up being 200 Test and 525 mg of Anadrol a week. From others I know who have run Anadrol, this should work pretty well.

What are your thoughts @blshaw, @iron_yuppie, @deanis55, @wsmwannabe, @unreal24278, @wanna_be and any others I may have forgot to include here.

I am thinking low test base with strong anabolic for short periods. I would do a strong anabolic injectable, but Nandralone or Tren or EQ don’t really appeal to me (I like my PP working).

I’m gonna copy and paste a long article I saved I found about genetics and test/orals. I find that I’m not a great responder to test and need higher amounts to get the same results most let from 150-175mg/week. It’s also prompted me to try short esters for TRT once my blast is over. With talking with the guy who wrote the thing, he things I fall into the category of short esters being better, and I’d be more of a responder to orals than most.

[Discussion] Genetic alterations modify our response to the use of PEDs, our athletic ability and our nutrition.

A few weeks ago I commented in the post about EQ the reasons why its response, mediated by the individual’s genetics, could cause such disparate effects depending on the person, since my answer was well accepted, I have decided to make a post developing the genetic characters that most influence the use of PEDs, weight loss and training.

TL;DR

Our genes can have various mutations that alter our response to different PEDs (making us good or bad responders), can increase our athletic performance (certain genetic alterations are repeated in most elite athletes) and finally can also influence factors nutrition related to weight and fat loss.

There are many different alterations, I only name the ones that I consider the most interesting ones.

Genetics and use of PEDs

Many people talk about the genetic response to steroids, of “good” and “bad” responders to these compounds, your product may not be underdosed but because of your genetics you do not respond in the same way as the rest (without having taking into account variables such as diet, training and rest), science has not delved much into this subject, but it has given us some answers that may be useful.

It has been found that most of the hydrolysis of esters is carried out by the PDE7B gene, in a study 500mg of testosterone enanthate was administered to see the different responses of users to this steroid.

The “good” responders who had the A allele obtained an average of 3.9 times higher levels than the basal level after the administration of 500mg of testosterone enanthate, the “bad” responders who had the G allele obtained an average increase of 2.5 times the baseline levels after the administration of 500mg of testosterone.

If we extrapolate this information we can get a very interesting piece of information and that is that the results, even having the same allele, varied, since the purpose of the experiment was only to take the average of the responders according to the allele, I would like to point out that it is very interesting that despite having the same allele and using the same methodology in the experiment the results had a small variability, this is because there are more factors at play.

We could imitate this test, injecting 500mg of testosterone enanthate and analyzing total testosterone concentrations 48 hours after administration (if its possible knowing that the testosterone concentration is correct or if we lack this data, we could compare our bloodwork with those subjects with the same batch and dose) if our levels are between 13-14ng / mL or close to these levels it would mean that we are bad responders ,close to 19ng / mL would mean that we are good responders and levels above this range would be what are known clinically as “outliers” .

If you are a “bad” responder, I would recommend using short esters (because the problem usually lies in the difficulty of hydrolyzing the ester) and using oral drugs as they lack an ester and have an immediate effect.

Our body has a large number of genes that modulate enzyme activity, two well-known are the CYP3A4 gene and the CYP2C9 gene, as has been proven in various clinical cases, the various mutations that can affect these genes can cause abolished, reduced, altered or increased enzymatic activity causing the metabolism of PEDs to be affected, for example in reference to the CYP3A4 gene we can detect at least 7 important mutations, which would divide the population into three different groups: “poor metabolizers, normal metabolizers and rapid metabolizers”, depending on the type of metabolism that the user has.

Another very interesting (and potentially dangerous) example is CYP2C19 * 17 polymorphism in the case that it causes a person to belong to the category called “ultra-rapid metabolizers”.

Genetics and weight loss

Below I am going to expose several genetic mutations and wild alterations that affect weight and fat loss.

FABP2 (rs1799883)

FABP2 refers to the intestinal fatty acid binding protein 2, which is a protein located in the cytosol of the intestinal epithelium and is associated with the metabolism of long chain fatty acids.

At rs1799883 a transition occurs at codon 54 resulting in a replacement of Alanine (Ala) with Threonine (Tr), the wild-type allele pattern for FABP2 is Ala / Ala while the mutant is Ala / Tr or Tr / Tr.

People with the mutant-type allele pattern would take advantage of a low-carb, high-fat diet while people with the wild-type allele pattern would take more advantage of a high-carb, low-fat diet.

PPARG2 (rs1801282)

This is the peroxisome proliferator activated receptor gamma-2 gene, which is an isoform of the PPARG gene. PPARG2 is found mainly in adipocytes and has a very important role in adipocyte differentiation.

At codon 12 of exon B in rs18001282 a mutation occurs consisting of a transition from alanine (Ala) to proline (Pro). The wild type allele pattern of PPARG2 is Pro / Pro, while the mutant type is Pro / Ala or Ala / Ala.

People with the mutant-type allele pattern would benefit more from a low-fat, high-carbohydrate diet.

ADRB3 (rs4994)

This is the beta-3 adrenergic receptor gene, which is found mainly in adipocytes and its function is related to lipid metabolism and thermogenesis.

At codon 64, a mutation can occur consisting of a transition from tryptophan (Trp) to arginine (Arg). The wild type allele pattern is Trp / Trp while the mutant type is Arg / Arg or Trp / Arg.

People with the mutant-type allele pattern would benefit more from a moderate carbohydrate and fat diet; those with a wild-type allele pattern would take advantage of a very high intake of PUFAs.

ADRB2 (rs1042713 and rs1041714)

This is the beta-2 adrenergic receptor gene which is distributed throughout the body, with a large presence in adipocytes and plays a very important role in lipid metabolism and thermogenesis.

The two most common genetic mutations in this gene occur at codons 16 and 27, respectively. At codon 16 (rs1042713) arginine (Arg) replaces glycine (Gly); the homozygous allele pattern for Glycine is that of the wild type (Gly / Gly) while the other two are of the mutant type.

At codon 27 (rs1041714) glutamic acid (Glu) replaces glutamine (Gln); the homozygous allele pattern for Glutamine is of the wild type (Gln / Gln) while the other two are of the mutant type.

People with a wild-type allele pattern at codon 16 would need a greater caloric deficit to achieve the same weight loss , the same would happen for those with a mutant-type allele pattern at codon 27.

Genes and sports performance

This is an excerpt from a list with more than 20 genes that can influence sports performance:

ACE gene:

Angiotensin converting enzyme gene has a very important role in muscle strength. Allele I is related to a lower concentration of ACE, while allele D is related to a higher concentration of ACE in serum and tissue. The ACE I / I genotype appears to be better for endurance athletes as it improves efficiency, while the D / D genotype favors strength and power athletes.

Vitamin D receptor gene:

A gene that has been studied in association with muscle strength, in fact the B allele of one of the forms of this gene has been associated with increased quadriceps strength.

Alpha actinin 3 (ACTN3):

The gene that encodes a protein called alpha actinin 3, two alleles have been discovered, X and R, the RR genotype is more favorable in strength and power sports, while the XX genotype is better for endurance sports. World-class endurance runners are more likely to contain the XX genotype.

Bibliography:

Kotsis V, Stabouli S, Papakatsika S, Rizos Z, Parati G (2010) Mechanisms of obesity-induced hypertension. Hypertens Res 33: 386-393.

Arkadianos I, Valdes AM, Marinos E, Florou A, Gill RD, et al. (2007) Improved weight management using genetic information to personalize a calorie controlled diet. Nutr J 6: 29.

Dopler Nelson M Prahakar P, Kornman K, Gardner C (2010) Genetic phenotypes predict weight loss success: the right diet does matter. AHA Abstracts: 79-80.

Luis DA Aller R, Izaola O, Sagrado MG, Conde R. (2008) Influence of Ala54Thr polymorphism of fatty acidbinding protein 2 on weight loss and insulin levels secondary to two hypocaloric diets: a randomized clinical trial. Diabetes Res Clin Pract 82: 113-118.

Yen CJ, Beamer BA, Negri C, Silver K, Brown KA, et al. (1997) Molecular scanning of the human peroxisome proliferator activated receptor gamma (hPPAR gamma) gene in diabetic Caucasians:

identification of a Pro12Ala PPAR gamma 2 missense mutation. Biochem Biophys Res Commun 241: 270274.

Evans RM, Barish GD, Wang YX (2004) PPARs and the complex journey to obesity. Nat Med 10: 355-361

PMID: 24910615

PMID: 21383644

PMCID: PMC6550675

PMID: 27419077

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How is baseline cholesterol?

Anadrol isn’t exactly well tolerated. Gastrointestinal irritation/appetite suppression can make it difficult to bulk on

It’ll probably fuck up your lipids

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In normal ranges, but not great. I’ve leaned up a bit, so it has probably improved. How long does it take to destroy lipids, and restore them after ceasing use of a drug like Anadrol? Part of the appeal of this method is it is only 6 weeks.

I have considered 50 mg/day if that becomes an issue.

How would you expect results to be of 500 mg/wk of Anadrol + 200 mg of test per week, as compared to 5-600 mg of test alone?

Around 5-7 days, probably takes 3-4 weeks to fully recover

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When we look at Anadrol or Dbol, we are looking at a drug that is a lot more anabolic than Test. To me, if Anadrol is 3X as anabolic, and we are using 525 mg/wk, with 200 test, it is like being on 1800 mg of test. I would think that would put size on almost everyone.

Now I know the mouse model that the anabolic / androgenic ratings come from are flawed. I don’t think mg/mg that Anavar is 3X as anabolic as test. From buddies that have run a lot of different compounds, it seems that Anadrol, Dbol and Tren are pretty close to what the study indicates.

Unsure, you’d probably accrue more water/glycogen retention from the anadrol. Albeit with a more aesthetic appearance in comparison to testosterone alone. Strength gains would probably also be superior with anadrol. Whether anadrol nets more long term gains? Ehhh, probably not…

Nephrotoxicity/hepatotoxicity with oxymetholone far exceeds that of testosterone and oxymetholone has a higher tendency to raise RBC count in comparison to test. 1800mg test/wk from what I’ve heard would knock 75mg drol/day out of the Park. Though it’d be a terribly irresponsible thing to do.

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Kidney health concerns me more than liver (liver seems to recover pretty well, and I don’t drink much, under a drink a day average).

RBC is a concern. My BP has been high on some readings, and normal on other readings with my monitor. I don’t know if it is something technique wise in my measurement. It can vary a lot (from no need to worry completely normal, to holy shit that is high). Maybe my monitor sucks? Seems like in a 10 minute period I can get 150/90 to 125/80. On TRT doses my Hematocrit is like 48-49 (200 mg/wk).

I am not so sure on that. The reason being is Anadrol is run for much shorter periods. The gains reported in 4 week kickstarts seem to be unreal. Huge strength gains, and scale weight shooting up. To me it seems comparable to running well over a gram of test, but I don’t actually have experience.

One of my freak gym buddies (deadlifts low 800s at 210 lbs) loves the A bombs. He has run high test (IIRC, 1200 mg/wk), and says it isn’t worth it (claims much over 700 mg just seems to bloat him). He now like to run test at 300 mg/wk, with about 100 mg/day of Anadrol. I don’t think I would go that high, but he is strong AF, and has capped delts and is shredded. I kinda got the idea from his experience.

Oxymetholone has a tendency for inducing hypertension within those predisposed. Baseline hypertension + oxymetholone is a bad idea

Get that sorted out prior to blasting, even if it requires medication (under the assistance/monitoring of a physician).

HCT will probably shoot up on oxymetholone too.

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Personally i have mostly avoided orals. Var is the only oral i have used and i doubt ill try any others.

If i had the 2 options you have mentioned above, id go with the dbol/test.

Im finding options limited as well. Anything heavy on the hairline is out, tren is definitely out, high dose test is likely out now too, eq is out (bad enough anxiety as it is so not risking it).

I seemed to tolerate deca well at 200mg/w so a higher dose of that and just above cruise dose test might be the best option for me.

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This is solid advice. I am still leaning out (and won’t do this cycle until I am about where I want to be). I’ll keep monitoring BP as I drop weight. Ideally I would be better than 120/80 when starting the blast. If I had to guess where I am now, it is probably 125-130/80-85 (based on lots of readings). I think the one or two times I got 150/80s were flukes.

If you’ve got the money, what about something like 200 test/800 primo? Might have some E2 issues with test that low, but you could play with the dosages.

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My hair line is loyal, but it still scares the shit out of me. I have really good hair for my age (33), and I want to keep it that way. I have heard Dbol and Drol are not too bad on the hair line. Nandrolone just scares me. Tren would not be allowed by my wife.

I get bad anxiety as well. I have considered EQ, but it just doesn’t seem worth it (results seem meh). It is also reportedly hard on kidneys. I don’t want to mess with kidneys much. Liver doesn’t scare me as much as I don’t drink much, and it can recover.

I could afford it. I really do want to keep the hair line loyal. That is my big concern with Primo. I would consider DHB and Test. DHB is a metabolite of Primo, but stronger. I guess it hurts like crazy though.

Primo is an analogue of DHB (1a methyl DHB) in the way proviron is an analogue of DHT (1a methyl DHT). DHB is a metabolite of EQ that forms in response to interaction with 5a reductase

Primo doesn’t have affinity for 3b-HSD and retains anabolic characteristics when interacting with AR in skeletal muscle. Proviron/DHT are broken down into pharmacologically inactive metabolites within skeletal muscle via 3b-HSD enzyme. Proviron isn’t oral masteron btw, this is a common misconception. Masteron is 2a methyl DHT, not 1a methyl DHT.

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It appears as usual that you are correct.

I just cut primo from my test c/NPP/Primo blast because of hair lost. Stopped the primo, hair loss slowed quite a bit.

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I love this idea. Short blasts that utilize orals for their one major purpose, which is to increase size and strength immediately, should be effective at adding real, appreciable muscle over the course of a year. Will you put on 10lbs of actual muscle over six weeks? No, of course not. But if you put on an extra two pounds and you do that three times a year you could end up with pretty solid gains without adding a ton of longer term stress to your system. I cannot comment on anadrol as I have never used it, but I know that with dbol you can dose it lower for longer (assuming it doesn’t cause BP issues) and get a ton out of it.

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This is the goal, and my thought process on it. Dbol or Anadrol are harsher than Test, but it is a short duration. It seems the main concern with these compounds is liver health. NAC or TUDCA can be added to help there, and the liver is a pretty amazing organ in its recovery ability.

Kidney on the other hand scares me a bit. It seems that doesn’t recover as well, and a 14-16 week test blast might do some damage at that duration if BP is high.

I am trying to get lean ATM, I have abs, but they are faint. I’ll probably try this in two months or so. Would like to have a good amount of ab definition when I do this. I think being lean helps a lot with BP which helps with heart and kidney health a lot.

I have run Anadrol once, my first cycle actually, and the distress went away after 4-5 days. Didn’t notice any lack of appetite. 50mg/day for 30 days

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What was your experience like on it? How were the gains? Strength increase?