Any Non-Responders Out There?

**V_Vandetta** · 09-22-2006, 08:23 PM

Originally Posted by Warrior21

22 now. I did the other cycles when I was younger, alot younger. Please don't flame. I know I fked up.

no bro i dont want to flame you at all... but this is starting to make sense .. with the early AAS use i am going to dig up some research But I am thinking that somthing is very wrong and that you have have caused some problems from the useing to young would explain the hair loss and some other problems ... but let me do a little research and I will post when i find out for sure

**guest589745** · 09-22-2006, 08:24 PM

Originally Posted by Kale

When are you thinking of starting ?

2-3 months. You?

**Kale** · 09-22-2006, 08:27 PM

Maybe the start of November, I want to get back in shape after this damn surgery I had then I am going to give it a go

**guest589745** · 09-22-2006, 08:28 PM

Originally Posted by Kale

Maybe the start of November, I want to get back in shape after this damn surgery I had then I am going to give it a go

It sucks because I am "back to normal" now and I will miss having so much energy but maybe tren /winny/masteron will be different. I also have to rehab this damn shoulder before I can go all out.

**Warrior21** · 09-22-2006, 08:32 PM

Vendetta I am damn sure that the steroids have prematurely brought on my hairloss. But it's in my genetics so it's inevitable. But most likely had I not fked with these strong compounds I would have had hair for at least 5-6 more years before it falling like crazy. Right now I'm shaving my head, but one day I will get hair implants. I will have my hair again.
Besides that I don't really think the fact that I started at a young age (16) would affect my receptors or me not gaining anything. I never gained anything back then, and I'm not gaining anything now. But it's not like early usage "shut" my receptors off or something.
Smiler I feel ya on the whole not responding to low dosages thing. Maybe thats just what is happening. I gotta say I had a short run with DNP one time and 400mg didn't do jack shit for me. Consequently, I couldn't run the stuff more than 4 days to really know whether I would have responded to that too, it was staining everything and I just exposed of it.

**Warrior21** · 09-22-2006, 08:34 PM

Originally Posted by Skullsmasher

It sucks because I am "back to normal" now and I will miss having so much energy but maybe tren/winny/masteron will be different. I also have to rehab this damn shoulder before I can go all out.

Skullsmasher maybe you want to inject vitamin B-12 while your off cycle? It gives an appetite and energy like hell. Try it, friend.

**Hellmaskbanned** · 09-22-2006, 08:34 PM

Originally Posted by Skullsmasher

It sucks because I am "back to normal" now and I will miss having so much energy but maybe tren/winny/masteron will be different. I also have to rehab this damn shoulder before I can go all out.

OUCH ....I feel sorry for your shoulder bro.

**V_Vandetta** · 09-22-2006, 08:36 PM

hypogonadism

The effects of male hypogonadism depend primarily on the stage of life at which they occur. They can occur during fetal development, puberty or adulthood. During each of these stages, the signs and symptoms are distinct.

Fetal development
The sex chromosomes X and Y — you receive an X from your mother and either an X or a Y from your father — determine whether the gonads in an embryo develop into ovaries (XX) or testicles (XY). If testicles form, the hormone testosterone is produced and male sex organs develop.

Production of too little hormone by the gonads during early fetal development may impair the growth or functions of the internal and external sex organs. This can cause a condition in which the sex of the child is not clear by external examination at birth (ambiguous genitalia).

Puberty
Male hypogonadism present at the time of puberty may slow growth and affect normal development. Body changes may include:

Decreased development of muscle mass
Lack of deepening of the voice
Impaired growth of body hair
Impaired growth of the penis and testicles
Excessive growth of the arms and legs in relation to the trunk of the body
Development of breast tissue (gynecomastia )
Adulthood
Hypogonadism in adult males may alter certain masculine physical characteristics and impair normal reproductive function. Signs and symptoms may include:

Erectile dysfunction
Infertility
Decrease in beard and body hair growth
Increase in body fat
Decrease in size or firmness of testicles
Decrease in muscle mass
Development of breast tissue
Loss of bone mass (osteoporosis )
Mental and emotional changes also can accompany hypogonadism. As testosterone decreases, some men may experience symptoms similar to those of menopause in women. These may include:

Fatigue
Decreased sex drive
Difficulty concentrating
Hot flashes
Irritability
Depression

Male hypogonadism with a deficiency of testosterone is a relatively common disorder in clinical practice and has significant effects on the fertility, sexual function, and general health of affected men.

Please note that it is extremely important to obtain an accurate diagnosis before trying to find a cure. Many diseases and conditions share common symptoms: if you treat yourself for the wrong illness or a specific symptom of a complex disease, you may delay legitimate treatment of a serious underlying problem. In other words, the greatest danger in self-treatment may be self-diagnosis. If you do not know what you really have, you can not treat it!

Knowing how difficult it is to weed out misinformation and piece together countless facts in order to see the "big picture", we now provide simple, inexpensive online access to The Analyst™. Used by doctors and patients alike, The Analyst™ is a computerized diagnostic tool that sits on a vast accumulation of knowledge and research. By combining thousands of connections between signs, symptoms, risk factors, conditions and treatments, The Analyst™ will help to build an accurate picture of your current health status, the risks you are running and courses of action (including appropriate lab testing) that should be considered. Full information is available here.

Hypogonadism can occur for a number of reasons, some relatively common and others rare. Certain men have hypogonadism from birth while others may develop this condition later in life. Types of hypogonadism include:

Primary hypogonadism (testicular failure) - Low serum testosterone levels with gonadotropins (FSH, LH) above the normal range. Klinefelters, surgical removal, bilateral mumps related orchitis, toxic damage by alcohol, heavy metals or chemotherapy.
Secondary (gonadotropin) hypogonadism - Caused by a pituitary failure or pituitary-hypothalamic injury from tumors, trauma, or radiation; characterized by low serum testosterone levels, but with gonadotropins in the normal or low range
Testicular atrophy may occur as the result of hernia repair, use of anabolic steroids , Klinefelter's syndrome and normal aging, although relatively little is known about the mechanisms underlying germ cell loss in aging. Sterility from mumps is rare even when both testicles are involved. Some degree of testicular shrinkage may be detectable after the mumps infection; however, it does not cause sterility.

In adult males with low serum testosterone and elevated gonadotropin levels, primary testicular failure should be suspected, whereas low or normal gonadotropin and low testosterone levels suggest a hypothalamic or pituitary disorder.

In men with clinical symptoms of primary or secondary hypogonadism, the deficiency of testosterone can be treated effectively with currently available preparations. Clomid and Arimidex act by reducing the conversion of testosterone to estrogens. HCG is being used to mimic luetinizing hormone to increase testosterone production in athletes and those with testicular atrophy. It must be used carefully and cyclically to prevent side effects.

**V_Vandetta** · 09-22-2006, 08:39 PM

i belive you damaged you natty test to the point on long term becasue the free test levels you posted seemed very low but I am no doctor but it would seem that hypogonadism is the case here

**guest589745** · 09-22-2006, 08:40 PM

Originally Posted by Warrior21

Skullsmasher maybe you want to inject vitamin B-12 while your off cycle? It gives an appetite and energy like hell. Try it, friend.

Might do that, thanks. I have heard it works for others.

**Warrior21** · 09-22-2006, 08:40 PM

I appreciate the effort V. But that can't be me hehe. My total test during last blood test was 1040 ng/dl, not bad. I grow body hair like crazy. My balls are big, I can't keep my penis down. Even in a month on Anavar alone at
90mg ED I can still get it up at the drop of a dime.

. I guess thats one of the few things I have to be greatful for.

**guest589745** · 09-22-2006, 08:41 PM

Originally Posted by Hellmask

OUCH ....I feel sorry for your shoulder bro.

We'll see. I gotta at least try.

***Narkissos*** · 09-22-2006, 08:44 PM

Originally Posted by V_Vandetta

i belive you damaged you natty test to the point on long term becasue the free test levels you posted seemed very low but I am no doctor but it would seem that hypogonadism is the case here

I dont' see that being applicable

As he grows on cycle as he should off cycle...

Even if he is hypogonadal.. if he supplements with just a replacement dose of test (re: HRT TRT) he would be seeing gains... namely because he is hypogonadal

I'd fathom he isn't.. Rather he is hyper-drug metabolism.. like what Tai proposed himself.

**Warrior21** · 09-22-2006, 08:45 PM

V don't confuse total test with free test. Keep in mind SHBG binds up to 98% of our nat. test. My total was 1040ng/dl, my free is 134ng/dl. Anybody care to post their free test while off cycle?
V you also mention that maybe I'm not gaining because my nat test has been lowered. If it were true, wouldn't I see much better gains from going on a cycle...given that my body would be so shocked by the surge of test. I'm also aware that if my nat test setpoint was low and I WOULD gain off of a cycle I wouldn't be able to maintain much mass while off AAS. But that's not even the case here. I'm not even gaining anything while on. I'd at least be happy if say while on I gained 20 lbs and only kept 10 while off. But I get nothing.

Again I want to thank you all for your kind responses, and genuine interest in helping me.

**fLgAtOr** · 09-22-2006, 08:45 PM

Originally Posted by Warrior21

I appreciate the effort V. But that can't be me hehe. My total test during last blood test was 1040 ng/dl, not bad. I grow body hair like crazy. My balls are big, I can't keep my penis down. Even in a month on Anavar alone at
90mg ED I can still get it up at the drop of a dime.

. I guess thats one of the few things I have to be greatful for.

Maybe you're too big for steroids ??? Eh? Ever think of that???

I say take a good amount of time off after your var cyc and then do some serious planning. Try "priming" beforehand like others have said, and go for a nice, basic and heavy cycle. I'm not qualified to give dosages, but there are some ideas floating around.

**V_Vandetta** · 09-22-2006, 08:46 PM

Originally Posted by Warrior21

I appreciate the effort V. But that can't be me hehe. My total test during last blood test was 1040 ng/dl, not bad. I grow body hair like crazy. My balls are big, I can't keep my penis down. Even in a month on Anavar alone at
90mg ED I can still get it up at the drop of a dime.

. I guess thats one of the few things I have to be greatful for.

maybe so but there is a reason this was done very quick but maybe it's nothing I have never heard or read anything that were AAS didnt make you grow ............. but also keep in mind that you do decribe some of the systems maybe not all But none the less to rule every thing out get a complete work up from head to toe and rule every thing out as nark stated you may be one of the ones that are a hard gainer

**Warrior21** · 09-22-2006, 08:48 PM

Originally Posted by Narkissos

I dont' see that being applicable

As he grows on cycle as he should off cycle...

Even if he is hypogonadal.. if he supplements with just a replacement dose of test (re: HRT TRT) he would be seeing gains... namely because he is hypogonadal

I'd fathom he isn't.. Rather he is hyper-drug metabolism.. like what Tai proposed himself.

Nark were seeing eye-to-eye. From context, I take it hyper-drug metabolism means my body flushes it out too quickly for anything to work? If this is the case, would mega dosing (2x or 3x normal amounts) be the solution? If so, I better get another job hehe. How would you explain my own brother's great results to just 60mg Var ED?

**Warrior21** · 09-22-2006, 08:51 PM

Originally Posted by fLgAtOr

Maybe you're too big for steroids ??? Eh? Ever think of that???

I say take a good amount of time off after your var cyc and then do some serious planning. Try "priming" beforehand like others have said, and go for a nice, basic and heavy cycle. I'm not qualified to give dosages, but there are some ideas floating around.

Too big for roids, heh I wish. Right now I'm 5'10 210-15 @ 14-5% bf. Nothing crazy. I was natural during my peak physique when I weighed 235@14%.

I will look into this "priming".

***Narkissos*** · 09-22-2006, 08:51 PM

Originally Posted by Warrior21

How would you explain my own brother's great results to just 60mg Var ED?

You're not identical twins... Sure you're from the same base stock..but your make up is not identical

That's my explanation.

**V_Vandetta** · 09-22-2006, 08:53 PM

Originally Posted by Narkissos

I dont' see that being applicable

As he grows on cycle as he should off cycle...

Even if he is hypogonadal.. if he supplements with just a replacement dose of test (re: HRT TRT) he would be seeing gains... namely because he is hypogonadal

I'd fathom he isn't.. Rather he is hyper-drug metabolism.. like what Tai proposed himself.

true but this has to be the frist time I ever heard that someone gained nothing? ( other than bunk gear) and even than they gained a little from training and eating... I mean i am no doc ... and I dont know everything....... i guess we learn something new every day .. just that I have seen guys grow on cycles AND DAMN SURE THEY DID'Nt diet right. i have scene were guys get low gains and worked hard on HIGH cycles but never nothing....... but maybe you are right and he has a hyper-drug metabolism

**Warrior21** · 09-22-2006, 08:56 PM

Well I'm an endomorph who gains fat very easily. I have a slow metabolism, but I'm sure that drug metabolism and nutrient metabolism are 2 diff things. Can you guys elaborate on hyper-drug metabolism?

This just keeps getting more pleasant by the minute.

**fLgAtOr** · 09-22-2006, 08:57 PM

And what about IGF? Would that be something that could help his situation?

**guest589745** · 09-22-2006, 08:58 PM

Originally Posted by Narkissos

I dont' see that being applicable

As he grows on cycle as he should off cycle...

Even if he is hypogonadal.. if he supplements with just a replacement dose of test (re: HRT TRT) he would be seeing gains... namely because he is hypogonadal

I'd fathom he isn't.. Rather he is hyper-drug metabolism.. like what Tai proposed himself.

You have a link nark?

**Warrior21** · 09-22-2006, 09:15 PM

I just made a connection with the hyper-drug metabolism connection. I notice that when I take an Anavar capsule I drink it with a whole bunch of water (usually at least 32 oz.). This makes me pee within 5 min. When I pee 5 min after taking the Anavar capsule I pee pretty dark. The very next pee after that, given I drank enough, is surprisingly clear.
I've interviewed (I guess you could say) my brother several times about his experience with Var the so that I could get to the bottom of this. One thing that sticks out is that his pee is consistently darker throughout the day, but never extremely dark.
I'm hypothesizing that I am a victim of this 'hyper-drug metabolism'. Maybe you guys can comment on this.

Another thought I may add is similar to Smiler's experience. I had gyno surgery when I was younger and the surgeon swore he put enough local anesthetic in my chest. Well I was screaming throughout that surgery. He put in some more because the nurses all suggested he should. Still nothing, after that he just told me to hold on and deal with it.

**Warrior21** · 09-23-2006, 06:15 AM

Bump, anyone know more about hyper drug metabolism?

**stupidhippo** · 09-23-2006, 07:59 AM

IMO if u dont gain shit from a cycle it must be sumin else than diet / training.. I mean u should put on at least some water weight and all... While ur training and diet might not be perfect but IMO it cant explain almost total unresponsiveness.. I mean I know ppl who dont eat shit, dont train good but when they take AAS they do grow (not as much as u should obviously bur there is a clear difference). This applies to u especially if u are not very big / strong... If I remeber correctly studies show that sedentary ppl achieve LBM increases even if they dont work out.. Once again I emphasize I am not saying to anybody that u shouldnt train... I just think in this case the answer prolly is sumin else than diet/training..

**stupidhippo** · 09-23-2006, 08:03 AM

complex question.... are u saying u have a very fast metabolism in all medication u have eaten. I find this pretty unbeliavable.. but does ur body have some sort of mechanism to deactivate certain compound? I dont have enough knowledge to completely rule it out.. sounds till unlikely.. To my understanding the metabolic pathways of local anaesthetics and aas are pretty different... but i dont know..

***Narkissos*** · 09-23-2006, 08:54 AM

Originally Posted by Skullsmasher

You have a link nark?

Ran a search... can't link to the thread cus it's in a private forum..sorry

Hit Tai with a pm

**AnabolicBoy1981** · 09-23-2006, 09:15 AM

warrior, ever have your thyroid tested?

**guest589745** · 09-23-2006, 10:18 AM

Originally Posted by Narkissos

Ran a search... can't link to the thread cus it's in a private forum..sorry

Hit Tai with a pm

I just spent over an hour searching then I see you said "RAN a search" not "RUN a search"................

Godamn tai has a lot of threads!

Yea, I PMed him, thanks.

**Warrior21** · 09-23-2006, 12:11 PM

Hippo I'm glad you see that this isn't a question of diet/training. Something is definately really wrong. I mean with the cycles that I've done my balls never went away, yes even on Deca and Fina as well. You're not as stupid as you say

I dunno if my body would have a mechanism to deactivate AAS. If it does I'll do whatever it takes to combat that mechanism. I've studied inhibiting
CYP P450 enzyme which may have something to do with this.

To anabolic boy, my thyroid has been tested, just 2 months ago. It is fine, my bloodwork is very good.

Nark can you elaborate on the hyper drug metabolism and how I can slow it down?

And Skullsmasher how is the search going? Did you find anything out? I'm sure you can benefit from getting to the bottom of this too.

**pumpd4lif** · 09-23-2006, 12:14 PM

Originally Posted by LmbrJak

Looks like your doseages are low and not run long enough.It can take 6 or so weeks for test e to kick in.

Maybe you should research more before next cycle

i must agree

**Warrior21** · 09-23-2006, 12:17 PM

That's your opinion. But I think you're switching the thread in the wrong direction. What would you tell me about the Dbol ? What would you say about Fina, Anavar ? They're known to kick in quick. Somethings not right, lets get to the bottom of this.

**Warrior21** · 09-23-2006, 01:05 PM

Cytochrome P450: genetic polymorphism and drug interactions.Belpaire FM, Bogaert MG.
Heymans Institute of Pharmacology, University of Gent Medical School, Belgium.

In this review, after a short discussion of our knowledge about cytochrome P450 isoenzymes, two important sources of variability in the metabolism of drugs by cytochrome P450 are described, i.e. genetic factors and drug-drug interactions. Many hepatic cytochrome P450 enzymes play an important role in the oxidative biotransformation of numerous drugs and other foreign compounds, and of many endogenous substrates. In humans more than 20 different isoenzymes of cytochrome P450 responsible for the hepatic metabolism of drugs, have been identified. They are classified into families and subfamilies on the basis of the degree of amino acid similarity. Cytochrome P450 isoenzymes are regulated by both genetic and environmental factors. Of particular interest is genetic polymorphism in drug oxidation. Two genetic polymorphisms in drug oxidation are well known, the sparteine/debrisoquine (CYP2D6) polymorphism and the mephenytoin oxidation (CYP2C19) polymorphism. As a result of these polymorphisms, two phenotypes exist in the population, poor and extensive metabolizers. Poor metabolizers may be prone to adverse reactions towards drugs with a narrow therapeutic range. In extensive metabolizers clinically significant drug interactions between drugs metabolized by the same isoenzyme can occur.

PMID: 8858891 [PubMed - indexed for MEDLINE]

NOW THE SECOND PART:

Update: genetic polymorphism of drug metabolizing enzymes in humans.Tanaka E.
Institute of Community Medicine, University of Tsukuba, Japan.

The cytochrome P450 (P450 or CYP) monooxygenases, CYP2D6, CYP2C19, CYP2E1 and CYP2C9, and non-P450 monooxygenases, N-acetyltransferase, thioprine methyltransferases and dihydropyrimidine dehydrogenase, all display polymorphism. CYP2D6 and CYP2C19 have been studied extensively and, despite their low abundance in the liver, they have been found to catalyse the metabolism of many drugs. CYP2D6 has many allelic variants, whereas CYP2C19 has only two. Most variants are translated into inactive, truncated proteins or fail to express protein. There is, as yet, no clear information about CYP2E1 polymorphism. In addition, genetic differences in certain foreign-compound metabolizing enzymes, such as Phase II enzymes, have been shown to be associated with an increased risk of developing environmentally and occupationally related diseases such as cancer. When two drugs that are substrates of a polymorphic CYP enzyme are administered concomitantly during drug therapy, each will compete for that enzyme and competitively inhibit the metabolism of the other substrate. This can result in toxicity. Patients who are poor metabolizers (PMs), extensive metabolizers (EMs) and ultrarapid metabolizers (URMs) can be identified. Having such information will help in determining the appropriate dosage of certain drugs when treating patients with an inherited abnormality of a drug-metabolizing enzyme. In view of the remarkable progress in this particular field, it is to be expected that more genetic polymorphisms will be discovered in the near future.

PMID: 10583694 [PubMed - indexed for MEDLINE]

**guest589745** · 09-23-2006, 01:13 PM

So what exactly is it that effects the metabolizing of drugs and what can we do to control the amount of it in our body ?

**guest589745** · 09-23-2006, 01:21 PM

In drug metabolism, cytochrome P450 is probably the most important element of Phase I metabolism in mammals (metabolism in this context being the chemical modification or degradation of chemicals including drugs and endogenous compounds). Many drugs may increase or decrease the activity of various CYP 450 isozymes in a phenomenon known as enzyme induction and inhibition). This is a major source of adverse drug interactions, since changes in P450 enzyme activity may affect the metabolism and clearance of various drugs. For example, if one drug inhibits the CYP-mediated metabolism of another drug, the second drug may accumulate within the body to toxic levels, possibly causing an overdose. Hence, these drug interactions may necessitate dosage adjustments or choosing drugs which do not interact with the CYP system. In addition, naturally occuring compounds may also cause a similar effect. For example, bioactive compounds found in grapefruit juice, including bergamottin, dihydroxybergamottin, and paradisin-A, have been found to inhibit CYP3A4-mediated metabolism of certain medications, leading to increased bioavailability and thus the strong possibility of overdosing. Because of this risk, avoiding grapefruit juice and fresh grapefruits entirely while on drugs is generally advised.

**guest589745** · 09-23-2006, 01:23 PM

The CYP2D6 function in any particular subject may be described as one of the following:

extensive metaboliser - these subjects have normal or reduced CYP2D6 function
poor metaboliser - these subjects have no CYP2D6 function
ultrarapid metaboliser - these subjects have multiple copies of the CYP2D6 gene expressed, and therefore greater-than-normal CYP2D6 function

**IIIIIIIIIIII** · 09-23-2006, 01:23 PM

this thread is WAYYY too technical for my little meathead mind..

all i have to say is..

**guest589745** · 09-23-2006, 01:25 PM

Furthermore ethnicity is a factor in the occurrence of CYP2D6 variability. The prevalence of CYP2D6 poor metabolisers is approximately 6-10% amongst Caucasian populations, but is lower in most other ethnic groups such as Asians (2%) [4]. In African Americans, however, the frequency of poor metabolizers is greater than for Caucasians (1.6% vs. 0.44%)

Cytochrome P450 CYP2D6 is responsible for the metabolism of approximately 20-25% of prescription medicine

microsomal vitamin D3 25-hydroxylase = (CYP2D25)

Substrates and inhibitors of CYP2D6

Substrates
Antidepressants*
Amitriptyline (Elavil)
Clomipramine (Anafranil)
Desipramine (Norpramin)
Doxepin (Adapin, Sinequan)
Fluoxetine (Prozac)
Imipramine (Tofranil)
Nortriptyline (Pamelor)
Paroxetine (Paxil)
Venlafaxine (Effexor)
Antipsychotics
Haloperidol (Haldol)
Perphenazine (Etrafon, Trilafon)
Risperidone (Risperdal)
Thioridazine (Mellaril)
Beta blockers
Metoprolol (Lopressor)
Penbutolol (Levatol)
Propranolol (Inderal)*
Timolol (Blocadren)
Narcotics
Codeine, tramadol (Ultram) Inhibitors
Antidepressants
Paroxetine > fluoxetine >
sertraline (Zoloft) > fluvoxamine
(Luvox),
Nefazodone (Serzone),
Venlafaxine > clomipramine
(Anafranil) > amitriptyline
Cimetidine (Tagamet)
Fluphenazine (Prolixin)
Antipsychotics
Haloperidol
Perphenazine

Inhibitors
Antidepressants
Paroxetine > fluoxetine >
sertraline (Zoloft) > fluvoxamine
(Luvox),
Nefazodone (Serzone),
Venlafaxine > clomipramine
(Anafranil) > amitriptyline
Cimetidine (Tagamet)
Fluphenazine (Prolixin)
Antipsychotics
Haloperidol
Perphenazine
Thioridazine

**guest589745** · 09-23-2006, 01:31 PM

I still am lost as to what increases or decreases Cytochrome P450 CYP2D6 if this is in fact the problem. an increase is what apparently causes hyper-drug metabolism unless Im missing something. And I suppose this is just one possible cause, not the definate reason.

this is getting comlpicated lol........