Oxandrolone post cycle?

Often I read threads regarding post cycles, how much clomid?, should I use HCG?, how can I avoid crashing, and losing strength?, as well as how long should I wait until next cycle?.

Legit questions of course and I know many people who go and start cycles without waiting even a month since their last. This brings me to my question.

Why not use Oxandrolone post cycle to help keep strength levels up? As I understand it does not shut down natural test levels, won't aromitize, and apart from cost, and being a 1 7-aa is pretty safe.

To you aa gurus, tell me your thoughts.

Thanks

Thats is my personal plan after my up and coming cycle, definately worthy of a discussion, I believe you can run clomid as ususal and then commence a mild 30-40mg ED dose with much benefit to strenght and will help keep the gains from the heavier cycle.

good question. good answer. Yes it is a good idea - you can run clomid as usual (in fact I recomend it ) but throwing oxy in is a good bridge to keep gains

ive been using chinese vars@30mgs ED,after my clomid therapy,about 3.5 weeks in i noticed a bit of testicular atrophy,and a loss of libido,but no erectile problems,ive kept ALL my gains in both strenght and lean mass,while dropping some bf.
im very happy,tho i think the theory about 30mgs and lower not effecting hpta levels is misleading,if that was the case i wouldnt have these testy and libido sides.
gonna run this for 8 weeks total then go back on for a couple months.
good luck with it.
Morg

i have heard the opposite on one thing... Var will shut u down...

Var WILL shut you down - it just depends on how much of it you are taking - another thing, I dont reccomiend taking it during clomid, go ahead and get your test production normal again, then begin anavar after - the dose for shutdown varies but have seen it as low as 10mg ED and as high as 25mg - taking even as high as 40 will not be too bad as it will recover quickly.

I agree with cycle here, Anavar from what I read will shut you down if you take to much, but cycle was only speakin of taking a small amount, and yes I believe it will help your keep your gains. I also (in the agreeing mood today), with cycle by not running it with your clomid cycle, simple cause your body needs to start it's own test. I mean hell you are just comin off a cycle, and the entire purpose of takin clomid is to get your test levels back to normal. Anavar will defeat the purpose IMO.

sort of off topic for this post, but my question is about anavar being 17aa..... would a cycle of anavar alone at say 25 - 40 mg ed for 5-6 weeks be that toxic to the liver? does anyone know how dangerous 17aa drugs really are? (like compared to alcohol for instance...) although winny can cause balding (if predeposed to it..) and joint problems, would winny at 50 mg ed for six weeks be more or less toxic compared to the var?

night op... i like the idea of var only cycles, depending on your goals... and if u want an opinion from a VET pm IRON GAME... i've seen him advicate anavar only cycles many times before on here.

peace, bg

Quote:

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Originally posted by big_guy
night op... i like the idea of var only cycles, depending on your goals... and if u want an opinion from a VET pm IRON GAME... i've seen him advicate anavar only cycles many times before on here.

peace, bg

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will do, thnx :)

just about anything you bridge with will decrease your natural test levels to some degree...the trick is to find what substance you can take and how much without shuting it down to a level that effects muscle development....
i like 30mg of anavar myself....i dont know how low my test levels decrease because of it, but i keep more of my gains than when i dont take it....it may just be that mentally i know im "on" something so i push harder and watch my diet more....either way, it works....

The key is not to start it untill your hpta has recovered... so you do the hcg, clomid, and then after your last shot of clomid start with around 20mg.... JJ is right 10mg is sometimes to much but I think if you wait till you are done with treatment then you should be fine, here again every one is diff...
I would do 15mg Dbol it works better and 50mcg of IGF-1r3 would work better...

Quote:

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Originally posted by Juice Junkie
If 10mg shuts you down 60% what do you think is going to happen with 30mg?

In my opinion the only options you have to bridge with are those that are completely non-hormonal. Insulin, IGF, Kyno, all non-hormonal. IGF has even been proven to aid in the recovery of HPTA. There is also another issue that is conviently left out. Whats the point of getting off a cycle? To clear receptor sites for the next cycle and prevent a permanent shut down of HPTA. If you get off test and start some anavar guess what!!! Receptors are still being occupied and you never clear. Thus the reason why you keep your so called gains because in all actuality you never came off. You might as well have just backed your test down to a lower dose and called that your recovery period or bridge.

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I agree with you here.

A "bridging" cycle that involves a 17AA is merely a light cycle. Anavar will shut down HPTA partially or fully, depending on the dose.

Anavar CAN BE liver toxic. It is a mild 17AA compared to dbol or winny, but it can have a negative effects on the liver.

I am considering a 40 day anavar cycle, NOT A BRIDGE, but a light cycle. I will not go back on injectibles until late april or early may. Huckleberrry Finaplex from Elite did a 45 day cycle and had good results.

I am still researching the best way to do the var only "light" cycle.

Quote:

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Whats the point of getting off a cycle? To clear receptor sites for the next cycle and prevent a permanent shut down of HPTA. If you get off test and start some anavar guess what!!! Receptors are still being occupied and you never clear.

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How long does it take to clear your receptors? If I come off and take clomid how long after that will I have clean receptors?

The clear receptor thing is a theory that's unproven. It doesn't really make sense because if it were true then all those on test replacement year after year would have to raise their doses every few months but the fact is they don't. I think the slow down in growth is just because your body needs a rest from the growth but I don't think that it has anything to do with receptors, it just needs a rest. Using Ox to bridge allows that rest without allowing muscular atrophy.

Boo, it's your dear firend. Thats what i like to see, anavar for bridging, anything else is a waste of time.

I already gave my reasons. If receptors downregulated then people who get hormone replacement therapy would need to raise their doses every few months and they don't. Are you saying they do?
You haven't shown any proof that the AR downregulates from AS. I am giving a real world example of why I am saying it doesn't.

You are confusing supersaturation with downregulating. Your example has nothing to do with the receptors downregulating. BTW 2gr will result in more growth than 1gr.
I have posted the studies showing an LH reading in boys using ox for several months about a dozen times in the last 2 years but if I get time to look them up again I will post again.
Your crack on Dr Scruggs is childish and unfounded. He doesn't make any money on Oxandrolone and I don't see what difference it would make, and as far as my quoting him goes, I have 12,000 posts on the boards and about 10 quote Dr Scruggs.

Here's one that showed 10 of 14 boys had lowered LH after 6 months of oxandrolone. It says "lowered" 34-89% . I am sure you're aware that if their HPTA is shut down there is 0 LH being produced. I assume from the wording that the other 4 boys didn't have any LH reduction whatsoever. This is consistent with the measurements at the VA Hospitals using it for alcoholics. But you would need to buy the whole study to see that.

1: J Pediatr 1979 Apr;94(4):657-62 Related Articles, Books, LinkOut


The effect of synthetic androgens on the hypothalamic-pituitary-gonadal axis in boys with constitutionally delayed growth.

Hopwood NJ, Kelch RP, Zipf WB, Hernandez RJ.

Serial concentrations of basal serum LH, FSH, testosterone, and LH and FSH responses to intravenous gonadotropin-releasing hormone were measured before and during six months of administration of fluoxymesterone or oxandrolone in 14 boys with constitutionally delayed growth and adolescence, in order to assess the effects of these androgens on maturation of the hypothalamic-pituitary-gonadal axis. Before therapy all boys had normal hormonal responses based on bone age. At the end of six months therapy 10 of the 14 boys had lower LH responses (34 to 89% reduction) to GnRH without consistent changes in FSH responses. With both androgens, there there was significant suppression of both basal serum FSH and testosterone. Eleven boys were restudied six months after completion of therapy; basal serum LH, FSH, and testosterone and responses to GnRH were equal to or greater than pretreatment levels, indicating recovery or progressive maturation of the HPGA. All boys had increased growth velocity and imporved weight gain without excessive bone age advancement; all had improved psychosocial adjustment.

PMID: 372514 [PubMed - indexed for MEDLINE]

Food for thought boys....

287. Lubischer, J. L.; Arnold, A. P. Axotomy transiently down-regulates androgen receptors in motoneurons of the spinal nucleus of the
bulbocavernosus. Brain-Res. 1995 Oct 2; 694(1-2): 61-8; ISSN:
0006-8993.

NETHERLANDS. Testosterone is an important trophic factor for
motoneurons in the spinal nucleus of the bulbocavernosus
(SNB), and SNB motoneurons are more responsive to
testosterone than are other motoneurons. Axonal injury during
early postnatal life prevents the normal development of
steroid-sensitivity by adult SNB motoneurons. Axonal injury
also causes changes in the expression by motoneurons of a
wide range of proteins, including the up-regulation of trophic
factor receptors. We have used a polyclonal antibody (PG-21;
G.S. Prins) to study the expression of androgen receptors in
SNB motoneurons after axonal injury. PG-21 labeled
motoneuronal nuclei in the lower lumbar spinal cord of rats in
a pattern that matched autoradiographic reports of androgen
accumulation in this region of the nervous system. A
population of numerous, small cells located dorsal to the
central canal also showed evidence of androgen receptor
expression. Cutting the axons of SNB motoneurons in adulthood
or in development caused a decrease in androgen receptor
immunoreactivity in SNB motoneurons. This is the first report
that a trophic factor receptor in motoneurons is down-
regulated after axonal injury, and is interesting in light of
reports that testosterone treatment can facilitate
motoneuronal regeneration after nerve cut. Androgen receptor
levels subsequently returned to normal, regardless of the age
at axotomy, providing no evidence for a lasting effect of
developmental axotomy on androgen receptor levels in SNB
motoneurons. Thus, axotomy-induced down-regulation of
androgen receptors does not underlie the inability of SNB
motoneurons to respond to androgen treatment several months
after pudendal nerve cut in development..

There are a lot of people who will say that there is no such thing as AR down-regulation. Which isn't true. It has been studied ad nauseum in prostate cancer studies. It does exist.

Though that is not an answer for whether or not this is applicable in Anavar's case and this discussion. Just wanted to clear that up.

I have seen that Mike but we're not talking about rats and we're not talking about cancer cells. But you're right about one thing I came way off topic here. Not intentionally but I did.

It doesnt matter whether or not these happened in cancerous situations, it was just in those studies that the idea of down regulation of androgen receptors proved very real.

And if you want a study done in HUMANS showing the effects of regulation of the androgen receptor (up or down) read this study.

Regulation of Androgen Receptor (AR) and Prostate Specific Antigen (PSA) Expression in the Androgen- Responsive Human Prostate LNCaP Cells by Ethanolic Extracts of the Chinese Herbal Preparation, PC-SPES

Whether or not prostate cancer is prevalent is irrelevant. The study was done FOR people with cancer patients. In those cancer patients their receptors do not act differently in this fundamental regard than it would in healthy subjects. It just happens to be the reason of study since nobody conducts clinical trials because there was an AnabolicReview.com debate :)

At any rate - this study does point out the regulation of AR in humans. I am not saying anyone is wrong - just thought I would post these to clear that up so you guys can get back on whether or not Var is a good thing or whatever the hell it was you guys were debating LOL