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Steroid use and bone mineral density

pengers84

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Does steroid use have any significant impact on bone mineral density? The reason I ask is because In the doctors waiting room reading the pamplets the other day and I was reading one on DEXAs and in the section headed 'who should have one,' one of the groups was 'long term steroid users.' Whats everyones opinions?
 
The answer goes like this:

Vitamin D plays an important role in maintenance of mineral bone matrix (hardness, density, remineralization, mobilization of mineral components).

I've chatted here about the side effects of anabolic steroid analogs: they tend to hit a lot of nuclear receptors in liver (home of vitamin D synthesis) and also in bone (site of stem cell blanks that are programmed by (other) nuclear receptors for their intended action (programming = early cell differentiation... late cell differentiation occurs once the cells migrate to their target location).

Nuclear receptors are a kinder, gentler form of cellular communication and autonomic/metabolic/energy control system. These receptors are meant to be kissed by loose binding, low abundance natural compounds (lipid like substances) in food.

Along come these anabolic steroids, which may bind much more tightly, and are present in very high concentrations, relative to the natural activators or deactivators of nuclear receptors in various tissues.

These anabolic steroid analogs "swamp" the signal of the natural ligands. The effect is often to block their activation.

Hence, the effect on bone (osteoclast) activity is to reduce the beneficial action of vitamin D on mineral deposition and matrix density.

Osteoporosis can occur with longterm steroid use.

Does this make sense?
 
Hmm interesting. What would you class as long term use? Is there anything that could be done to counter this negative effect of steroid use?

Thanks heaps
 
I think anything less than 2 times the amount of time off cycle vs. on cycle would be considered long term. But I would love to hear T's thought on this. You have to allow your body time to return to normal, and I'm not sure if double the time off vs on would even do it.
 
VDR is the nuclear receptor in question. The activation of this receptor is complex and its regulated, as are many other steroid activated nuclear receptors, by a co-activator, AP-1.

See: http://endo.endojournals.org/cgi/content/full/140/1/63

This sentence, from the opening paragraph in the introduction section, really says it all:

"The AP-1 class of transcription factors can inhibit the activation of the receptors for glucocorticoid, progesterone, estrogen, androgen, thyroid, and retinoids."

AP-1 itself is activated by anabolic steroid analogs (AAS). A quickie search on Google using the terms AP-1 and anabolic steroids confirmed this suspicion.

Just how much these anabolic steroids affect AP-1 transcriptional regulational will vary somewhat within individuals due to differences with receptor polymorphisms for various targets (named above). They read like a who's who list responsible for the desired primary and undesired secondary tissue specific effects of anabolic steroids.

Note that we now have 3 levels of AAS action (to produce the side effect):

AAS steric binding blockade of VDR receptor activation

AAS initiation of AP-1 transcriptional regulation

AAS steric binding to estrogen, glucocorticoid and retinoid receptors, all of which also co-active VDR in bone cells.

Because regulation can go either way - activation or inhibition, depending on the degree of ligand "fit" - physical / chemical match between the natural activator and the wannabe (such as AAS) into a receptor binding pocket - there will be some AAS agents that may have a positive effect on bone (osteoclast) function.

The National Institutes of Health apparently was thinking along these lines, in this 2002 request for research proposals (RFP):

http://grants.nih.gov/grants/guide/pa-files/pa-03-008.html

So I can't really answer your questions on how long to estabilish potential feedback regulatory effect on mature and developing bone cells. I can't even tell you if all AAS have negative consequences. I guess the SERMs and some SARMs (estrogen- and androgen-like agents, respectively) have a potential positive effect as PCT. BUT, whether they can compete with other AAS on-cycle? You would need studies (like the ones proposed with the RFP) to answer that question.

What I have given you, and other who will have the patience to read this response, is a moment of pause, as you come to appreciate the potential for long term effects from AAS use.

You got the signals for densification from structural compressive forces during heavy exertion (training). And you have probable alteration of the receptor that answsers that signal. For some steroids, its a positive effect (nadrolone acting through estrogen receptor), for some, acting on the glucocorticoid and vitamin D receptors, it maybe a negative effect.

Can't say for sure how long these AAS compounds take to exert their effects. In various studies I looked at, the net gain in those with osteoporosis (men and women) was 3% increase in density per annum (thats without the mechanical induction signals for bone densification), expressed with the first few months of treatment with AAS. Negative impact on liver from anabolic steroids is the primary negative action that dictates the period of use as a theraputic agent; that is manifest in a matter of a few months of steroid use.

Reversibility of side effects induced by these agents depends on a variety of factors.

Sorry, not the answer you wanted, Pengers and dg, but its what you get.
 
That is what I expected. It is based on many factors. Lets just say the more gear you do, the more chances of Osteoporosis/bone loss you have.
 
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