HelloNelson and the gang,
I just read an article entitled, "Can I get brain disease from steroiduse?" by Jerry Brainum. I found it very interesting so I looked upthe paper cited.
The full paper is available if you search for the name:
"Brain Nerve Growth Factor Unbalance Induced by Anabolic Androgenic Steroids in Rats"
I found some odd details in the paper that I was hoping you might be able toexplain.
1) The author gave mice 5mg/kg/dayx 1 monthof nandrolone or stanozolol claiming this to be a bodybuilder dose. Given thatmice have a life expectancy of about 2 years and humans about 80 that wouldmean a 100 kg man would be taking 3,500mg a week for 40 months straight! Thatseems like an absurdly high dose for an absurdly long duration. I have heard of 800 mg/week of nandrolone run for 16weeks among bodybuilders. According to Tamaki's 2003 paper “Nandolone decanoate enhances hypothalamicbiogenic amines in rats” the standardtherapeutic dose in humans is 0.4 mg/kg/day. For a 100 kg man that would be 40mg/day or 280 mg/wk. Based on the dose and duration. I wonder how applicable thesefindings are to humans, if at all.
2) The authors did not supply the data but noted no difference in body weight changes between control groups and AAS groups?! At that dosage and duration? Maybe they mean no difference in total weight but certainly there should be some differences in lean body mass and fat mass, even without exercise right?
3) If you look at the left hand of figure 5 you will see that both AAS groups had lower latency times to find the platform in the Morris water maze task. TheAAS groups were actually more efficient at completing the task. If the goal ofthe rat is, as we assume, to get on that platform as quickly as possible thenshouldn't we conclude that AAS administration actually benefited performance onthis task?
4) If you look at the right hand of figure 5 you will see the AAS treatmentrats had less time to extinction. That is, during the probe several days after"learning acquisition" the rats were timed to see how much time theywould spend in the quadrant that the platform had been placed in all previoustrials. The authors assume that this is a measure of the rat's memory and that longertimes in this quadrant reflects a better memory or learning than the shortertime. The trouble is there are other plausible interpretations of this data.For example, if you wanted to get out of the water fast and you swam to thelocation you thought a platform was in but didn't find it, you might quicklydecide to search elsewhere. Does that necessarily imply that you did not rememberwhere the platform was? My interpretation may suggest that the AAS groups were"thinking faster" and "employing multiple strategies" toproblem solve.
4) The authors state that there was NGF abnormality in specific brain regionsof AAS treated mice. This appears to be true. However, considering the"abnormal" state of the mice's hippocampal NGF which was actually anincrease compared to controls, wouldn't this be beneficial? I would expect that my above interpretation ismore plausible than the authors given that the hippocampus is stronglyassociated with spatial learning and transfer of memory from short to long term.
The decrease in NGF in the basal frontal region does appear to be a legitimatenegative impact of high dose, long duration AAS administration
BUT....
This study, which Jerry Brainum did not mention but which you can findthe full paper if you search for :
High-Dose Anabolic Androgenic Steroids
Modulate Concentrations of Nerve Growth
Factor and Expression of Its Low Affinity
Receptor (p75-NGFr) in Male Rat Brain
Gave testosterone or nandrolone at 5mg/kg/wk (Thisdose seems more reasonable). For 6 weeks (equivalent to 60 months or 5 years ofcontinuous use in humans, if my calculations and assumptions arecorrect). If you look at table 1 of the study you will see that in thenandrolone group the only significant reduction in NGF was in the hypothalamuswhich I would expect considering that nandrolone down-regulates fsh and lhproduction in the HPTA. And again, as in the study cited by Jerry Brainum thereis an increase in hippocampal NGF, but with no accompanying decrease of NGF inthe frontal cortex.
In this study, testosterone showed a different pattern of NGF effect on thebrain with only increases in septum and occipital cortex, which to me seemspositive. I wonder if the common bodybuilding practice of co-administration oftestosterone with nandrolone might help to offset any potentially deleteriouseffects of nandrolone use on the brain. I wish they had a fourth study groupwhich was nandrolone+testosterone, oh well.
Also, in his article Jerry Brainum asked the question, are these changesreversible? To which he implied there was no answer. If you look in the studythat I linked you can see the researchers interrupted AAS administration forfour weeks and then retested the brains of the mice. Lo and behold! Thenandrolone treated mice brains went back to “normal” where there werereductions in NGF BUT remained elevated in the septum. Doesn't this seem likegood news for nandrolone users? Am I misreading or misunderstanding something?
I understand that animal studies do not always translate to human physiology .However, there is a lack of well controlled human studies on this matter. So,if one wants to speculate on an answer using the available scientific data oneis forced to, at least in part, rely on the animal studies.
Finally, if someone were to choose to use nandrolone at 100mg/wk x 8 weeks oncea year on top of their regular TRT dose of testosterone for joint and tendon issues, do you believe that the co-administration of Alpha-lipoic acid or alphalipoic acid rich foods would help to ameliorate any negative impact nandroloneuse could have on the brain?
I ask because of this paper:
1)
Lipoic acid and pentoxifylline mitigate nandrolonedecanoate-induced neurobehavioral perturbations in rats via re-balance of brainneurotransmitters, up-regulation of Nrf2/HO-1 pathway, and down-regulation ofTNFR1 expression
Doyou know of anything else that might help to mitigate any potential adverseeffects nandrolone may have on the brain?
I just read an article entitled, "Can I get brain disease from steroiduse?" by Jerry Brainum. I found it very interesting so I looked upthe paper cited.
The full paper is available if you search for the name:
"Brain Nerve Growth Factor Unbalance Induced by Anabolic Androgenic Steroids in Rats"
I found some odd details in the paper that I was hoping you might be able toexplain.
1) The author gave mice 5mg/kg/dayx 1 monthof nandrolone or stanozolol claiming this to be a bodybuilder dose. Given thatmice have a life expectancy of about 2 years and humans about 80 that wouldmean a 100 kg man would be taking 3,500mg a week for 40 months straight! Thatseems like an absurdly high dose for an absurdly long duration. I have heard of 800 mg/week of nandrolone run for 16weeks among bodybuilders. According to Tamaki's 2003 paper “Nandolone decanoate enhances hypothalamicbiogenic amines in rats” the standardtherapeutic dose in humans is 0.4 mg/kg/day. For a 100 kg man that would be 40mg/day or 280 mg/wk. Based on the dose and duration. I wonder how applicable thesefindings are to humans, if at all.
2) The authors did not supply the data but noted no difference in body weight changes between control groups and AAS groups?! At that dosage and duration? Maybe they mean no difference in total weight but certainly there should be some differences in lean body mass and fat mass, even without exercise right?
3) If you look at the left hand of figure 5 you will see that both AAS groups had lower latency times to find the platform in the Morris water maze task. TheAAS groups were actually more efficient at completing the task. If the goal ofthe rat is, as we assume, to get on that platform as quickly as possible thenshouldn't we conclude that AAS administration actually benefited performance onthis task?
4) If you look at the right hand of figure 5 you will see the AAS treatmentrats had less time to extinction. That is, during the probe several days after"learning acquisition" the rats were timed to see how much time theywould spend in the quadrant that the platform had been placed in all previoustrials. The authors assume that this is a measure of the rat's memory and that longertimes in this quadrant reflects a better memory or learning than the shortertime. The trouble is there are other plausible interpretations of this data.For example, if you wanted to get out of the water fast and you swam to thelocation you thought a platform was in but didn't find it, you might quicklydecide to search elsewhere. Does that necessarily imply that you did not rememberwhere the platform was? My interpretation may suggest that the AAS groups were"thinking faster" and "employing multiple strategies" toproblem solve.
4) The authors state that there was NGF abnormality in specific brain regionsof AAS treated mice. This appears to be true. However, considering the"abnormal" state of the mice's hippocampal NGF which was actually anincrease compared to controls, wouldn't this be beneficial? I would expect that my above interpretation ismore plausible than the authors given that the hippocampus is stronglyassociated with spatial learning and transfer of memory from short to long term.
The decrease in NGF in the basal frontal region does appear to be a legitimatenegative impact of high dose, long duration AAS administration
BUT....
This study, which Jerry Brainum did not mention but which you can findthe full paper if you search for :
High-Dose Anabolic Androgenic Steroids
Modulate Concentrations of Nerve Growth
Factor and Expression of Its Low Affinity
Receptor (p75-NGFr) in Male Rat Brain
Gave testosterone or nandrolone at 5mg/kg/wk (Thisdose seems more reasonable). For 6 weeks (equivalent to 60 months or 5 years ofcontinuous use in humans, if my calculations and assumptions arecorrect). If you look at table 1 of the study you will see that in thenandrolone group the only significant reduction in NGF was in the hypothalamuswhich I would expect considering that nandrolone down-regulates fsh and lhproduction in the HPTA. And again, as in the study cited by Jerry Brainum thereis an increase in hippocampal NGF, but with no accompanying decrease of NGF inthe frontal cortex.
In this study, testosterone showed a different pattern of NGF effect on thebrain with only increases in septum and occipital cortex, which to me seemspositive. I wonder if the common bodybuilding practice of co-administration oftestosterone with nandrolone might help to offset any potentially deleteriouseffects of nandrolone use on the brain. I wish they had a fourth study groupwhich was nandrolone+testosterone, oh well.
Also, in his article Jerry Brainum asked the question, are these changesreversible? To which he implied there was no answer. If you look in the studythat I linked you can see the researchers interrupted AAS administration forfour weeks and then retested the brains of the mice. Lo and behold! Thenandrolone treated mice brains went back to “normal” where there werereductions in NGF BUT remained elevated in the septum. Doesn't this seem likegood news for nandrolone users? Am I misreading or misunderstanding something?
I understand that animal studies do not always translate to human physiology .However, there is a lack of well controlled human studies on this matter. So,if one wants to speculate on an answer using the available scientific data oneis forced to, at least in part, rely on the animal studies.
Finally, if someone were to choose to use nandrolone at 100mg/wk x 8 weeks oncea year on top of their regular TRT dose of testosterone for joint and tendon issues, do you believe that the co-administration of Alpha-lipoic acid or alphalipoic acid rich foods would help to ameliorate any negative impact nandroloneuse could have on the brain?
I ask because of this paper:
1)
Lipoic acid and pentoxifylline mitigate nandrolonedecanoate-induced neurobehavioral perturbations in rats via re-balance of brainneurotransmitters, up-regulation of Nrf2/HO-1 pathway, and down-regulation ofTNFR1 expression
Doyou know of anything else that might help to mitigate any potential adverseeffects nandrolone may have on the brain?
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