Nandi

[jimmyinkedup]

Once upon a time, long before many were around or in this game there was a forum with a member named Nandi (Karl Hoffman). The man did more for this game than anyone other than Dan Duchaine and did so more safely than ducahine. IMO he was a genius. I will be ref diff posts from him as they still hold true today and have become the foundation of the principles vets like Austin and all the senior guys like Marcus and Matt and BG and the list goes on will share regarding aas and ancillary use. Here is an amazing post he made re: Tamoxifen and Ocular Toxicity. While most get vision sides with clomid it could be specuated that an anti oxidant would help alleviate this with clomid as it did here with nolvadex. Enjoy and RIP Nandi:

Tamoxifen, ocular toxicity, & oxidative stress

The article linked to below proposes that the ocular damage caused by tamoxifen is due to oxidative stress. The authors suggest that the use of antioxidants may help prevent such damage.

Exp Biol Med (Maywood). 2004 Jul;229(7):607-15.

Oxidative stress plays an important role in the pathogenesis of drug-induced retinopathy.

Toler SM.

Clinical Safety and Risk Management, Pfizer Inc., Pfizer Global Research and Development, 50 Pequot Avenue, New London, CT 06320. [email protected]

Several pharmaceutical agents have been associated with rare but serious retinopathies, some resulting in blindness. Little is known of the mechanism(s) that produce these injuries. Mechanisms proposed thus far have not been embraced by the medical and scientific communities. However, preclinical and clinical data indicate that oxidative stress may contribute substantially to iatrogenic retinal disease. Retinal oxidative stress may be precipitated by the interaction of putative retinal toxins with the ocular redox system. The retina, replete with cytochromes P450 and myeloperoxidase, may serve to activate xenobiotics to oxidants, resulting in ocular injury. These activated agents may directly form retinal adducts or may diminish ocular reduced glutathione concentrations. Data are reviewed that suggest that indomethacin, tamoxifen, thioridazine, and chloroquine all produce retinopathies via a common mechanism-they produce ocular oxidative stress

Full article can be accessed here:

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Originally posted by Nandi

[jimmyinkedup]

btw a tid bit. Nandi is THE SOURCE for e2 managment being the key to gyno control. Years ahead of his time he touted and supported the position with solid references when it came to the myth of prolactin or progesterone induced gyno....

[austinite]

Thanks for the mention, Jimmy.

I really wish I would have had the pleasure of meeting this great man. I would have settled for online interaction. I hear nothing but good things, from multiple places, and I've read enough from him to know what an outstanding advocate for everyone's health and education he was. He certainly made an impact on the industry as a whole. Great leader with many followers.

Thank you for starting this thread. RIP Nandi.

Subscribed.

[marcus300]

Legend and defiantly ahead of his time

[jimmyinkedup]

Austin woulldnt be right based on your knowledge and contributions not to mention you man. ...and you Marcus. The man really was a pioneer and a genius imo. I have learned more from reading him then I have from duchaine or anyone else. He supported EVERYTHING with rock solid refs as well. Astounding.

[jimmyinkedup]

Another Gem by Nandi. This was posted in 2003. Think about that. Think about how far ahead of his time this guy was and how true these still ring:

I compiled a short list off the top of my head based on posts and threads that appear regularly on this board. Some of these may be better characterized as controversial rather than false, but I'd like to hear your ideas.

1) The use of thyroid hormone damages the thyroid

See mind and muscle #10

2) GH administration builds muscle mass

No studies have ever confirmed this. Several have refuted it. Hepatic IGF-1 is probably not important to muscle growth

3) Estrogen promotes fat accumulation

Estrogen has been shown to be both anorectic and lipolytic, the latter via reduction of lipoprotein lipase levels

4) Aromatase inhibitors and SERMS reduce the anabolic effects of steroids

Again, there is no research to support this. The effect is claimed to be due to reduction in IGF-1. As mentioned, hepatic IGF-1 is probably relatively unimportant for muscle growth

5) Proviron prevents gynecomastia

This is based on the fact that Proviron is 5 alpha reduced, like DHT. Numerous other AAS are 5 alpha reduced and they are not claimed to prevent gyno. Proviron has never been used in a study to treat or prevent gyno

6) Winstrol prevents "progestigenic gyno"

There is no evidence that synthetic progestigenic androgens cause gyno, or even contribute to it. Winstrol has been shown to be a progesterone receptor agonist in the one study that looked at this effect

7) Insulin use damages your pancreas

Insulin is routinely used in type 2 diabetes to lower blood sugar. It has not been shown to harm the pancreas in these patients or in any other subjects.

8) Antiestrogens prevent bloat from AAS use

Rather than a myth, this is probably better called a half truth. Androgens can directly promote water retention without aromatizing

9) Androgen receptors need to be "cleaned out" periodically

Androgen receptors are continually being turned over in the body. There is no need to clean out existing receptors because they only have a halflife of a few hours

[Sgt. Hartman]

Wow. Nice find jimmy.

[jimmyinkedup]

Are the cardiac effects of AAS use reversible?

Heart. 2004 May;90(5):496-501.

Are the cardiac effects of anabolic steroid abuse in strength athletes reversible?

Urhausen A, Albers T, Kindermann W.

Institute of Sports and Preventive Medicine, University of Saarland Saarbruecken, Germany. [email protected]

OBJECTIVE: To investigate the reversibility of adverse cardiovascular effects after chronic abuse of anabolic androgenic steroids (AAS) in athletes. METHODS: Doppler echocardiography and cycle ergometry including measurements of blood pressure at rest and during exercise were undertaken in 32 bodybuilders or powerlifters, including 15 athletes who had not been taking AAS for at least 12 months (ex-users) and 17 currently abusing AAS (users), as well as in 15 anabolic-free weightlifters. RESULTS: Systolic blood pressure was higher in users (mean (SD) 140 (10) mm Hg) than in ex-users (130 (5) mm Hg) (p < 0.05) or weightlifters (125 (10) mm Hg; p < 0.001). Left ventricular muscle mass related to fat-free body mass and the ratio of mean left ventricular wall thickness to internal diameter were not significantly higher in users (3.32 (0.48) g/kg and 42.1 (4.4)%) than in ex-users (3.16 (0.53) g/kg and 40.3 (3.8)%), but were lower in weightlifters (2.43 (0.26) g/kg and 36.5 (4.0)%; p < 0.001). Left ventricular wall thickness related to fat-free body mass was also lower in weightlifters, but did not differ between users and ex-users. Left ventricular wall thickness was correlated with a point score estimating AAS abuse in users (r = 0.49, p < 0.05). In all groups, systolic left ventricular function was within the normal range. The maximum late transmitral Doppler flow velocity (Amax) was higher in users (61 (12) cm/s) and ex-users (60 (12) cm/s) than in weightlifters (50 (9) cm/s; p < 0.05 and p = 0.054). CONCLUSIONS: Several years after discontinuation of anabolic steroid abuse, strength athletes still show a slight concentric left ventricular hypertrophy in comparison with AAS-free strength athletes.

On the other hand,

Int J Sports Med. 2003 Jul;24(5):344-51. Related Articles, Links


Prospective echocardiographic assessment of androgenic-anabolic steroids effects on cardiac structure and function in strength athletes.

Hartgens F, Cheriex EC, Kuipers H.

Netherlands Centre for Doping Affairs, Capelle aan den IJssel, The Netherlands. [email protected]

Since the abuse of androgenic-anabolic steroids (AAS) has been associated with the occurrence of serious cardiovascular disease in young athletes, we performed two studies to investigate the effects of short-term AAS administration on heart structure and function in experienced male strength athletes, with special reference to dose and duration of drug abuse. In Study 1 the effects of AAS were assessed in 17 experienced male strength athletes (age 31 +/- 7 y) who self-administered AAS for 8 or 12 - 16 weeks and in 15 non-using strength athletes (age 33 +/- 5 y) in a non-blinded design. In Study 2 the effects of administration of nandrolone decanoate (200 mg/wk i. m.) for eight weeks were investigated in 16 bodybuilders in a randomised double blind, placebo controlled design. In all subjects M-mode and two-dimensional Doppler-echocardiography were performed at baseline and after 8 weeks AAS administration. In the athletes of Study 1 who used AAS for 12 - 16 weeks a third echocardiogram was also made at the end of the AAS administration period. Echocardiographic examinations included the determination of the aortic diameter (AD), left atrium diameter (LA), left ventricular end diastolic diameter (LVEDD), interventricular septum thickness (IVS), posterior wall end diastolic wall thickness (PWEDWT), left ventricular mass (LVM), left ventricular mass index (LVMI), ejection fraction (EF) and right ventricular diameter (RVD). For assessment of the diastolic function measurements of E and A peak velocities and calculation of E/A ratio were used. In addition, acceleration and deceleration times of the E-top (ATM and DT, respectively) were determined. For evaluation of factors associated with stroke volume the aorta peak flow (AV) and left ventricular ejection times (LVET) were determined. In Study 1 eight weeks AAS self-administration did not result in changes of blood pressure or cardiac size and function. Additionally, duration of AAS self-administration did not have any impact on these parameters. Study 2 revealed that eight weeks administration of nandrolone decanoate did not induce significant alterations in blood pressure and heart morphology and function. Short-term administration of AAS for periods up to 16 weeks did not lead to detectable echocardiographic alterations of heart morphology and systolic and diastolic function in experienced strength athletes The administration regimen used nor the length of AAS abuse did influence the results. Moreover, it is concluded that echocardiographic evaluation may provide incomplete assessment of the actual cardiac condition in AAS users since it is not sensitive enough to detect alterations at the cellular level. Nevertheless, from the present study no conclusions can be drawn of the cardiotoxic effects of long term AAS abuse.

[songdog]

Good job JimmY!