[GUIDE]: Preventing Cardiovascular & Neurotoxic effects of AAS via Antioxidants

ChemBB

Member
After my heart scare, I've been slowly accumulating research on compounds to help reduce/prevent damage from AAS.

There is mounting evidence that the majority of adverse effects of AAS are by-products of oxidative damage/stress.

Here is the collection of papers I've been able to find on using specific anti-oxidants to prevent/reduce impact on various organs:
(Personally, I was already taking Taurine and Ashwagandha, but I've ordered ALA, NAC, and ALCAR.)

Quick Overview by Compound
  • TaurineNandrolone models
    Signals: ↓ systolic BP; blunts ACE; ↑ NOx; normalizes hypercoagulability; multi-organ histology improvements
    Mechanisms: RAAS/NO modulation; mild antiplatelet effects
  • α-Lipoic Acid (ALA)Nandrolone & methandienone models
    Signals: ↓ renal oxidative stress & injury; ↓ cardiac injury markers; neurobehavioral rescue when paired with pentoxifylline
    Mechanisms: Antioxidant; ↑ Nrf2/HO-1; ↓ NF-κB/TNF-α
  • N-Acetylcysteine (NAC)Nandrolone model
    Signals: ↓ cardiac apoptosis & DNA damage; ↓ TLR4–NF-κB–NLRP3 activation; ↓ CK-MB/LDH
    Mechanisms: Glutathione repletion; inflammasome down-modulation
  • MelatoninStanozolol model + exercise stress
    Signals: Prevents BP rise; improves ECG axis; boosts cardiac antioxidative enzymes
    Mechanisms: Antioxidant; autonomic/circadian modulation
  • AshwagandhaNandrolone neurotoxicity model
    Signals: ↓ neuronal cell death; ↓ prodynorphin mRNA; ↓ AChE; histologic neuroprotection
    Mechanisms: Antioxidant/anti-excitotoxic; cholinergic normalization
  • Silymarin ± “Antox” (Se + vit A/C/E)Nandrolone hepatic/renal models
    Signals: Best overall improvements when combined (enzymes, urea/Cr, histology)
    Mechanisms: Multi-antioxidant synergy; membrane stabilization
  • Silymarin + FenugreekNandrolone myopathy model
    Signals: Ameliorates cardiac & skeletal muscle damage; combo favorable
    Mechanisms: Antioxidant/anti-inflammatory
  • Curcumin (nano ferrite–chitosan–curcumin NPs)Nandrolone nephrotoxicity
    Signals: Improved renal function, redox status, and inflammation (nano-formulation > standard)
    Mechanisms: Free-radical scavenging; ↓ TNF-α/PCNA
  • Damiana ExtractTrenbolone hepatic/renal model
    Signals: Improved ALT/AST, urea/Cr; restored SOD/CAT/GSH; better histology
    Mechanisms: Antioxidant/anti-inflammatory; membrane stabilization

AgentAAS modelModel & dosing (abridged)Primary endpointsOutcome (protective?)Mechanistic notesSource
AshwagandhaNandroloneMale rats; ND regimen (brain injury model); WS extract alongside NDHippocampal histology; cell death; prodynorphin mRNA; AChE activity↓ cell death; ↓ prodynorphin mRNA; ↓ AChE; histology improved → neuroprotectionAntioxidant / anti-excitotoxic; cholinergic normalizationhttps://op.niscair.res.in/index.php/IJTK/article/view/30919/465479530 (Withania somnifera ameliorates nandrolone-decanoate-induced brain damage in rats by inhibiting cell death, prodynorphin mRNA expression and acetylcholinesterase activity)
Damiana extractTrenboloneMale rats; Tren ± DamianaSerum ALT/AST, urea/creatinine; hepatic/renal histology; SOD/CAT/GSH/MDAImproved liver/kidney tests; restored antioxidant enzymes; histology improvedAntioxidant / anti-inflammatory; membrane stabilizationAmeliorating Effect of Damiana (Turnera Diffusa) Extract against Trenbolone-induced Nephrotoxicity and Hepatotoxicity in Male Albino Rats
Nano ferrite–chitosan–curcumin NPsNandrolone48 rats; ND 25 mg/kg/wk ×4; then CurNPs 50 mg/kg q48h ×2 wk or NF-CH-CurNPs 24 mg/kg q48h ×2 wkUrea/Cr, electrolytes; MDA, CAT/SOD/GSH; PCNA, TNF-α; renal histologyBoth nano-formulations improved renal function, redox status, inflammation; NF-CH-CurNPs bestFree-radical scavenging; anti-inflammatory (↓TNF-α, ↓PCNA)Ameliorating and therapeutic impact of nano ferrite-chitosan-curcumin nanoparticles against nandrolone decanote induced renal toxicity, inflammation, and oxidative stress in male rats
Silymarin + “Antox” (Se + vit A/C/E)Nandrolone110 rats; ND 7.93 or 11.9 mg/kg; 8 wk ± silymarin and/or AntoxBody/organ weights; ALT/AST, bilirubin; urea/Cr; liver/kidney histologyCombo Silymarin+Antox gave largest improvements (enzymes, urea/Cr, histology)Multi-antioxidant / free-radical-scavenging synergyEffect of Nandrolone Decanoate (Anabolic Steroid) on the Liver and Kidney of Male Albino Rats and the Role of Antioxidant (Antox-Silymarin) as Adjuvant Therapy
Silymarin + FenugreekNandroloneAdult male rats; ND cardiotoxicity model ± silymarin and/or fenugreekCardiac/skeletal muscle histology; oxidative stress markersBoth agents ameliorated ND-induced myopathy; combo favorableAntioxidant / anti-inflammatoryThe toxic effects of anabolic steroids “nandrolone decanoate” on cardiac and skeletal muscles with the potential ameliorative effects of silymarin and fenugreek seeds extract in adult male albino rats
MelatoninStanozololRats; STA 5 mg/kg s.c. 5 d/wk ×6 wk; melatonin 10 mg/kg i.p. 5 d/wkBP, ECG axis; cardiac SOD/CATMelatonin prevented BP rise and axis deviation; modulated CATAntioxidant; autonomic modulationMelatonin Reduces Oxidative Stress and Cardiovascular Changes Induced by Stanozolol in Rats Exposed to Swimming Exercise
TaurineNandrolone32 rats; 12 wk ND ± taurine in drinking waterSystolic BP, ACE activity, NOxTaurine prevented ND-induced BP rise and blunted ACE activityRAAS modulation; NO biologyImpact of chronic administration of anabolic androgenic steroids and taurine on blood pressure in rats
TaurineNandroloneRats; chronic ND ± taurineThromboelastography (R, K, α, CI); clot lysisND induced hypercoagulability; taurine normalized clot kineticsAnti-platelet / antithrombotic actionsInfluence of chronic administration of anabolic androgenic steroids and taurine on haemostasis profile in rats: a thrombelastographic study
TaurineNandrolone40 rats; control, taurine, ND, ND+taurineCK-MB; testicular MDA/SOD/TNF-α; hippocampal/heart/testis histology & IHCTaurine attenuated ND toxicity across biochemical & histologic endpointsROS/RNS quenching; anti-inflammatoryAmeliorative Effect of Taurine on Nandrolone Decanoate Induced Toxicity on Brain, Heart and Testis in Adult Male Albino Rats
TaurineNandrolone30 rats; 8 wk ND ± taurineLiver enzymes; histologyPartial hepatoprotection reportedAntioxidantEffect of Nandrolone Decanoate on the liver of Adult Male Albino Rats and the Possible ameliorating role Of Taurine
α-Lipoic acid (ALA) ± PentoxifyllineNandroloneRats; ND 15 mg/kg q3d; ALA 100 mg/kg p.o.; PTX 200 mg/kg i.p.Open-field, water maze, aggression; monoamines/GABA/ACh; MDA, TNF-α, AChE; Nrf2/HO-1, TNFR1ND: anxiety, memory deficits, aggression, oxidative/inflammatory changes; ALA+PTX reversed↑Nrf2/HO-1; ↓TNF-α/TNFR1; antioxidant & anti-inflammatoryLipoic acid and pentoxifylline mitigate nandrolone decanoate-induced neurobehavioral perturbations in rats via re-balance of brain neurotransmitters, up-regulation of Nrf2/HO-1 pathway, and down-regulation of TNFR1 expression
α-Lipoic acid (ALA)NandroloneRat ND nephrotoxicity model ± ALASerum urea/Cr; renal MDA; antioxidant enzymes; histologyALA attenuated ND nephrotoxicityAntioxidant; possible NF-κB dampeningBIOCHEMICAL AND HISTOPATHOLOGICAL ASPECTS OF NANDROLONE DECANOATE NEPHROTOXICITY AND POTENTIAL IMPACT OF ALPHA LIPOIC ACID
α-Lipoic acid (ALA)Dianabol (Methandienone)20 rabbits; Methandienone 0.35 mg/kg ± ALA 10 mg/kg p.o.CPK, CRP, troponin; heart/aorta histologyALA lowered cardiac injury markers; histology improvedAntioxidant / anti-inflammatoryhttps://www.ejhm.journals.ekb.eg/article_287317.html (The Essential Role of Alpha Lipoic Acid on the Cardiovascular System in Rabbits Subjected to Methandienone Administration)
N-acetylcysteine (NAC)Nandrolone18 rats; Control, ND, NAC+ND (6 wk)Cardiac TUNEL apoptosis; 8-OHdG; TLR4/NF-κB/NLRP3; CK-MB/LDHND ↑ apoptosis, DNA damage, TLR4-NF-κB-NLRP3, injury enzymes; NAC reduced allGlutathione repletion; TLR4-NF-κB-NLRP3 down-modulationNandrolone decanoate induces heart injury via oxidative damage and mitochondrial apoptotic pathway by regulation of TLR4/NF-κB/NLRP3 axis in male rats: The rescue effect of N-acetylcysteine
 
Inject glut or NAC.

That sounds a bit pricey compared to just drinking raw powdered ALA/ALCAR/NAC/Taurine

Also, each of these compounds has unique/complementary mechanisms, as there's not just a blanket "anti-oxidant" mechanism.
 
Interesting, thanks. What is your dose of taurine? Have you started using NAC?
 
I have been taking just 1 500mg NAC capsule a day for allergies. I can't finish my meals. Has anyone else experienced similar?
 
What is your dose of taurine? Have you started using NAC?
I take 3g in the AM with my morning pills, and then another 3g a few hours later pre-workout.

NAC I recently started, 1,200mg pre-bed.

My current antioxidant stack is:

- 3g + 3g Taurine
- 600mg ALA
- 1,200mg NAC
- 1,000mg Vitamin C
- 400mg Pomegranate Extract (POMELLA)

Also take 3g ALCAR + 20-25g Creatine pre-workout

Wouldn't it be better to focus on statins and ARBs which are proven to reduce inflammation in the arteries?
It's not an either-or scenario. I'd hope that everyone using AAS in BB'ing doses is taking medications for LDL and BP.

Plus, oxidative stress is a systemic thing -- it causes a whole host of issues across various tissues/organs.
 
Thanks. What's your thinking on NAC vs injectable Glutathione?

Thats a lot of creatine. Is that based on the more recent idea of higher doses for the brain?
 
I have loaded up on injectable Glutathione - arrived from Korea faster than the pre-workout I ordered from Amazon. Great price also. Have some other brands to get through first. Will be pinning it pre-workout when I do my L-Car MWF.

Thanks for starting this thread @ChemBB - incredibly important topic (obvi)
 
Thanks. What's your thinking on NAC vs injectable Glutathione?
I've not used or read much on inj. Glutathione, but my understanding is it's about the most potent thing you can get.

Is that based on the more recent idea of higher doses for the brain?
Yes exactly. Don't have any negative effects from it, and Creatine is so cheap it costs basically nothing to take 20-25g a day of unflavored
 
idk if this been mentioned.

but ofc you can take all of this but still have dogshit cholesterol/blood pressure.

make sure to to control those 2 with whatever medications you want if you're getting trouble from aas and you're golden. its upto genetics then.

you can also add glps for better cardiovascular health

"The GLP-1 receptor is present on multiple cardiovascular cell types, including cardiomyocytes, endothelial cells, and smooth muscle cells, allowing the hormone to exert direct protective effects"

"GLP-1 receptor agonists (GLP-1 RAs) have been shown to significantly lower the risk of a composite of cardiovascular death, nonfatal heart attack, or nonfatal stroke"

"Clinical trials have demonstrated that GLP-1 RAs can improve exercise capacity and reduce levels of NT-proBNP in patients with heart failure, suggesting a role in managing HF symptoms"

"GLP-1 RAs have been found to have anti-inflammatory effects and reduce atherosclerotic risk by impacting cells like macrophages and smooth muscle cells in the artery walls"

this is just on glp-1 receptor. gip offers some more benefits for the heart but we dont understand it yet, and the "bad" speculating effects of gccr yet
 
I have loaded up on injectable Glutathione - arrived from Korea faster than the pre-workout I ordered from Amazon. Great price also. Have some other brands to get through first. Will be pinning it pre-workout when I do my L-Car MWF.

Thanks for starting this thread @ChemBB - incredibly important topic (obvi)
I need to look into this but I've came across the Korea link to inj Glutathione before. Is it thought to be superior?
 
idk if this been mentioned.

but ofc you can take all of this but still have dogshit cholesterol/blood pressure.

make sure to to control those 2 with whatever medications you want if you're getting trouble from aas and you're golden. its upto genetics then.

you can also add glps for better cardiovascular health

"The GLP-1 receptor is present on multiple cardiovascular cell types, including cardiomyocytes, endothelial cells, and smooth muscle cells, allowing the hormone to exert direct protective effects"

"GLP-1 receptor agonists (GLP-1 RAs) have been shown to significantly lower the risk of a composite of cardiovascular death, nonfatal heart attack, or nonfatal stroke"

"Clinical trials have demonstrated that GLP-1 RAs can improve exercise capacity and reduce levels of NT-proBNP in patients with heart failure, suggesting a role in managing HF symptoms"

"GLP-1 RAs have been found to have anti-inflammatory effects and reduce atherosclerotic risk by impacting cells like macrophages and smooth muscle cells in the artery walls"

this is just on glp-1 receptor. gip offers some more benefits for the heart but we dont understand it yet, and the "bad" speculating effects of gccr yet
Very interesting. Need to schedule a deep dive on this. 'gccr' bad effects...I will look into this whats the basic speculation?
 
Very interesting. Need to schedule a deep dive on this. 'gccr' bad effects...I will look into this whats the basic speculation?
its me who cant spell. but gcg-r the gcg receptor reta plays on.

it can both be bad and good for heart. no telling yet without enough data.

phase 3 trials come out in 2026-27
 
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Very interesting. Need to schedule a deep dive on this. 'gccr' bad effects...I will look into this whats the basic speculation?

GLP-1 is the heavy hitter, with nearly 40 years of evidence it's the "fountain of youth" receptor in countless tissues. There are some links from an old post of mine below.

GIP plays a minor role in similar processes.

Glucagon, on the other hand, has a pile of failed drugs that tried to utilize it (for "free" calorie burn basically) in the trash heap because it proved to be dangerous. Reta managed to utilize it in a balanced way with GLP and GIP that finally did more good than harm, but I kind of wonder what's going on with Lily dragging their feet on bringing Reta to the market, and the very latest GLPs in development moving on from glucagon as the magic ingredient to other things (mostly related to muscle retention and growth).

GLP receptors are everywhere, and it seems when activated, they improve the associated organ in function, protect against further degeneration. and in many cases reverse existing damage.

Liver


Heart


Nerves

(eyes specifically, but the protective and regeneration mechanism has been observed in nerves generally throughout the body. A "rare development" in the prevention and treatment of vision loss.)


Brain

("clear clinical improvement" in patients with neurodegenerative conditions)

 
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GLP-1 is the heavy hitter, with nearly 40 years of evidence it's the "fountain of youth" receptor in countless tissues. There are some links from an old post of mine below.

GIP plays a minor role in similar processes.

Glucagon, on the other hand, has a pile of failed drugs that tried to utilize it (for "free" calorie burn basically) in the trash heap because it proved to be dangerous. Reta finally managed to utilize it in a balanced way with GLP and GIP that finally did more good than harm, but I kind of wonder what's going on with Lily dragging their feet on bringing Reta to the market, and the very latest GLPs in development moving on from glucagon as the magic ingredient to other things (mostly related to muscle retention and growth).
As popular as Reta is, I see it as the Ferrari 458 Italia. For some, it’s THE car (in red only). But it’s just another accomplishment that eventually led to the development of the la Ferrari and all the subsequent innovations. I think years down the line people will still be using Reta but there will be better options that do even more (likely orally also). What I can say is that I tolerate Reta much better than tirz. With Tirz I was getting 24-36 Hours of post injection fatigue / malaise once I hit the 5 mg dosage. After a month of that and 2 weeks on the 7.5 I switched to Reta and feel much better. However, I do find I have a bit more reflux on Reta, but I can at least tolerate some dietary fat. On tirz if I tried to eat a steak or even a piece of fish prepared at a restaurant (with some olive oil) it was instant diarrhea. If tirz was all that I had available I’d be fine but I much much prefer Reta. I’ve also noticed some better blood markers on Reta. After only a few weeks of 2 mg my fasting glucose dropped 25% compared to what it was on 7.5 tirz.

This is an embarrassment of riches. Even if sema was all we had we’d be way ahead of the game
 

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