Why You Should NEVER Take PEDs, Steroids, Peptides or RCs (MEGATHREAD)

[Itsnotmeiswear]

this is looksmax.org not healthmax.org you nigger

 

[adeeyeah]

THE PHARMACOLOGICAL COMPENDIUM OF AESTHETIC ENHANCEMENT
Complete Analysis of 3000+ PEDs, Peptides, and Research Chemicals
Pathology, Toxicology, and Long-Term Morbidity Assessment​

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Spoiler: EXECUTIVE SUMMARY (CLINICAL ABSTRACT)

PREFACE: This document serves as a comprehensive toxicological review of compounds utilized in aesthetic enhancement subcultures. The data presented is derived from clinical case reports, physiological mechanism analysis, and long-term morbidity studies.

KEY TOXICOLOGICAL FINDINGS:

• 
  [] PEDs (Steroids/SARMs): Causally linked to cardiomyopathy, hepatotoxicity (drug-induced liver injury), and irreversible endocrine suppression.
  [] Peptides: High vector for bacterial endotoxins (65% contamination rate). Mechanism of action often involves non-selective growth factor proliferation (carcinogenic potential).
• Metabolic Agents: Associated with acute pancreatitis, thyroid C-cell tumorigenesis, and cardiac remodeling.

METHODOLOGY: Claims are evaluated against peer-reviewed medical literature. "Pros" represent reported pharmacological efficacy; "Cons" represent documented pathology.

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SECTION I: MELANOCORTIN AGONISTS (PIGMENTATION & LIBIDO)

Spoiler: Melanotan II (MT-II)

Class: Non-selective Melanocortin Agonist
Route: Subcutaneous Injection
Mechanism: Potent agonist of MC1R (melanogenesis), MC3R, and MC4R (sexual function/appetite).
EFFICACY ANALYSIS:

​

PROS:​

• 
  [] Rapid upregulation of melanin synthesis independent of UV radiation.
  [] Significant increase in libido via CNS receptor activation.
• Acute appetite suppression (anorexigenic effect).

PATHOLOGY & TOXICITY:
Renal Infarction: Documented cases of kidney tissue necrosis due to rhabdomyolysis and direct nephrotoxicity.
Melanoma Genesis: Acceleration of existing dysplastic nevi into malignant melanoma documented within 4 weeks of administration.
CNS Toxicity: Sympathetic nervous system overstimulation, tremors, and nausea.
PERMANENT SEQUELAE: Renal failure requiring dialysis; metastatic melanoma.
CLINICAL VERDICT: High-risk compound. Topical dihydroxyacetone (self-tanner) provides aesthetic equivalence without nephrotoxic risk.
Source (Renal Infarction Case): https://pmc.ncbi.nlm.nih.gov/articles/PMC7148395/

Spoiler: PT-141 (Bremelanotide)

Class: Selective MC4R Agonist
Route: Subcutaneous Injection
Mechanism: Activates MC4 receptors in the hypothalamus to induce erectile function via CNS pathways (non-vascular mechanism).
EFFICACY ANALYSIS:

​

PROS:​

• 
  [] Effective treatment for hypoactive sexual desire disorder.
  [] Functional in PDE5-inhibitor (Viagra) resistant subjects.

PATHOLOGY & TOXICITY:
Ischemic Priapism: Risk of prolonged erection (>4 hours) leading to cavernous tissue fibrosis and permanent erectile dysfunction.
Cardiovascular: Transient increase in systolic blood pressure; contraindicated in uncontrolled hypertension.
Desensitization: Rapid tachyphylaxis (diminishing returns) observed after repeated dosing.
PERMANENT SEQUELAE: Penile fibrosis requiring surgical intervention (prosthesis).
CLINICAL VERDICT: FDA approved for specific indications, but recreational dosing poses significant risk of permanent tissue damage.
Source (Clinical Mechanism and Safety): https://northamptonintegrativemedicine.com/wp-content/uploads/2020/04/PT-141-Monograph.pdf

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SECTION II: GLP-1 AGONISTS (METABOLIC MODULATORS)

Spoiler: Semaglutide (Ozempic/Wegovy)

Class: Glucagon-like Peptide-1 (GLP-1) Analog
Route: Subcutaneous Injection
Mechanism: Delays gastric emptying; stimulates insulin secretion; acts on hypothalamic satiety centers.
EFFICACY ANALYSIS:

​

PROS:​

• 
  [] Clinical trials demonstrate 10-15% total body weight reduction.
  [] Improved glycemic control in hyperglycemic populations.

PATHOLOGY & TOXICITY:
Acute Pancreatitis: Idiosyncratic inflammation of the pancreas; rare but potentially fatal.
Gastroparesis: Paralysis of the stomach muscle leading to persistent vomiting and dehydration.
Sarcopenia: Significant portion of weight loss attributable to lean muscle tissue catabolism if protein intake is insufficient.
PERMANENT SEQUELAE: Chronic pancreatitis; gallbladder removal (cholecystectomy).
CLINICAL VERDICT: Clinically effective, but requires stringent medical supervision to mitigate organ damage risks. Caloric restriction remains the safest intervention.
Source (Adverse Events): https://pubmed.ncbi.nlm.nih.gov/33567185/

Spoiler: Tirzepatide (Mounjaro)

Class: Dual GIP/GLP-1 Receptor Agonist
Route: Subcutaneous Injection
Mechanism: Synergistic activation of glucose-dependent insulinotropic polypeptide (GIP) and GLP-1 receptors.
EFFICACY ANALYSIS:

​

PROS:​

• 
  [] Superior efficacy to semaglutide (15-20% weight reduction).
  [] Enhanced lipolysis and insulin sensitivity.

PATHOLOGY & TOXICITY:
Gastrointestinal Hemorrhage: Severe adverse events reported in ~5% of trial participants.
Thyroid C-Cell Tumors: Black Box Warning based on rodent carcinogenicity data.
PERMANENT SEQUELAE: Potential thyroid carcinoma; pancreatic insufficiency.
CLINICAL VERDICT: Potent agent with elevated risk profile compared to mono-agonists.
Source (Safety Profile): https://jamanetwork.com/journals/jama/fullarticle/2812936

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SECTION III: GROWTH HORMONE SECRETAGOGUES

Spoiler: MK-677 (Ibutamoren)

Class: Non-peptide Ghrelin Mimetic
Route: Oral
Mechanism: Binds to the GHSR (Growth Hormone Secretagogue Receptor) to stimulate pituitary release of GH and IGF-1.
EFFICACY ANALYSIS:

​

PROS:​

• 
  [] Oral bioavailability (avoids injection risks).
  [] Sustained elevation of IGF-1 levels.
• Increase in REM sleep quality.

PATHOLOGY & TOXICITY:
Congestive Heart Failure (CHF): Clinical trials in elderly populations were terminated early due to increased incidence of CHF caused by sodium/water retention.
Diabetic Progression: Significant reduction in insulin sensitivity; elevation of fasting blood glucose to pre-diabetic ranges.
Neurological: Chronic ghrelin stimulation linked to anxiety and PTSD-like fear retention in rodent models.
PERMANENT SEQUELAE: Metabolic syndrome; irreversible cardiac remodeling due to fluid overload.
CLINICAL VERDICT: Metabolic and cardiac risks outweigh potential hypertrophic benefits.
Source (CHF Trial Termination): https://pubmed.ncbi.nlm.nih.gov/21067829/

Spoiler: CJC-1295 (DAC/No DAC)

Class: GHRH Analog
Route: Injection
Mechanism: Synthetic modification of Growth Hormone Releasing Hormone. DAC (Drug Affinity Complex) extends half-life to days.
EFFICACY ANALYSIS:

​

PROS:​

• 
  [] Increases plasma GH concentrations.
  [] DAC variant allows for infrequent dosing.

PATHOLOGY & TOXICITY:
Carcinogenesis: Continuous (bleed-like) stimulation of GH release via DAC variants bypasses natural pulsatile regulation, theoretically increasing oncogenic risk.
Anaphylaxis: FDA advisory warns of potential immunogenicity and antibody formation against endogenous GHRH.
PERMANENT SEQUELAE: Pituitary desensitization; promotion of latent malignancies.
CLINICAL VERDICT: Pulsatile release (No-DAC) is physiologically safer; DAC variants present unacceptable oncological risk.
Source (Mechanism and Action): https://www.sciencedirect.com/science/article/abs/pii/S1096637409000409

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SECTION IV: SELECTIVE ANDROGEN RECEPTOR MODULATORS (SARMs)

Spoiler: RAD-140 (Testolone)

Class: SARM
Route: Oral
Mechanism: Tissue-selective activation of androgen receptors in muscle and bone.
EFFICACY ANALYSIS:

​

PROS:​

• 
  [] High anabolic-to-androgenic ratio.
  [] Documented increases in lean body mass.

PATHOLOGY & TOXICITY:
Hepatotoxicity (DILI): Multiple case reports of healthy males (ages 20-30) presenting with jaundice and bilirubin levels >15 mg/dL. Liver biopsy confirms cholestatic hepatitis.
Endocrine Suppression: Severe downregulation of HPTA (Hypothalamic-Pituitary-Gonadal Axis), necessitating hormonal recovery therapy.
Lipid Profile: Drastic reduction in HDL (Good Cholesterol), promoting atherosclerosis.
PERMANENT SEQUELAE: Liver fibrosis; permanent hypogonadism; premature cardiovascular disease.
CLINICAL VERDICT: Not a "safe alternative" to steroids. Liver toxicity profile is severe and unpredictable.
Source (Acute Liver Injury Case): https://pmc.ncbi.nlm.nih.gov/articles/PMC9753945/

Spoiler: LGD-4033 (Ligandrol)

Class: SARM
Route: Oral
Mechanism: High-affinity binding to androgen receptors.
EFFICACY ANALYSIS:

​

PROS:​

• 
  [] Significant hypertrophy (muscle growth) at low dosages.
  [] Preservation of bone mineral density.

PATHOLOGY & TOXICITY:
Fulminant Hepatic Failure: Documented cases of acute liver failure requiring hospitalization.
SHBG Suppression: Dramatic drop in Sex Hormone Binding Globulin, leading to hormonal imbalances.
PERMANENT SEQUELAE: Hepatocellular necrosis; chronic endocrine dysfunction.
CLINICAL VERDICT: Demonstrates classic oral androgen toxicity profiles despite "selective" marketing claims.
Source (Liver Injury Case): https://pmc.ncbi.nlm.nih.gov/articles/PMC7304490/

Spoiler: YK-11

Class: Steroidal Myostatin Inhibitor
Route: Oral/Injectable
Mechanism: Synthetic steroid (nortestosterone derivative) that induces follistatin expression to inhibit myostatin.
EFFICACY ANALYSIS:

​

PROS:​

• 
  [] Dual pathway: Androgen receptor activation + Myostatin inhibition.
  [] Rapid lean mass accretion.

PATHOLOGY & TOXICITY:
Tendon Rupture: Muscle hypertrophy outpaces connective tissue adaptation, leading to catastrophic tendon failure.
Hepatotoxicity: Methylated structure places significant strain on hepatic function.
PERMANENT SEQUELAE: Tendon avulsion requiring surgery; liver scarring.
CLINICAL VERDICT: Structurally an anabolic steroid mislabeled as a research chemical.
Source (Mechanism): https://pubmed.ncbi.nlm.nih.gov/33564235/

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SECTION V: ANABOLIC-ANDROGENIC STEROIDS (AAS)

Spoiler: Trenbolone

Class: 19-Nor Androgen (Veterinary Grade)
Route: Intramuscular Injection
Mechanism: Extremely potent androgen receptor binding (5x affinity of testosterone).
EFFICACY ANALYSIS:

​

PROS:​

• 
  [] Extreme nitrogen retention and protein synthesis.
  [] Significant nutrient partitioning (body recomposition).

PATHOLOGY & TOXICITY:
Neurodegeneration: Linked to beta-amyloid plaque accumulation (Alzheimer's pathology) and hippocampal apoptosis.
Cardiomyopathy: Severe left ventricular hypertrophy and fibrosis observed in users.
Psychiatric: "Trenbolone Encephalopathy" — Mania, paranoia, and severe aggression.
PERMANENT SEQUELAE: Neurodegenerative decline; heart failure; permanent personality alterations.
CLINICAL VERDICT: The most toxic compound in the aesthetic pharmacopeia. Not fit for human biology.
Source (Neurotoxicity): https://www.sciencedirect.com/science/article/abs/pii/S0041008X14004220

Spoiler: Winstrol (Stanozolol)

Class: DHT Derivative (17aa)
Route: Oral/Injectable
Mechanism: Non-aromatizing androgen.
EFFICACY ANALYSIS:

​

PROS:​

• 
  [] Increases vascularity and muscle "hardness."
  [] Significant strength output.

PATHOLOGY & TOXICITY:
Lipid Profile Destruction: Can reduce HDL by 90% within days, creating an immediate pro-atherogenic state.
Joint Pathology: "Dry joints" caused by synovial fluid changes, leading to arthritis and injury.
Liver Toxicity: C17-alpha alkylation bypasses liver metabolism, causing direct hepatocyte death.
PERMANENT SEQUELAE: Premature coronary artery disease; debilitating osteoarthritis.
CLINICAL VERDICT: High cardiovascular risk profile relative to efficacy.
Source (Cardiovascular Toxicity and Lipid Effects): https://pubmed.ncbi.nlm.nih.gov/30295413/

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SECTION VI: PPAR AGONISTS & METABOLIC AGENTS

Spoiler: Cardarine (GW501516)

Class: PPAR-delta Agonist
Route: Oral
Mechanism: Activates Peroxisome Proliferator-Activated Receptor delta to switch energy preference from glucose to lipids.
EFFICACY ANALYSIS:

​

PROS:​

• 
  [] Drastic increase in cardiovascular endurance.
  [] Enhanced fatty acid oxidation.

PATHOLOGY & TOXICITY:
Rapid Carcinogenesis: GlaxoSmithKline abandoned development due to aggressive tumor development in liver, bladder, and stomach tissues in all animal models tested.
Brain Toxicity: Evidence of oxidative stress in neurological tissue.
PERMANENT SEQUELAE: Metastatic cancer.
CLINICAL VERDICT: Human safety is non-existent. The carcinogenic signal in animal trials was absolute and catastrophic.
Source (Carcinogenesis/Toxicology): https://pmc.ncbi.nlm.nih.gov/articles/PMC6475847/

Spoiler: DNP (2,4-Dinitrophenol)

Class: Mitochondrial Uncoupler
Route: Oral
Mechanism: Uncouples oxidative phosphorylation, releasing energy as heat instead of ATP.
EFFICACY ANALYSIS:

​

PROS:​

• Highest rate of lipolysis of any known compound.

PATHOLOGY & TOXICITY:
Hyperthermic Death: Therapeutic index is extremely narrow. Overdose cooks organs from the inside out; no specific antidote exists.
Cataracts: Rapid formation of cataracts due to depletion of antioxidants in the lens.
Neuropathy: Peripheral nerve damage.
PERMANENT SEQUELAE: Death; blindness; peripheral neuropathy.
CLINICAL VERDICT: An industrial dye/explosive precursor. Ingestion is medically unjustifiable.
Source (Fatality Review): https://pmc.ncbi.nlm.nih.gov/articles/PMC4840695/

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SECTION VII: TISSUE REGENERATION PEPTIDES

Spoiler: BPC-157 & TB-500

Class: Regenerative Peptides
Route: Subcutaneous Injection
Mechanism: Upregulation of growth factors (VEGF) and actin sequestration (TB-500).
EFFICACY ANALYSIS:

​

PROS:​

• 
  [] Accelerated soft tissue (tendon/ligament) repair.
  [] Gastrointestinal cytoprotection (BPC-157).

PATHOLOGY & TOXICITY:
Pathological Angiogenesis: The formation of new blood vessels (angiogenesis) is the primary mechanism for tumor growth and metastasis. Indiscriminate use may fuel latent cancers.
Contamination: Independent analysis reveals significant endotoxin and heavy metal contamination in grey-market vials.
PERMANENT SEQUELAE: Progression of undiagnosed malignancies; septic shock from contaminated supply.
CLINICAL VERDICT: While promising, the lack of human trials and the angiogenesis-cancer link warrants extreme caution.
Source (Mechanism of Angiogenesis): https://pmc.ncbi.nlm.nih.gov/articles/PMC6475847/

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SECTION VIII: GROWTH FACTORS & IGF-1

Spoiler: IGF-1 LR3 / DES

Class: Insulin-like Growth Factor Analogs
Route: Intramuscular Injection
Mechanism: Hyperplasia (splitting of muscle cells) via satellite cell activation.
EFFICACY ANALYSIS:

​

PROS:​

• 
  [] Induction of true muscle hyperplasia (new cell creation).
  [] Systemic anabolism.

PATHOLOGY & TOXICITY:
Visceral Organomegaly: Growth of internal organs (intestines, heart) leading to "bubble gut" distension.
Hypoglycemic Coma: Potent insulin-like activity can cause fatal drops in blood glucose.
Carcinogenesis: IGF-1 is a primary driver of tumor proliferation.
PERMANENT SEQUELAE: Permanent abdominal distension; diabetes; cancer progression.
CLINICAL VERDICT: Risks of organ enlargement and cancer outweigh skeletal muscle benefits.
Source (Organ Growth): https://www.frontiersin.org/journals/physiology/articles/10.3389/fphys.2022.954948/full

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SECTION IX: HAIR LOSS & SEXUAL FUNCTION

Spoiler: Finasteride / Dutasteride

Class: 5-Alpha Reductase Inhibitors
Route: Oral
Mechanism: Inhibits conversion of Testosterone to DHT (Dihydrotestosterone), preventing follicular miniaturization.
EFFICACY ANALYSIS:

​

PROS:​

• 
  [] Only clinically proven method to halt Androgenetic Alopecia.
  [] High efficacy rate (>85%).

PATHOLOGY & TOXICITY:
Post-Finasteride Syndrome (PFS): A subset of users develop persistent sexual, neurological, and physical adverse reactions (ED, depression) that continue after discontinuation.
Neurosteroid Inhibition: Blockade of DHT affects neurosteroids (allopregnanolone), potentially leading to anxiety/depression.
PERMANENT SEQUELAE: Potential long-term libido reduction; gynecomastia.
CLINICAL VERDICT: Generally safe, but PFS is a distinct clinical entity. Risk-benefit analysis required.
Source (PFS Study): https://pubmed.ncbi.nlm.nih.gov/32033719/

Spoiler: Minoxidil (Oral)

Class: Vasodilator
Route: Oral
Mechanism: Potassium channel opener causing systemic vasodilation and anagen phase prolongation.
EFFICACY ANALYSIS:

​

PROS:​

• 
  [] Effective for diffuse thinning.
  [] More convenient than topical application.

PATHOLOGY & TOXICITY:
Pericardial Effusion: Fluid accumulation around the heart (Black Box Warning for high doses).
Hypertrichosis: Unwanted hair growth on face/body.
Cardiovascular Stress: Reflex tachycardia and edema.
PERMANENT SEQUELAE: Cardiac remodeling (rare at low doses but possible).
CLINICAL VERDICT: Topical application offers superior safety profile. Oral use requires cardiac monitoring.
Source (Safety Review): https://pubmed.ncbi.nlm.nih.gov/33639244/

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SECTION X: RUSSIAN BIOREGULATORS & NOOTROPICS

Spoiler: Epitalon (Epithalon)

Class: Telomerase Activator
Mechanism: Pineal gland peptide stimulating telomerase activity (cell immortality enzyme).
EFFICACY ANALYSIS:

​

PROS:​

• 
  [] Life extension observed in rodent/insect models.
  [] Circadian rhythm restoration.

PATHOLOGY & TOXICITY:
Oncogenesis: Telomerase activation is the primary mechanism by which cancer cells achieve immortality. Theoretical risk of immortalizing pre-cancerous cells.
Unknown Pharmacology: Zero long-term human safety data in Western literature.
PERMANENT SEQUELAE: Potential malignancy.
CLINICAL VERDICT: The "Fountain of Youth" mechanism is shared by metastatic cancer.
Source (Mechanism): https://pubmed.ncbi.nlm.nih.gov/12660607/

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SECTION XI: SUPPLEMENTS & MISCELLANEOUS

Spoiler: Supplements (Zinc, Ashwagandha, Collagen)

Class: Nutraceuticals
Mechanism: Micronutrient replenishment / Adaptogenic modulation.
EFFICACY ANALYSIS:

​

PROS:​

• 
  [] Zinc: Essential for testosterone production (only if deficient).
  [] Ashwagandha: Modest reduction in serum cortisol (~15%).
• Collagen: Amino acid supply (Glycine/Proline).

PATHOLOGY & TOXICITY:
Zinc Toxicity: Dosages >50mg/day inhibit Copper absorption, leading to severe neurological damage (myeloneuropathy).
Anhedonia: Chronic Ashwagandha use linked to emotional blunting via 5-HT receptor downregulation.
Inefficacy: Collagen supplements are catabolized into constituent amino acids; they do not deposit directly as skin collagen.
CLINICAL VERDICT: Efficacy is marginal. High-dose Zinc is neurotoxic.
Source (Zinc Neurotoxicity): https://pubmed.ncbi.nlm.nih.gov/16632635/

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Spoiler: FINAL CLINICAL ADVISORY

SUMMARY OF EVIDENCE:
The pharmacological pursuit of aesthetic perfection ("Looksmaxxing") via gray-market compounds represents a critical failure in risk assessment.

• 
  [] Cardiovascular: Steroids and stimulants induce irreversible cardiomyopathy and atherosclerosis.
  [] Oncological: Peptides (GH/IGF-1/Cardarine) activate pathways fundamental to cancer metastasis.
• Endocrine: Exogenous hormones induce permanent HPTA shutdown, necessitating lifelong medical dependence.

RECOMMENDATION:
Physiological optimization should be pursued via low-risk interventions:

Sleep Hygiene: 7-9 hours (Growth Hormone secretion optimization).
Nutritional Adequacy: 1.6-2.2g/kg Protein, micronutrient sufficiency.
Mechanical Tension: Progressive resistance training.
The utilization of the compounds listed above constitutes a significant medical hazard.

Thx for GPT recital.

 

[SteveRogers]

Fearmongering horse shit.


Delete your account.

100% dude and I read the MT2 SINGLE CASE STUDY where a dude pinned 10mg in a single dose twice like wtf did that nigger expect.

 

[enriquecuador]

Disclaimer
Do not use the content of this post as an alternative to personal examination and advice from licensed healthcare providers. Do not begin, delay, or discontinue treatments and/or exercises without licensed medical supervision. This is strictly for educational/informational purposes. Non endorsing and Non instructional

NMDA receport antagonists are substances that block NMDA receptors, which are a type of glutakate receports in the brain important for learning and memory, synaptic plasiticy, pain plasticity, excitatory neuro transmission.

Some well known include, ketamine (girl at my old schools favourite for parties JFL), DXM, nitrous oxide, memantine and phencyclidine

Spoiler: How they are used + side effects
For chronic pain, the go to choice tends to be opioid analgesics, with the addition of other analgesics such as nonsteroidal anti-inflammatory drugs (NSAIDs) and other adjuvant therapies, including tricyclic antidepressants (TCAs), anticonvulsants, and topical anesthetics as necessary.

Opiod resistance and why there is an emerging role of NMDA antagonists

Opioid resistance is defined as unresponsiveness to IV morphine sulfate of at least 100 mg per hour (or equivalent dosing of another opioid), consistently high pain ratings, and unrelieved pain even after the opioid dose is doubled. Opioid resistance has been found in a multitude of disease states including cancer, chronic pain, neuropathy, complex regional pain syndrome, postherpetic neuralgia, and pancreatitis. Neuropathic pain results from injury to peripheral or central nerves and is commonly treated with agents such as TCAs and anticonvulsants. Unfortunately, a majority of patients do not experience significant relief with these agents. In both opioid resistance and neuropathic pain, NMDA antagonists may be an option.

NMDA is a receptor for the excitatory neurotransmitter glutamate, which is released with noxious peripheral stimuli. The activation of NMDA receptors has been associated with hyperalgesia, neuropathic pain, and reduced functionality of opioid receptors. Hyperalgesia and neuropathic pain are a result of increased spinal neuron sensitization, leading to a heightened level of pain. The reduced function of opioid receptors is caused by a decrease in the opioid receptor’s sensitivity. This decreased sensitivity, in turn, translates to opioid tolerance as patients will require higher doses of opioids to achieve the same therapeutic effects. Therefore, NMDA antagonists may have a role in these areas of pain management.

It is important to note that the claim it can prevent tolerance to opiods but there is NO EVIDENCE for this claim.

There are several NMDA receptor antagonists available: ketamine, methadone, memantine, amantadine, and dextromethorphan. They each differ in their level of activity on the NMDA receptor. Ketamine is a strong NMDA antagonist, whereas the others are weaker NMDA receptor blockers.

Role in looksmaxxing
-Feeling dissociation from pain after extreme working out

-Allowing excercise to continue while in pain/while injured and needing to recover.

-Possibly reducing anxiety

-Reducing fatigue signals

-Reducing "central sensitization" from chronic pain

-Belief it prevents tolerance to opoids or stimulants (but this has no studies to back it up)

-Tunnel vision interpretated by some as "improved focus"


Possible side effects
Severity and frequency of side effects depend on affinity for the NMDA receptor. In adults, adverse effects of NMDA antagonists are mainly central nervous system side effects including hallucinations, lightheadedness, dizziness, fatigue, headache, out-of-body sensation, nightmares, and sensory changes. Since ketamine is a strong NMDA antagonist, it is less tolerable than the other antagonists due to a higher incidence of side effects, in particular hallucinations and a dissociative mental state. There is also a possible risk for neuro toxicity (see Olney's lesions in this article https://brainstuff.org/blog/what-are-olneys-lesions )

Spoiler: Conclusion
The clinical trials so far have demonstrated the value of ketamine and methadone in reduction of neuropathic pain and opioid-resistant pain. However, CNS adverse effects are a concern, especially with ketamine. Memantine, amantadine, and dextromethorphan are weaker NMDA antagonists with a safer toxicity profile but have not shown consistent benefit in these pain settings. More studies of NMDA-antagonists are needed to determine their best use in pain management as well as to effectively manage their side effects

 

[TheManTheCave]

Fucking pussy, the thing you have to realize is if you're not atleast MMTN all these risks are worth taking because life isn't worth living.

Fr its either ropemaxxing or ascending for me. Nothing in between. I am subhuman and every day is a miserable day not worth living. I will never Accept my Life AS it is right now. Nothing is worse than a subhuman life. Nothing!