Anabolic Steroids: Uses, Side Effects, And Alternatives

Anabolic Steroids – What They Are, How They’re Used, Their Benefits, Risks, and Legal Status

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1. What are anabolic steroids?

Anabolic steroids are synthetic derivatives of the male sex hormone testosterone.

Medical use: prescribed for conditions that cause low testosterone (hypogonadism), delayed puberty in boys, gitea.noname-studios.es certain types of anemia, and muscle wasting disorders.

Non‑medical use: taken by athletes, bodybuilders, and fitness enthusiasts to increase muscle mass, strength, and performance.

2. How are they typically used?

Purpose	Typical dosage & route
Medical (e.g., hypogonadism)	Low doses, usually 50–100 mg testosterone enanthate per week, intramuscular injection or transdermal gel.
Performance enhancement	Higher doses, often 200–800 mg of anabolic steroids per week. Common forms: nandrolone decanoate, stanozolol, trenbolone acetate, etc. Administration via intramuscular injections, oral pills, or patches.

> Note: Dosing can vary widely; "stacking" multiple steroids is common among bodybuilders.

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3. What Are the Potential Side Effects?

Category	Possible Adverse Effects
Cardiovascular	↑Blood pressure, ↑LDL cholesterol, ↓HDL cholesterol → increased risk of atherosclerosis and heart disease.
Hepatic (liver)	Oral anabolic steroids can cause cholestasis, elevated liver enzymes, peliosis hepatis, or hepatocellular adenoma.
Endocrine	Suppression of natural testosterone production → infertility, decreased libido, gynecomastia, testicular atrophy.
Psychiatric	Mood swings, irritability ("roid rage"), anxiety, depression; possible addiction.
Dermatologic	Acne, oily skin, hirsutism (excessive hair growth).
Cardiovascular	Hypertension, increased LDL/low HDL ratio → atherosclerosis risk.

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2. How the Brain Processes an Anabolic Steroid

Absorption and Distribution

- After oral ingestion, steroids are absorbed through the gastrointestinal tract into portal circulation.

- First‑pass metabolism in the liver reduces bioavailability; however, many synthetic analogues (e.g., oxandrolone) were designed to resist glucuronidation or hydroxylation.

Crossing the Blood–Brain Barrier (BBB)

- Steroids are lipophilic and readily cross the BBB via passive diffusion.

- The degree of crossing depends on lipid solubility, molecular size, and plasma protein binding.

Binding to Nuclear Receptors

- Within neurons and glia, steroids bind intracellular androgen receptors (AR) or estrogen receptors (ER). Oxandrolone has a higher affinity for AR with minimal aromatization to estradiol.

- The steroid–receptor complex translocates to the nucleus and acts as a transcription factor binding hormone response elements (HREs).

Transcriptional Regulation

- Binding initiates up‑regulation of genes such as:

- BDNF – promotes synaptic plasticity.
- Neurotrophin‑3, GDNF – support neuron survival.
- Synaptophysin, PSD‑95 – enhance synapse formation.
- Genes involved in mitochondrial biogenesis (PGC‑1α) and antioxidant defense (e.g., SOD2, GPx) are also up‑regulated, improving neuronal resilience.

Post‑Translational Modifications

- Steroid receptor activation triggers phosphorylation cascades that modulate:

- CREB → increases transcription of neuroprotective genes.
- MAPK/ERK → promotes dendritic spine growth.
- PI3K/Akt → supports cell survival and reduces apoptosis.

Cellular Outcomes

- Enhanced synaptic plasticity (long‑term potentiation).

- Reduced excitotoxic damage and oxidative stress.
- Improved learning/memory performance in animal models.
- Potential reversal of age‑related cognitive decline.

Conclusion:

Neuroactive steroids can act as modulators of cognition by engaging nuclear receptors to alter gene expression, influencing synaptic plasticity, and providing neuroprotection. These mechanisms offer a compelling basis for developing steroid‑based therapeutics aimed at mitigating cognitive deficits associated with aging or neurological disease.