Anabolic Steroids: Uses, Side Effects, And Alternatives
Anabolic Steroids – What They Are, How They’re Used, Their Benefits, Risks, and Legal Status
---
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.
---
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. |
---
2. How the Brain Processes an Anabolic Steroid
- Absorption and Distribution
- 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)
- The degree of crossing depends on lipid solubility, molecular size, and plasma protein binding.
- Binding to Nuclear Receptors
- The steroid–receptor complex translocates to the nucleus and acts as a transcription factor binding hormone response elements (HREs).
- Transcriptional Regulation
- 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
- CREB → increases transcription of neuroprotective genes.
- MAPK/ERK → promotes dendritic spine growth.
- PI3K/Akt → supports cell survival and reduces apoptosis.
- Cellular Outcomes
- 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.
