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Team USP Rep
Hypotheses About Why Androgens Cause Cardiovascular Disease
BY: Type-IIx
We all love gear. Those of us who still love androgens in all their might and glory, after decadeslong use patterns, continue to do so against all odds because we have a rational understanding that — like Prometheus' fire
— with this power come real risks that must be traded-off wisely.
One major aspect, the biggest, is the risk of cardiovascular-thrombotic disease or fatal event. Here are the major competing, perhaps overlapping, models that have been synthesized to explain why androgens increase this risk:
1. The Atherogenesis Model
This model focuses on the relationship between AAS and hepatic triglyceride lipase (HTGL), an enzyme that regulates serum lipids and lipoproteins.
Mechanism: AAS administration enhances HTGL activity.
Effect: This leads to a suppression of "good" high-density lipoprotein (HDL) levels and an elevation of "bad" low-density lipoprotein (LDL) levels.
Outcome: These changes decrease the regression of atherosclerotic plaques, increasing the risk of heart disease.
2. The Thrombosis Model
This model explains injury through changes in the haemostatic system (the process of blood clotting).
Mechanism: AAS use has a strong effect on platelet aggregation.
Outcome: This leads to enhanced blood-clot formation, which increases the risk of cardiovascular events like strokes or heart attacks.
3. The Coronary Artery Vasospasm Model
This model attempts to explain cases of sudden cardiac death where neither atherosclerosis nor thrombosis is present.
Mechanism: AAS may inhibit the properties of nitric oxide, which acts as a relaxing factor for the smooth muscles of the arteries.
Effect: This can induce a vasospasm (a sudden constriction of a blood vessel).
Physical Compression: AAS increases myocardial muscle mass but decrease capillary density, meaning the heart muscle itself may compress its own coronary vessels, triggering an infarction.
4. The Direct Injury Model
This model suggests that AAS causes structural damage directly to the heart cells.
Mechanism: AAS induces direct myocardial cell injury, leading to cell death.
Effect: Dead cells are replaced by scar tissue, a process known as fibrosis.
Outcome: Fibrotic areas predispose the athlete to arrhythmias (irregular heartbeats), which can lead to fatal events.
5. Other Potential Models
Recent research has suggested additional pathways for injury, including:
Catecholamine myotoxicity: AAS use may be associated with ventricular fibrillation due to myocardial necrosis and degenerative changes within the heart's sympathetic neurons.
Secondary Endocrine Effects: These include insulin resistance and impaired thyroid function, though their direct role in cardiac injury is less defined than the four primary models.
BY: Type-IIx
We all love gear. Those of us who still love androgens in all their might and glory, after decadeslong use patterns, continue to do so against all odds because we have a rational understanding that — like Prometheus' fire
— with this power come real risks that must be traded-off wisely.One major aspect, the biggest, is the risk of cardiovascular-thrombotic disease or fatal event. Here are the major competing, perhaps overlapping, models that have been synthesized to explain why androgens increase this risk:
1. The Atherogenesis Model
This model focuses on the relationship between AAS and hepatic triglyceride lipase (HTGL), an enzyme that regulates serum lipids and lipoproteins.
Mechanism: AAS administration enhances HTGL activity.
Effect: This leads to a suppression of "good" high-density lipoprotein (HDL) levels and an elevation of "bad" low-density lipoprotein (LDL) levels.
Outcome: These changes decrease the regression of atherosclerotic plaques, increasing the risk of heart disease.
2. The Thrombosis Model
This model explains injury through changes in the haemostatic system (the process of blood clotting).
Mechanism: AAS use has a strong effect on platelet aggregation.
Outcome: This leads to enhanced blood-clot formation, which increases the risk of cardiovascular events like strokes or heart attacks.
3. The Coronary Artery Vasospasm Model
This model attempts to explain cases of sudden cardiac death where neither atherosclerosis nor thrombosis is present.
Mechanism: AAS may inhibit the properties of nitric oxide, which acts as a relaxing factor for the smooth muscles of the arteries.
Effect: This can induce a vasospasm (a sudden constriction of a blood vessel).
Physical Compression: AAS increases myocardial muscle mass but decrease capillary density, meaning the heart muscle itself may compress its own coronary vessels, triggering an infarction.
4. The Direct Injury Model
This model suggests that AAS causes structural damage directly to the heart cells.
Mechanism: AAS induces direct myocardial cell injury, leading to cell death.
Effect: Dead cells are replaced by scar tissue, a process known as fibrosis.
Outcome: Fibrotic areas predispose the athlete to arrhythmias (irregular heartbeats), which can lead to fatal events.
5. Other Potential Models
Recent research has suggested additional pathways for injury, including:
Catecholamine myotoxicity: AAS use may be associated with ventricular fibrillation due to myocardial necrosis and degenerative changes within the heart's sympathetic neurons.
Secondary Endocrine Effects: These include insulin resistance and impaired thyroid function, though their direct role in cardiac injury is less defined than the four primary models.
