Which Halo (fluoxymesterone) effect most increases its cardiovascular risks?

Which Halo (fluoxymesterone) effect most increases its cardiovascular risks?


  • Total voters
    12
  • Poll closed .
1. 11β-Hydroxysteroid dehydrogenase type 2 (11β-HSD2) is an enzyme that converts active cortisol into its inactive form, cortisone, helping to regulate cortisol's effects on mineralocorticoid receptors, especially in the kidneys. Inhibition of 11β-HSD2 can lead to increased active cortisol levels, which may cause sodium retention, potassium loss, and elevated blood pressure. This inhibition is relevant in contexts such as hypertension, metabolic disorders, and pharmacological research, as it can amplify cortisol's effects and has potential therapeutic implications, though it may also lead to side effects.


2.
GR antagonism refers to the blocking of glucocorticoid receptors, which are proteins that cortisol binds to in the body. This process can help reduce the effects of cortisol, particularly in conditions like Cushing's syndrome and certain psychiatric disorders.


3. Hepatic triglyceride lipase activity (HTGLA) inhibition refers to the reduction of the enzyme's ability to hydrolyze triglycerides, which can affect lipid metabolism and cholesterol levels in the body. This inhibition can lead to increased levels of triglycerides and potentially contribute to cardiovascular issues.


4. Stroke volume can be increased by factors such as increased venous return, which enhances preload, and improved contractility of the heart. Prolonged aerobic exercise training can also lead to a higher stroke volume by allowing more blood to be ejected with each heartbeat.


Calcium accumulation could have a negative effect of cardiovascular health because halotestin reduces excretion through urine. I couldn't find any correlation with any of these so I opted for option 3 based on negative effects on lipids. I'm still unclear on that also.
 
Last edited:
Back
Top