Effect of High Levels of Test on blood LDL

[Sampei]

You are extremely well educated in many of these topics. I have enjoyed your thyroid posts.

To your point we recently discussed the TyG calculator which does as good a job as fasting insulin. The OPs hdl-c suggests Test abuse. But we don't have his baseline. I'd guess it was higher. His diet appears decent.

It's all thanks to you ppl that I have learned so many things. I feel we are some jack of all trades lol

 

[espresso123]

This is correct. Dietary saturated fat is more of an issue for some vs dietary cholesterol. As you correctly pointed out, LDL synthesis and reuptake happens in the liver in response to various conditions in the body.



The actual reason plaques accumulate is well understood by the scientific community. It's less well understoood and communicated by cardiologists and the medical community in general. At the level of the lay person there are all kinds of wacky theories.

In short, endothelial damage occurs from any number of various reasons like hypertension, metabolic syndrome, chronic inflammation, or oxidative stress. Once damaged, atherogenic particles enter the subendothelial space and from there the process begins. I'll spare you the details of the process.

There are two primary aspects to this that are individually necessary, but not sufficient to cause ASCVD which requires both. That is to say, there must be endothelial damage and there must be atherogenic particles. There are people with elevated biomarkers for atherogenic particles that are otherwise genetically gifted with regard to the endothelial resilience that do not suffer from ASCVD. There are people that lost the genetic lottery in that sense or suffer from any number of conditions that exacerbate endothelial damage (like smoking) that a small number of atherogenic particles is sufficient to cause a great deal of disease.



This is why outcome trials are necessary for any particular intervention. Niacin, for example, improves biomarkers, but negatively impact outcomes. Generally speaking, outcome trials are the final step in drug development.

Most recently, the drug bempedoic acid show positive outcomes in the CLEAR outcomes trial which was completed in late 2023. Prior to that, Repatha (evolocumab) demonstrated positive outcomes in the FOURIER trial.

Highly appreciate this valuable information. Thanks so much for sharing.

 

[PressureTest]

I wish I knew why my cholesterol levels seem to be so affected. Prior to starting TRT, I was 52 HDL/ 76 LDL. Six months later, on 200mg/wk with .25 Arimidex 1 or 2x/weekly, I had gone to 23 HDL/ 114 LDL.

I did 280 Test/ 280 Primo/ .25 AI for 10 weeks and got checked. I was “non-detect <15 HDL” and 224 LDL. After a month of Primo cessation I was back with HDL in 30-40’s and borderline high LDL.

I think the AI may be the culprit, even though my E2 was hovering in the 30’s. I’ve had at least two HDL readings in the 20’s on T and AI only. After skipping AI for a month or so it was back in the 40’s.

I’m on a small dose of Rosuvastatin now. I may try T/Primo again w/ no AI and see what happens. All my other blood work was totally fine.

 

[espresso123]

I wish I knew why my cholesterol levels seem to be so affected. Prior to starting TRT, I was 52 HDL/ 76 LDL. Six months later, on 200mg/wk with .25 Arimidex 1 or 2x/weekly, I had gone to 23 HDL/ 114 LDL.

I did 280 Test/ 280 Primo/ .25 AI for 10 weeks and got checked. I was “non-detect <15 HDL” and 224 LDL. After a month of Primo cessation I was back with HDL in 30-40’s and borderline high LDL.

I think the AI may be the culprit, even though my E2 was hovering in the 30’s. I’ve had at least two HDL readings in the 20’s on T and AI only. After skipping AI for a month or so it was back in the 40’s.

I’m on a small dose of Rosuvastatin now. I may try T/Primo again w/ no AI and see what happens. All my other blood work was totally fine.

AIs (e.g. Exemestane) also have a negative impact on your lipids. They are not necessarily less "bad" on your blood work than DHT derivatives.

Also, if using Primo, your E2 should be lowered anyways. I do not know how much it impacts you individually, so Id say do your bloodwork.
Not trying to be offensive, but I get the impression some people think AIs are like additional pills to throw in without thinking about their impact entirely - not referring to you since I dont know anything about your aromatase activity at all.

I am not a fan of statins, but regarding that, there are people out here who know better than me.

 

[PressureTest]

AIs (e.g. Exemestane) also have a negative impact on your lipids. They are not necessarily less "bad" on your blood work than DHT derivatives.

Also, if using Primo, your E2 should be lowered anyways. I do not know how much it impacts you individually, so Id say do your bloodwork.
Not trying to be offensive, but I get the impression some people think AIs are like additional pills to throw in without thinking about their impact entirely - not referring to you since I dont know anything about your aromatase activity at all.

I am not a fan of statins, but regarding that, there are people out here who know better than me.

I started on arimidex after my E2 was coming back in the 70’s on 200mg test, then when I got the first low HDL test, switched to exemestane. I want to not take any AI’s but I’m a high aromatizer. A 185mg/wk TRT dose w/o AI puts me at mid-700 T and 49 E2, which is enough to make me feel not great and have continuous acne breakouts on my back. The time I added the primo to the test/AI, it knocked my E2 down to 15.

I’ve found data on the AI’s and their effects on lipids but it’s usually talking about a decrease of <10% vs. mine going down 50+%. I actually found a decent paper about anabolics and HDL and emailed the primary author who was pretty much like “I don’t know.. AI and low E2 might affect it but I wouldnt expect that impact outside of oral anabolics.”