I told you this would happen (not trying to be a know it all but… yeet!) Masteron is pretty harsh on lipids too. It’s primarily the anavar, but mast doesn’t help.
RYR (if legitimate) will get it down quickly. Keep an eye on LFT’s, kidney function etc. Stop taking it if you start getting myalgia or generalised weakness.
Imagine this, HDL was probably tanked (due to mast/var) and LDL was through the roof… Whilst particle size/sub-fractions matter, no matter the cause that HDL/LDL ratio is awful.
You can try get a doc to prescribe a statin, though given AAS mediated lipid profile alteration is transient it probably isn’t necessary. Try see what lipids are 6 weeks from now/without anavar, if they’re still ehhhh (say HDL below 40, LDL above 130-160 or HDL/LDL ratio worse than 1:3) you could opt to take a statin. They’ve got a bad rap and they do have potential side effects (as do all drugs) but they dramatically lower mortality rates in relation to CVD if risk is initially elevated. Red yeast rice is literally identical to taking unregulated lovastatin, if you can take that you can (probably) handle a low dose of say… Atorvastatin.
You’d need to be honest with your doc though. Slightly altered lipids may not be the end of the world (depending on sub-fractions) if lifestyle is decent and no other risk factors are present… But AAS use is a risk factor, and a pretty fat one at that. I don’t have a definitive number to give, but I’d argue depending on the compounds used anabolic steroids probably increase the odds of developing cardiovascular disease by 3-10x+ that of those who are otherwise healthy (higher end for chronic use of orals/stronger drugs like tren).
Anavar is probably one of the harsher orals in terms of inducing dyslipidemia, though all (generally) have a pronounced effect in lipids. Literature shows oxandrolone is generally quite a bit harsher than oxymetholone, methyltestosterone in terms of inducing dyslipidemia… Stanozolol appears harsher than oxandrolone (actually stanozolol simply appears to be the worst drug for cholesterol)
I’ll add to that one thing. You should be careful with drugs that stress or inhibit the liver and statins. With some statins you could provoke rhabdomyolysis.
Not great but there is a genetic factor here as both parents lived a healthy lifestyle (no drinking, no smoking, not obese) and were treated for lipids.
I’ll drop the mast too. I get retested in about 4 - 6 weeks.
FWIW, my lipid panel taken six weeks after a four week run of 75mg oxandralone was the best it’s ever been in my life.
HDL: 60
LDL: 78
Total: 152
Not sure what it looked like while on the var cycle, but if it bounces back this quickly and this well, I’m not that concerned, although I do still intend to keep any future var cycles limited to 4 weeks.
It is paramount, in my opinion, to use diet as much as possible to mitigate any side effects arising from AAS usage, especially if incorporating orals. Low, low fat. Good carbs and lean protein with supplemental fish oil (and a lot of it).
My cruise for a couple of years now has been test and mast with a blast of anavar every few months. For my blood work, I’ve already stopped the anavar and will drop or cut in half the mast. I’m not good at fasting, but I am modifying my diet somewhat and we’ll see what happens
I’ll respectfully disagree. This is like saying somebody who needs TRT can get lean and add muscle just like anybody else. We all know that is not true.
I don’t know how old you are but, at 55, I can tell you that shit I “knew” to be true at 30 suddenly isn’t so locked in anymore.
It’s not “like” anything else. It’s a standalone statement. Unless an individual has some kind of disease, then diet is the single biggest variable impacting lipids. This is not a controversial claim. It’s exactly why lipids are supposed to be measured in a fasting state.
Nobody wants to eat healthy foods (because they’ve become dependant on the dopamine release provided by consuming high fat/sugar foods), so doctors prescribe statins to everyone so they can keep pounding shitty meals.
For you, probably, but I’ve seen lean guys with shitty lipid profiles and fat guys with good lipids. Its rarely “one” thing that determines the outcome of something and, if you spend any amount of time on this forum you will see that each of us has individual reactions to the same drugs.
My claim is simple: diet impacts lipids, and the fact that lipids change dependant on fasting state shows this.
Every time I make a blatantly obvious claim on this forum that people don’t prefer to acknowledge as true I get push back. If your cholesterol is shitty, then your diet is shitty.
I’ve actually read your linked post several times previously and have found it informative and useful. I do expect that my lipids get pretty trashy while on (which is why I only run it for 4 wks max). Next time I run oxandrolone I’ll have a full blood workup pulled and report back - will probably be some time next year though.
The main point I’m trying to help communicate (and I don’t think it’s lost on you) is that correcting lipids, in my experience and observation, can sometimes take dramatic and permanent dietary changes. Changes that are dramatic enough that many people will never make them. But if someone has trashy lipids outside of a diseased state then I would challenge them to first and foremost radically alter their nutrition.
Lean fish, lean chicken, oats, low-fat yogurts, rice, broccoli, spinach, carrots, fiber, egg whites, whole grains. If an individual has not developed the discipline to eat from this list almost exclusively for weeks and months, then in my opinion they have not done the due diligence in modifying their diet to support their lipid/cardiovascular health. I’m not saying someone has to eat like this 24/7/365 (although I do and love it), but don’t come complaining about LDL if you haven’t done the work.
If my own DNA has anything to do with my lipid profile, it is such that I have to eat as listed above to achieve the results I get. I’ve spent years fucking around on my nutrition and dealing with statins and poor results.
On the contrary, anything you post gets my immediate attention, usually above anyone else. The contributions from you and @unreal24278 are highly valued.
It’s interesting to me that it didn’t move like HDL did around 2015.
You know, none if this even touches on the idea that lipids alone may not even be the best indicator for cardiovascular health outcomes. Inflammation plays a massive role to my understanding. Anyone have any thoughts or links?
