Test C, NPP, and Anavar

Just to finish this topic, here’s the breakdown with some examples:

image

Check out the “diff” column which shows how much someone’s LDL-calc will be overestimated if they have average to a little high on Total Cholesterol and low triglycerides.

First equation is Friedewald and second equation is modified form for “group A” patients. Huge bias as you get into the 200s for total and are below 100 for triglycerides.

But like @spinup states, what this tells you about CVD risk is pretty hard to determine. My Lp(a) on oxandrolone was zero, but @unreal24278 has made some great posts about all the pieces that go into this. Inflammation to be continued.

The remaining % is genetics?

Pretty much. You can’t treat familial hypercholesterolemia with diet etc.

@unreal24278
Well that’s me then…

No matter how healthy i eat my LDL is always over the ref. ranges and my HDL is always barely in range , around 39-43…

Now i got myself some anavar to go with Primo.(i’m already on TRT)
And i’m trying a very low carb diet for 3 months along with a lot of cardio and supplements like bergamot , q-10 etc…
(Tried no flush niacin, gave me blurry vision for an hour straight.)

My plan was to try and lower cholesterol before going for anavar and primo but i really doubt i will accomplish that.

Oh and my mother has no cholesterol issues. Not sure about my father since he died at 48 from colon cancer. My grandfather however had cardiovascular issues.

Don’t tell @spinup this. It will upset his blanket statement that all cholesterol is controlled by diet.

I think a point can be made that one could have a great diet and have worse cholesterol than someone eating junk. However, if someone eating junk has bad cholesterol, diet should be something looked to, to control it. It should be the first thing looked at, but might not be enough.

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That’s not a statement I ever made. In fact, I explicitly mentioned disease states.

Are you being contentious for the sake of it?

It was clearly your implication when I disagreed with you. You refused to consider what I had already told you…that everybody is different and responds differently and that we shouldn’t make statements like you did.

You’re being intentionally obtuse for the purpose of argument. Like my children when they’re in a bad mood.

Honestly, if this forum is going to continue to be a place where people with bad attitudes copy and paste quotes without any intent on truth-seeking or contribution, I’ll happily spend my time elsewhere. It’s tedious.

@studhammer @spinup come one guys let’s love and heal one another. Life is short and there’s so much to read and learn. You guys probably have so much in common; let’s all empathize with each other and seek to understand and correct the science/art rather than attack each other. Spend that extra energy posting some extra super fine content.

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FHC is a one or two allele genetic disease. It’s not rare but I think you are way oversimplifying here. The combination of gene variations that could worsen “cholesterol” is endless. So I agree that it plays a big role but 10-15% is way too low in my experience. For most people a proper diet would go a long way and I’m not talking about people being 10% out of range but being really hypercholersterolemic.

I’d sign that. Doctors most often don’t even bother telling their clients what they could do because they KNOW that they aren’t going to change shit. They are right with that. I’d get frustrated too.

@readalot you can count on my contribution to the inflammation saga as that is something that I want to go off on everytime I read about cholesterol on here. I also have some questions regarding this subject.

Well yeah… If you’ve got both alleles the disease is far more severe. Multiple types of genetic mutations exist of which can result in dyslipidemia as you’ve specified. Generally speaking heterozygous familial hypercholesterolemia however cannot be treated with diet alone.

Homozygous FH is quite rare, those with homozygous FH usually drop dead at an early age of left untreated. Ditto with heterozygous FH, but there’s a difference between a heart attack at 55 and a heart attack at 25.

As to dietary intervention, literature generally specifies 10-15% to be the norm unless extreme measures are taken. Granted some do manage to attain superior results.

One also needs to register the vast majority of people aren’t capable of rigorously adhering to an extremely strict diet (i.e esselstyn diet), they give into craving henceforth sustainability is an issue.

A combination of losing weight and eating clean can make quite a big difference however if the patient is overweight and/or has insulin resistance to begin with. But for a relatively healthy male/female with dyslipidemia, diet will only take them so far.

I see problems with the point you’re making and the literature it’s based on.

The first study relies partly on self reported adherence which everybody knows is more than a bit flawed regarding diet adherence. If you’re not adhering, you’re not getting results.

Now the difference in the point I am making and where I think we differ:

Step 2 diet of the American Heart Association or its equivalent (<30% of total energy intake as fat, with 7% or less as saturated fat; ratio of polyunsaturated to saturated fatty acid >1.4; cholesterol intake <200 mg/day; and energy intake to achieve desirable body weight).

This is the intervention they analyzed which shows what they also imply elsewhere in the paper and what I think is what you are getting at:

They changed only WHAT the subjects ate

That’s a difference in definition because if we on here talk about diet, we not only talk about what to eat but especially HOW MUCH.

So I get it, you are fat, you eat too much and I tell you: just eat less of that! That may be sustainable but not particularly effective as you stated (10% reduction).

But if you’re fat and you change your ways, get lean, eat “healthy” food and not too much, I bet the reduction in cholesterol is way higher.

In other words, if you get to the root of the problem, the inability to take up LDL-C into cells and metabolize it, you’ll end up getting more out of the diet.

Dietary compliance might be expected to be better in patients at higher risk of cardiovascular disease, but the reduction in blood cholesterol concentration was similar in the five comparisons among patients with coronary heart disease

And this statement from the review shows something we all know, you can’t get people to change their ways for their lives, literally. Even if it’s just diet.

Edit: I’ll add some literature later

Edit 2: Literature

However, in six patients given treatment by diet alone (no colestipol), comparable weight loss (-6 +/- 1 kg) did not alter plasma HDL cholesterol or total triglyceride concentrations, but reduced total cholesterol (-9% +/- 3%) and LDL cholesterol (-11% +/- 3%) levels. These results suggest that weight reduction increases plasma HDL cholesterol levels only in those patients with hypercholesterolemia given colestipol but not in those given treatment by diet alone. Nevertheless, the effects of weight loss on plasma total cholesterol and LDL cholesterol levels were comparable in the two groups of patients.

So minus 6 kg (13 lbs) equaled a 11% LDL reduction. That’s a lot.

Now what if we go to the extremes?
What if a man with 450 lbs goes down to a healthy weight of 180 lbs?

I don’t know what his lipids were but I bet they were sky high before and in range afterwards.

I already made the point about sustainability but if people would get down to low BF and a healthy weight, I bet most would have good LDL and total cholesterol. They are just not willing to do it.

Edit 3: not trying to completely generalize because I read some studies that couldn’t confirm a LDL decrease because of weight loss alone. Some also were in the ballpark of unreals statements.

This even went against what I’m saying partly but there are problems with the study.

My point is: Get healthy. Do sports, eat good food and get your weight down and that will do it for most people. Not all, but the vast majority. Because we are not talking about public policy here but the advice for individuals that are dedicated enough to do what it takes.

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Well it’s been 16 days since the eye incident (but I didn’t realize that the valsalva maneuver was causing the issue and kept training for another 3 training days, 5 calendar days, so maybe really only 11 days). My vision seems to be getting better, but at a MUCH slower rate that I thought it would. I am off of everything besides my cruise dose of 250 mg/wk test C. I took one full week off from everything and just pinned again for the first time today. From reading through some of the good stuff that @readalot supplied, I may have to come off of even that cruise to get my vision fully back. I do have another appointment with the eye doctor on Thursday, and I fully expect the fluid level to have gone WAY down based on how well I can see now vs 11 days ago. I do not expect the fluid to be gone though.

I am still lifting weight, but it’s pretty much all machine movements with bodybuilding/BFR in mind. The heaviest weight I used yesterday on leg day was 50 lbs on the leg press and today heaviest was 45 lbs total on machine chest press. Tempo kills.

What’s your TT and E2 at this dose (steady state peak/ trough on TT and rough E2)?

Glad to hear you are on the mend. Take care of yourself.

I am not entirely sure what it is at 250, but I know that at 200 I’m around 1300 and at 180 I’m around 1000 (I don’t know what my peak and trough values are, I do not test that often, but each of those are a day after pinning each one so I would imagine those are close to peak values). so maybe 250 will have me around 1700? I know it isn’t necessarily a linear increase but I think that may be a good guesstimate

Close enough, thanks. So what’s your reasoning for running so high while trying to rehab your eye? E2 levels? Just curious your thinking as I would be back to physiologic ASAP but maybe I am missing something.

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Honestly? Fear of losing all of this lean tissue I put on. I know I probably shouldn’t be running more than 150/wk to help rehab my eye. but I was hoping that I could quickly see marked improvement even at 250.

Sometimes I need to be reeled in though. If I am being stupid, just say so

I would never say you are being stupid, just bouncing ideas. I have no definitive proof your trajectory to recovery will be faster by dropping T/E2 down to physiologic, but to me it doesn’t sound like a bad idea.

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In one of the studies you posted (I don’t remember which) it mentioned the man that has the CSR issue came off of his HRT altogether and his eye healed. Now that is just a sample size of 1, but unfortunately that is the largest “trial” I have seen. I suppose it wouldn’t hurt to come back down to 180. At the very least I should be able to maintain what I have at that level. I’m big but I’m not THAT big. However, I don’t think I’ll be making anymore change until after my eye appointment this Thursday (which I don’t pin again until that night anyways). For full disclosure, I always run HCG as well, whether on TRT or on cycle. I don’t believe that makes a difference, but it can’t hurt to have it all in the open.

And for the record, I always run HCG because my sexual health feels better and I don’t want severe shrinkage, which I get when I don’t run it.