"Temporarily" bad lipids may be worse than you think

by /u/pedsaccountonreddit

NOTE: I'm not a medical professional of any sort and I have NO background or expertise in this area at ALL. This is NOT medical advice. This isn't intended to be advice at all. I'm providing my OWN PERSONAL NOTES here for educational purposes ONLY. You should consult with a physician and take THEIR advice.

As an additional note, I do NOT condone the use of illegal anabolic steroids or other illegal drugs. To put it briefly, I don't think you should do steroids or other anabolics outside of the care of a physician.

"The first principle is that you must not fool yourself - and you are the easiest person to fool." - Richard Feynman

You're going to die someday, and it's probably going to be heart disease that kills you.

"Heart disease" can mean a few different things, but for our purposes we'll take "heart disease" to mean coronary artery disease / atherosclerosis ("CAD"), e.g. the gradual accumulation of plaque in arteries. When most people think of CAD they think of something you suddenly "have" rather than a slow process that occurs over years. In reality, atheroscleroic plaques begin to accumulate in early childhood, and by age 10 almost all children have fatty streaks in their arteries[1]. Sub-clinical CAD can exist for many years before clinical symptoms of heart disease, such as hypertension, present themselves.

Recommended reading: Peter Attia's series on cholesterol

I highly recommend reading M.D. Peter Attia's blog series on cholesterol which can be found here:

That being said, the blogs are long and take some serious attention to process. They're worth it, though.

Bad lipids are bad

What I've learned from reading the above posts (besides the different values that can be measured, e.g. LDL-P, HDL-C/P, etc) is that it looks likely that the main driver of atherosclerosis over time is area under the curve. E.g. not just the amount of time you spend with some atherosclerosis-inducing cholesterol ratio, but rather the magnitude of those lipids summed over time [2].

As I dug further, I found more evidence that this area under the curve should be a worry for folks. E.g. https://www.fightaging.org/archives/2018/10/can-atherosclerosis-be-prevented-via-early-large-reductions-in-ldl-cholesterol/, https://www.heart.org/en/news/2018/10/04/researchers-suggest-way-to-possibly-eliminate-artery-clogging-condition, https://www.ahajournals.org/doi/10.1161/JAHA.118.009778 (REALLY interesting).

So what's incredible here is that there's researchers testing the following: they take somewhat younger people, e.g. 35-50 years old, and give them statins to lower their LDL-C down to <= 25 for > 1 year. Then they take these people off the statins, have them go off and lead a normal life and then measure their cardiac risk over time. The theory is that this sustained period of ultra-low LDL allows "HDL" (& associated machinery) to possibly clean up early aterial plaque development before it progresses. So in these peoples' cases, their "curve" would dip down into the 'negative', hopefully allowing them prolonged life/health span.

Of course we don't know whether or not this will work, but what stuck with me in this reading is that the classic picture of "getting" heart disease or being of sufficient age / bad cholesterol levels to require e.g. statin treatment almost certainly comes too late to stop the progression of atherosclerosis.

So how's this effect PED usage? Well obviously a ton of anabolics jack up LDL-C and lower HDL-C, which likely leads to a "tall" y-value in this "area under the curve." Lots of guys "cruse," reducing their anabolic dosage for some period of time to "let their blood recover." But it seems a drastically more aggressive approach could be helpful to users of anabolics.

We don't really know what these studies will show us, but it could mean that guys should aim for ultra-low LDL values for sustained periods of "cruising," values FAR beyond what exist in the typical western population. The common perception is that bad lipid elevations are benign, akin to something like temporary liver enzyme elevations. This may not be true.

And no, "sustained period" here does NOT mean "time on = time off." Think of what the curve looks like. Here's your typical person who develops clinical CAD in his 40s and dies of a heart attack:

https://ibb.co/x5v9W4c

The red line is where he dies. At the point where the red line is, his Total Cholesterol: HDL-C [3] ratio is 7 and he's not on a statin.

And here's someone who's healthy and lives to 85 and then suffers from congestive heart failure secondary to CAD:

https://ibb.co/cT2hPMz

The red line is where he dies. At the point where the red line is, his Total Cholesterol: HDL-C ratio is 2.5 and he's on a statin.

And here's someone who's 55 years old, is otherwise healthy but did a couple of AAS cycles:

https://ibb.co/4fC4XwQ

This graph isn't quite right but you should hopefully get the idea. The red line is where he dies. At the point where the red line is, his Total Cholesterol: HDL-C ratio is 3 and he's not on a statin. He eats right, does his cardio and checks his lipids regularly.

But the key is:

  1. Lipids are a "snapshot" in time. They tell you what some numbers are right now but they don't tell you about what happened before and the damage that was done.
  2. Standard lipid tests don't tell the whole picture, as detailed in the Peter Attia blogs. A bit more on this below.
  3. To see the "area under the curve" something akin to a coronary calcium scan ("CAC" or "heart scan") would be needed. See https://www.mayoclinic.org/tests-procedures/heart-scan/about/pac-20384686, https://www.youtube.com/watch?v=NSPcuGjstN4.
  4. Temporary "bad lipids" could have a sustained impact on lifespan due to accumulation of atheroscleroic plaque. This could be compounded by insufficient time on "cruise" or in recovery where lipids are good enough to "clean up" accumulation (e.g. with lipids as good as the AHA study above). "Standard" / "in range" lipids on "cruise" may be insufficient to "clean up" accumulation because CAD -- aka the reaper -- is coming for us all, it's just a matter of area under the curve. AND, in fact, it may be impossible to "clean up" the accumulation done by a period of bad lipids - we don't know!

Caveats here:

  1. I'm NOT an expert of ANY sort here. These are my OWN OPINIONS, SHARED FOR EDUCATIONAL PURPOSES ONLY.
  2. It's totally possible that "area under the curve" isn't quite right and there are other factors that correlate with age that lead to acceleration of CAD such as LDL receptor degradation with age.

Being that, again, I am NOT an expert or ANY kind of medical professional, what I've gleaned for myself from my recent reading is that the following tests are important to get:

There is lots of variability here so it's important to know what cards you're dealt genetically and the best way to do that is to get tested.

Personally, I'll be getting all of the above annually (sans Lp(a) which I tested just one). If I was an AAS user I would definitely get a CAC done to assess my "area under the curve."

Layne Norton just got a CAC done and found out he has calcified plaque in his arteries. The good thing is that he is seeing the impact NOW so that he can make changes to prolong his life. John Meadows had a CAC done last year and found out he has calcified plaque in his arteries.

Again, I am NOT an expert and I welcome any and all comments here. These are truly my own personal beliefs and notes, shared purely for educational and discussion purposes and are NOT advice.

Notes:

Some people think that the reductions in HDL-C on cycle don't matter as they won't contribute to an increase in atheroscleroic plaque. The evidence we have right now is that reductions in HDL-C with AAS are associated with atheroscleroic plaque and reduction of HDL function

Footnotes:

  1. https://www.youtube.com/watch?v=AkWd0R05ZEs, https://www.ncbi.nlm.nih.gov/pubmed/11063473, https://www.ncbi.nlm.nih.gov/pubmed/1619200, https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2812791/
  2. Note that we don't really know what this ratio is, which is part of the problem. LDL-P (which is ~LDL-C in most cases) seems to be an independent driver of atherosclerosis development. Figures I've read state that LDL-C <= 25 /may/ be "atherosclerosis-proof." I'm not sure if we know whether a good ratio does or doesn't drive atherosclerosis.
  3. FYI this is called the Castelli Index (TC: HDL-C) and it's the most-used general CAD risk marker. Of course, if you read the Peter Attia posts you'll see this does NOT paint the whole picture of CAD risk. But this is just an illustration and so I'm using the Castelli Index as a storytelling tool here.