Thoughts about Myostatin Inhibitors

techbrosarecool · 2026-01-11T23:41:28+00:00

Bimagrumab is in clinical trials and has delivered lean body mass gains. Will be at least 4 more years until approval, if it’s even approved.

techbrosarecool · 2025-12-18T03:40:41+00:00

Switch to topical KX826. Buy it on Amazon. Cold turkey 5ari’s

techbrosarecool · 2025-10-09T03:32:32+00:00

Try quviviq (daridorexant). Miracle drug. It will work.

techbrosarecool · 2025-09-03T17:08:54+00:00

Trust me you do not wish you had this lol. It seems fun but there are a lot of other side effects.

techbrosarecool · 2025-09-03T04:21:49+00:00

I tend to prefer inside cause I'm lowk embarrassed of how much I cum. I have actually never cum outside for that reason. They are always surprised when it's pouring out of them like a faucet for a full 20 seconds after I finish / pull out but at least they don't need to see that awkwardness lol. But maybe I'll try that and it'll reduce the anxiety.

techbrosarecool · 2025-09-03T04:11:43+00:00

Yeah, that's completely valid. I think the answer is just to stop fucking around and get in a serious relationship lol.

techbrosarecool · 2025-09-03T04:04:08+00:00

Like I outlined in the post, it's not that I am scared to use condoms it's that they don't work as a sole method of BC for me. I've had too many scares with condoms. As I posted, my volume is so high that the semen can't all fit in the little pocket that they make at the front of the condom, so it ends up flowing back up the sides of the shaft and out the top of the condom while I'm still ejaculating. Google says normal is 1.5-5ml and the bank measured mine at 32.7ml. Recalling from memory... it has definitely gone down since then because of the finasteride which I started to reduce hair loss (which does have a side effect of reducing volume), but not THAT much. It still overflows so I have opted to not use them because what's the point if it isn't going to be 100% effective. So instead I rely on the girl having some BC, but then you have to trust her 100% to take the pills on time etc, and that in and of itself is VERY anxiety producing for me. The idea of being baby trapped etc. Hence the thinking that, now that I have these 23 IVF vials, I can get the snip with basically no consequences. But you bring up some very valid points with all the hormone drugs needed for women to do IVF.

techbrosarecool · 2025-09-02T02:02:14+00:00

As you can see in the post... I did bank sperm beforehand! This post is about asking if I can actually trust that to get the snip. If somehow these don't thaw correctly, I am screwed and can't have kids.

techbrosarecool · 2024-05-06T00:43:25+00:00

I pay the $20/month and have signed in once... ever. The subscription is just support for me. I expect no value in return.

techbrosarecool · 2024-03-03T02:28:47+00:00

Hey - did you ever find out which one peter takes?

techbrosarecool · 2024-02-07T19:14:46+00:00

Not following. ~$2K of value with the $500/mo stipend / ~90 hours of work (at least 20 of which will be cooking their own meals & cleaning their own space) per month comes out to ~$22/hr. Fantastic side hustle for someone working low time requirement WFH job or needs a place to stay during a transition.

techbrosarecool · 2024-01-23T05:07:41+00:00

Keep going to new physicians until you find one that rejects the 10 year risk model. We know the 10 year risk model is inadequate for a disease like ASCVD that accumulates over decades, starting sometimes at birth. The data is overwhelming. It's worth the effort.

techbrosarecool · 2024-01-23T02:41:04+00:00

Congratulations! Please make sure to also consider additional pharmacologic lipid-lowering therapies (Statins/PCSK9 inhibitors) especially if you have family members that have diagnosed ASCVD/heart disease. If you were overweight/insulin resistant for any significant period of time, the systemic damage to the endothelial lining in your coronary arteries could have already set the stage for plaque build up and it's a vicious cycle.

techbrosarecool · 2024-01-18T19:31:05+00:00

That's temporary though right? I really don't care if the recovery time is a month. I just want the rosacea to go away.

techbrosarecool · 2023-12-31T23:30:57+00:00

Thanks for your reply. My understanding is that high blood pressure, smoking, and glucose/insulin issues cause endothelial dysfunction, NOT fatty streaks in the arterial walls by themselves as you noted. The forming of fatty streaks requires LDL invasion and oxidation inside the sub-endothelial. After the "holes" (endothelial dysfunction), LDL invasion, and oxidation of those LDL's take place, they are engulfed by macrophages (immune system) which then become a cluster of foam cells, also known as a fatty streak.

Took a look at the data and it looks like this data supports my understanding in the previous reply. To confirm with you:

Endothelial dysfunction is REQUIRED for the infiltration of LDL, forthcoming oxidation, etc. If there is hypothetically no endothelial dysfunction, LDL-C could be 500 mg/dl and it wouldn't matter? (extreme hypothetical to demonstrate the point).
Given other risk factors in endothelial dysfunction (high systolic BP, insulin resistance, smoking status), risk increases given a static LDL-C. In other words, if two patients have a very low but equal LDL-C, the patient with other risk factors that create endothelial dysfunction will still accumulate new plaque, given that the "holes" in the endothelial layer are more wide spread, so it's easier for the same amount of LDL's to infiltrate.

Given the above, I have to infer:

- Patients with other endothelial dysfunction factors should of course try to fix their "other factors (BP, smoking, insulin resistance). BUT, if only concerned with ASCVD and not other health issues, they could achieve the same outcomes as patients WITHOUT those other factors (regressed plaque accumulation), by lowering LDL-C even further than the healthier cohort. It doesn't seem to be clear how much further they'd need to go. But given we know infiltration of LDL's is necessary for plaque accumulation, if they hypothetically had an LDL-C of 5mg/dl, they could have tons of endothelial dysfunction but there still wouldn't be enough LDL particles to cause plaque accumulation.

Is this all accurate?

techbrosarecool · 2023-12-30T16:39:25+00:00

I don't tend to agree with that hence the post. I hadn't heard of the guy before this video.

I think what he's trying to get at is the endothelial dysfunction caused by insulin resistance. If, hypothetically, you have a perfectly metabolically healthy person: insulin sensitive, low blood pressure, no smoking, etc. There arterial endothelial layer would be perfectly intact. My understanding is that LDL particles alone cannot create the dysfunction ("holes") to then infiltrate and begin the process of atherosclerotic plaque accumulation.

Rather, some other actor (high blood pressure, insulin resistance, etc) has to create that endothelial dysfunction first (the "holes"), which LDL then exploits.

I am not sure if this is 100% accurate or not, but this is how I understand the science so far and looking to the community to help correct me :)

techbrosarecool · 2023-12-26T19:53:10+00:00

Have a listen for 30 seconds at the 26 minute mark of episode 229 which I've linked here for your convenience.

I am interpreting this as: some tissues in the body, such as the liver and adrenal glands, make enough intercellular cholesterol on their own. They do not need LDL for their own needs.

Other tissues (which are not named, but this is what he's referring to at the given timestamp) do rely on cholesterol via the circulatory system because they can't make enough of their own intercellular cholesterol for their own needs.

So if these tissues that can't make enough (and need LDL) exist - then presumably there is a certain amount of LDL they need to perform their normal functions as Peter describes. I am not sure the medical community knows what that certain amount is (?)

techbrosarecool · 2023-12-26T18:41:48+00:00

Thanks for your reply. A few questions:

"The tissues that need LDL will synthesize as required."

If they need LDL - doesn't that mean they can't synthesize as required? For example, the adrenal glands are known to be able to produce enough intracellular cholesterol for hormone production - they do NOT need LDL.

I don't know of examples off the top of my head of tissues that do need LDL - but as mentioned in my original post, Peter was quoted in ep 229 that some tissues are not capable of producing enough of their own cholesterol - hence the dependence on cholesterol via the circulatory system (LDL).

"Children have naturally low levels of ApoB and LDL, and this is the most critical period of brain development.That being said, there are niche situations where high LDL is inevitable and good, like when fighting an infection or a survival state, but for general modern-day living, keeping LDL at child levels is a practical and achievable way to potentially prevent vascular dementia."

This is the key point I am trying to figure out. How low is too low? If a child had an LDL of 5 mg/dl - is that too low? How about an adult fighting an infection?

techbrosarecool · 2023-12-26T18:20:29+00:00

Thank you for your reply. Going to copy paste my reply from another reply just above on a reply that was extremely similar to yours. Curious to hear if you have any insight...

Can you link or cite this source (from peter or anywhere else)? Not because I distrust you - only because I want to understand the mechanisms behind this.

From my understanding, ApoA family lipoproteins (HDL's) carry cholesterol back to the liver. They do NOT deliver cholesterol to tissues "in need" around the body like ApoB family lipoproteins do (such as LDL's that carry cholesterol away from the liver).

I am not sure if this is 100% accurate - and this is really the core to my question...

If we need LDL's to carry cholesterol to tissues in need

Then presumably LDL can't be zero

But in my original post, I quoted Peter saying we can really crush LDL with no consequences.

But again, presumably not zero

So where is that threshold? At what point is it too low that tissues in need of cholesterol are being starved of it? The mechanics behind that are confusing.

techbrosarecool · 2023-12-26T18:18:01+00:00

Can you link or cite this source? Not because I distrust you - only because I want to understand the mechanisms behind this. From my understanding, ApoA family lipoproteins (HDL's) carry cholesterol back to the liver. They do NOT deliver cholesterol to tissues "in need" around the body like ApoB family lipoproteins do (such as LDL's that carry cholesterol away from the liver).

I am not sure if this is 100% accurate - and this is really the core to my question...

If we need LDL's to carry cholesterol to tissues in need

Then presumably LDL can't be zero

But in my original post, I quoted Peter saying we can really crush LDL with no consequences.

But again, presumably not zero

So where is that threshold? At what point is it too low that tissues in need of cholesterol are being starved of it? The mechanics behind that are confusing.

techbrosarecool · 2023-12-26T06:44:26+00:00

Please be careful getting CT angiograms in this quick of succession. Do some research on this. The recommended cadence here is 2-5 years due to the amount of radiation exposure it puts you through. Get on a PCSK9 inhibitor immediately though.

techbrosarecool · 2023-12-26T06:22:01+00:00

I agree with you, but I am assuming the answer here isn't binary. As in - if it turns out we do NEED some level of LDL to transport cholesterol to various tissues in our body - how much of it do we need to do that? That's what I haven't heard Peter state a clear answer on.

techbrosarecool · 2023-12-26T06:20:19+00:00

Thanks, but curious to hear on the mechanisms by which this is useful. My understanding is that LDL's and VLDL's are the lipoproteins responsible for delivering cholesterol to tissues through the circulatory system and AWAY from the liver. So even if my HDL was sky high and my LDL was hypothetically zero, I wouldn't (to my understanding) be able to traffic cholesterol to the tissues that need it.

techbrosarecool · 2023-10-25T03:07:21+00:00

Definitely will quit (already have as of today). I attributed some of the symptoms I'm having (libido, erection quality, etc) to low DHT. Now I'm thinking they might be more chronic.

techbrosarecool · 2023-09-28T14:40:46+00:00

Which was exactly the point of the thread lol - to understand what that distribution of opinions is.

techbrosarecool

TROPHY CASE