BTW these are the papers on which I based my hypothesis about IGF-1 LR3. Can anyone get the full text of the 2023 paper??
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This is a fascinating finding if that’s the reason it went down so much. There is a doctor (Dr. Andrew Winge from Man Medicine) makes good YouTube videos, who said his Lp(a) dropped by 40% on oral estradiol
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Yeah I follow him and agree with him on most things except high hematocrit. I’d be concerned that the increased risk of thrombosis from oral estrogen would offset or even have a net detrimental effect when weighed against a 40% decrease in Lp(a).
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Lpa_IGF1.pdf (355.7 KB)
I had to pay $25 for what ended up being a 1.5 page article 
. Anyway, some good tidbits of info. In a small study of children and adults with Laron syndrome, once-daily IGF-1 administration decreased Lp(a) by 65 +/- 15%, which is huge.
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Sorry, I did not respond earlier.
You can find many medical papers, especially ones two years or older, here for free.
https://sci-hub.se/
“Sci-Hub has the largest (> 88 million documents) database of full-text scientific papers, available for free. Approximately 80% of the collection are articles from scientific journals, most of them dedicated to the subject of medicine. That is followed by physics, chemistry and biology, humanities, etc. The entire collection is available for download on the torrent network, and takes up about 100 terabytes of space.”
Amazingly, you can download the entire collection if you have the time and space.
Sorry, here is the paper you paid for.
“https://sci-hub.se/https://pubmed.ncbi.nlm.nih.gov/9150696/”
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A great paper.
Thanks for sharing… I have been on HGH for nine months to rebuild the thymus…
RapAdmin found and posted where rapamycin does similar thymus regeneration in a female mouse study.
CAD prevention and benefits on top would be fantastic.
I’m familiar w/sci-hub and have used it many times. They have the 1997 paper (the one you linked to) but not the 2023 paper, which is the one I paid for and posted above.
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Emily Latella, says sorry!
HGH increases Lp(a), and IGF-1 lowers it, so HGH therapy either increases it or has minimal to no effect since GH increases IGF-1 production by the liver. Giving IGF-1 itself (or possibly its longer-acting analog IGF-1 LR3) lowers Lp(a) because IGF-1 doesn’t raise GH.
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Interesting David… I am getting a Coronary Calcium Scan in January 2026. Will see if anything has changed.
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The designer cytokine IC7Fc attenuates atherosclerosis development by targeting hyperlipidemia in mice
https://www.science.org/doi/10.1126/sciadv.adx3794
Designer drug targets both heart disease and diabetes
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Anecdotally, I have checked Lp(a) on HGH and without HGH and there isn’t much of a difference. I’m fortunate enough to have a low level either way though.
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Right, I’ve also heard from others that there’s essentially no effect on Lp(a) from either GH itself or GH secretagogues, which is consistent with the literature. Only IGF-1 itself, without GH, lowers it. And to my knowledge, this is the first time anyone has looked at Lp(a) changes from IGF-1 LR3, which should be more potent due to its longer half-life from the LR3 modification.
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Just sharing this article about a study that shows exposure to light at night might increase heart attacks. It was just in Jama 10/25
The study
https://jamanetwork.com/journals/jamanetworkopen/fullarticle/2840489
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Back in 2005 (age 49) I was diagnosed with a coronary artery spasm via angiogram. It was in the artery next to the widow maker so I got lucky. That artery had about 60% blockage as well so they did not insert a stent. Apparently various type of stress can cause this, physical and emotional. At that time my “emotional” stress was through the roof.
Side note, 6 weeks after that, I went on a solo 2 day motorcycle ride covering 1,000 km. It was not a slow ride, life begins at 200km/hr is my philosophy. My wife asked the logical question, why? It will either set me free or kill me, was my reply and it set me free from the emotional roller coaster I had been on.
In 2013 I was having pain in my left arm, went to a cardiologist and did the tests and he gave my heart a clean bill of health, had no idea what the pain was. Six months later it was diagnosed as a referred pain from a injury to my ininfraspinatus, took a year to work that out but all good ever since.
2025, July my PCP asked when the last time I’d been to a Cardiologist and she then referred me to one as a precaution for this old guy.
I have no symptoms, no shortness of breath, no chest pains, I’m a fully functioning, hard working, old guy LoL! she loves to refer me to specialists!
July did a stress test with ultrasound. 2 dark spots were detected, 4 months later a repeat test, only 1 dark spot, Apparently ultrasound imaging is not the best option for this type of imaging as it provided 1 false positive. Oct 27 I was sent for a nuclear heart scan. That came back with a definitive blockage that the radiologist deemed to be medium to high risk.
Nov 3 went for an angiogram. Three possible outcomes 1) nothing needs to be done, 2) insert a stent, 3) by-pass surgery
Was pretty cool watching the process, at one point they pulled the dye thingy out and inserted something that vibrated (later identified as the drill thingy), then pulled that out and reinserted the dye thingy 
don’t mind the highly technical description of the process,
Diagnosis was a CTO, chronic total obstruction. With collateral circulation or arteriogenesis that was basically a “fix” my body was providing. There are levels to this and mine is pretty high as I do not have any of the symptoms that poor collateral regrowth provides.
I attrite this to more good luck, good genes and my last 2 years of peptide therapy, specifically daily BPC 157 + TB500 (aa43) to keep my old body primed to heal. Both these peptides support arteriogenisis.
And of course the 1000km ride at speed
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New from Christine Glorioso. A really good story:
The discovery of PCSK9’s role began in 2003 when researchers identified gain-of-function mutations in the PCSK9 gene in French families with familial hypercholesterolemia, a condition that causes dangerously high cholesterol from birth. Shortly after, scientists discovered the flip side: people with loss-of-function mutations in PCSK9 had remarkably low LDL cholesterol and dramatically reduced cardiovascular disease risk.
In one landmark 2006 study, participants with these protective mutations had 28% lower LDL cholesterol and an 88% reduction in cardiovascular disease risk.
This genetic evidence was so compelling that it launched a pharmaceutical race to inhibit PCSK9- and remarkably, the first drugs were approved just 12 years after the initial discovery.
PCSK9 Inhibitors prevent PCSK9 from doing its job, which in turn increases the number of receptors available to clear cholesterol, lowering LDL levels. Statins work through different mechanisms by inhibiting HMG CoA reductase as well as other effects. Together the two classes of drugs are synergistic when used in combination.
The PCSK9 longevity gene- therapeutics, heart health, brain health, and supplements
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