Lipoprotein(a) / LP(a): Elevated From HGH (During & After?)

I just received the results from an LP(a) blood test, and unfortunately, it's on the high side at around 52 ng/dL / 110 nmol/L.

I had previously been running HGH for around 18 months at around 2 IU/day but had around a 6-week unrelated break before running the LP(a) bloods.
I was blissfully unaware that HGH can affect LP(a), but it seems that HGH does in fact raise LP(a) significantly.

My case may well be hereditary, but I'm curious as to any other experiences running LP(a) during or after running HGH.

Here is the literature I came across. There is evidence of LP(a) returning to baseline after 6 weeks to 3 months:

Study 1:

Three months after the cessation of GH therapy, serum Lp(a) levels were not significantly different from the pre-treatment values.

Study 2:

Serum Lp(a) concentrations increased in all patients after only 6 weeks of treatment (205 ±13% of pretreatment values, mean±SEM) and remained increased after 26 weeks of treatment (196±16% of pretreatment values).In the four patients who started on active treatment, Lp(a)concentrations decreased to pretreatment concentrations 6 weeks after rhGH withdrawal (Figure 2).

Study 3:

Overnight fasting blood samples were collected immediately before and after 6 months hGH treatment. In all but one of the children there was a significant increase in serum Lp(a) over the 6 month treatment period -(+)66.7% over the basal levels (range 14 to 180%). After the hGH treatment, in six children Lp(a) levels were elevated to above 300 mg/l, the cut-off level for increased coronary artery disease (CAD) risk.

Study 4:

However, after 12 months of treatment, the Lp(a) concentration had increased by 44% and 101% above baseline and the control group, respectively. Men and women responded differently to GH, with a more marked increase in Lp(a) concentration and fat-free mass and a more pronounced decrease in body-fat mass in men.
 
I've started running my own Lp(a) experiments. I also didn't know HGH impacted this. I thought it was just AAS.

My tests so far:
1. Test 175mg, Primo 105mg: Lp(a) < 10
2. Test 120mg, No AAS, HGH 4IU: Lp(a) 31
Interesting - thanks for posting. Assume you were actively taking HGH while testing at 31 ng/dl? I have a feeling mine may be hereditary, especially seeing as the one trial above showed a return to baseline after 6 weeks, and I'd been off exactly that long.

Has me questioning whether I should continue running HGH, AAS, etc, despite the benefits. Not to mention other risks factors: life's pleasures, such as booze and excess food, amongst other things, which I like to enjoy from time to time.
 
I just received the results from an LP(a) blood test, and unfortunately, it's on the high side at around 52 ng/dL / 110 nmol/L.

I had previously been running HGH for around 18 months at around 2 IU/day but had around a 6-week unrelated break before running the LP(a) bloods.
I was blissfully unaware that HGH can affect LP(a), but it seems that HGH does in fact raise LP(a) significantly.

My case may well be hereditary, but I'm curious as to any other experiences running LP(a) during or after running HGH.

Here is the literature I came across. There is evidence of LP(a) returning to baseline after 6 weeks to 3 months:

Study 1:

Three months after the cessation of GH therapy, serum Lp(a) levels were not significantly different from the pre-treatment values.

Study 2:

Serum Lp(a) concentrations increased in all patients after only 6 weeks of treatment (205 ±13% of pretreatment values, mean±SEM) and remained increased after 26 weeks of treatment (196±16% of pretreatment values).In the four patients who started on active treatment, Lp(a)concentrations decreased to pretreatment concentrations 6 weeks after rhGH withdrawal (Figure 2).

Study 3:

Overnight fasting blood samples were collected immediately before and after 6 months hGH treatment. In all but one of the children there was a significant increase in serum Lp(a) over the 6 month treatment period -(+)66.7% over the basal levels (range 14 to 180%). After the hGH treatment, in six children Lp(a) levels were elevated to above 300 mg/l, the cut-off level for increased coronary artery disease (CAD) risk.

Study 4:

However, after 12 months of treatment, the Lp(a) concentration had increased by 44% and 101% above baseline and the control group, respectively. Men and women responded differently to GH, with a more marked increase in Lp(a) concentration and fat-free mass and a more pronounced decrease in body-fat mass in men.
Thanks for sharing these. I was unaware of this connection at all.
 
I don't think it is as simple as it increases lp(a) and therefore is bad enough to stop GH.

One of the studies says "high density lipoprotein cholesterol concentrations increased during treatment and were significantly higher than pretreatment levels after 26 weeks of treatment." This would help counteract the lp(a) increase. Growth hormone treatment of growth hormone-deficient adults results in a marked increase in Lp(a) and HDL cholesterol concentrations - PubMed

Another study straight up concludes that other changes counteract the lp(a) increase: "Our study shows an unfavorable effect of rhGH replacement therapy on Lp(a) levels, which is, however, counteracted by a favorable effect of rhGH on TC, LDL-C and the TC/LDL-C and LDL-C/HDL-C ratios." The effect of recombinant human GH replacement therapy on lipoprotein(a) and other lipid parameters in adults with acquired GH deficiency: results of a double-blind and placebo-controlled trial - PubMed
 
I don't think it is as simple as it increases lp(a) and therefore is bad enough to stop GH.

One of the studies says "high density lipoprotein cholesterol concentrations increased during treatment and were significantly higher than pretreatment levels after 26 weeks of treatment." This would help counteract the lp(a) increase. Growth hormone treatment of growth hormone-deficient adults results in a marked increase in Lp(a) and HDL cholesterol concentrations - PubMed

Another study straight up concludes that other changes counteract the lp(a) increase: "Our study shows an unfavorable effect of rhGH replacement therapy on Lp(a) levels, which is, however, counteracted by a favorable effect of rhGH on TC, LDL-C and the TC/LDL-C and LDL-C/HDL-C ratios." The effect of recombinant human GH replacement therapy on lipoprotein(a) and other lipid parameters in adults with acquired GH deficiency: results of a double-blind and placebo-controlled trial - PubMed

This is true. AAS, by the way, decrease Lp(a) with statistical significance, but without apparent clinical significance. We'd hardly regard androgens as beneficial for cardiovascular risks.

There is a class of drug known as antisense oligonucleotides (ASOs) that reduce Lp(a) to the tune of 50 - 80%. These hold potential for treating dyslipidemia by a novel mechanism, and could be used in combination with statins for a potent reduction in cardiovascular disease risk for long-term AAS users.
 
This is true. AAS, by the way, decrease Lp(a) with statistical significance, but without apparent clinical significance. We'd hardly regard androgens as beneficial for cardiovascular risks.

There is a class of drug known as antisense oligonucleotides (ASOs) that reduce Lp(a) to the tune of 50 - 80%. These hold potential for treating dyslipidemia by a novel mechanism, and could be used in combination with statins for a potent reduction in cardiovascular disease risk for long-term AAS users.
Yes, the ASOs look very promising, although I'd imagine some way off from being available. From the Attia/Benoît Arsenault podcast in 2022:
1733587650975.webp

Do you know which AAS, in particular, are known to lower LP(a)?
 
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