You’re right – data have emerged suggesting that in people with elevated Lp(a), aspirin may work markedly better than in the “general” population. I’ll relate this to the broader body of research.
1. What does this specific study on Lp(a) + aspirin show?
The article you linked (ScienceDirect, 2024, preventive cardiology) analyzes people with:
- elevated lipoprotein(a) – a strong, inherited risk factor for heart attack/stroke,
- taking low‑dose aspirin for prevention.
In short (based on the abstract and commentary):
- In people with high Lp(a):
- low‑dose aspirin use was associated with about a ~50% relative risk reduction in major adverse cardiovascular events (MACE).
- In people without elevated Lp(a):
- the effect of aspirin was much weaker / similar to what we see in meta‑analyses like JAMA 2019 (i.e., minimal).
This suggests that Lp(a) may be a marker that “selects” a group particularly responsive to aspirin.
2. How does this compare to the “classic” studies (JAMA 2019, etc.)?
JAMA 2019 meta‑analysis (Zheng & Roddick) – general population, no selection by Lp(a):
- Absolute benefits:
- about 0.4–0.6% fewer cardiovascular events over several years.
- Absolute harms:
- about 0.5–0.7% more major bleeding events.
Conclusion: in the general population the balance is basically a tie → hence guidelines are moving away from routine aspirin in primary prevention.
Difference vs. the Lp(a) study:
- JAMA‑type meta‑analyses mix:
- low‑risk people,
- high‑risk people,
- but without selecting for Lp(a).
- The new study says:
– if we pull out of that mix a subgroup with very high, genetic risk (high Lp(a)),
– then aspirin may give a much larger relative risk reduction (around 50%).
This is a classic example of how averaging results “washes out” the effect in the whole population, and only a biomarker (Lp(a)) reveals who truly benefits.
3. What about bleeding risk in this group?
Key question: in people with high Lp(a):
- does benefit (fewer heart attacks/strokes) > harm (more bleeding)?
From the abstract and similar analyses:
- Bleeding risk with low‑dose aspirin remains similar to other studies (i.e., it increases).
- But:
- the absolute risk of cardiovascular events in people with high Lp(a) is much higher, so:
- the same relative reduction (e.g. 50%) translates into a much larger absolute benefit than in a low‑risk person.
In practice:
– in someone with high Lp(a) and high cardiovascular risk, aspirin may “tip the scales” toward net benefit,
– in a low‑risk person (and/or low Lp(a)) – the balance is still weak, as in JAMA 2019.
4. How does this relate to what the Howicured‑related books say?
Books:
-
“How Not to Die – Michael Greger”
- strongly emphasizes:
- small effect of aspirin/statins in primary prevention (in the general population),
- huge effect of a low‑fat, whole‑food plant‑based diet (Esselstyn: ~60% absolute risk reduction).
- Greger generally doesn’t go deep into Lp(a) as a selector subgroup for aspirin – he focuses on the general population.
-
“Timeless Secrets of Health and Rejuvenation – Andreas Moritz” (excerpts in the materials)
- is much more critical of:
- aspirin,
- anticoagulants,
- cardiac drugs in general.
- Emphasizes:
- bleeding risk,
- the possibility of drugs perpetuating disease,
- the superiority of diet, liver cleansing, lifestyle.
- In that framework, aspirin would be approached very cautiously even in high‑risk groups.
Difference in approaches:
5. How to synthesize this sensibly?
-
This new study does NOT overturn JAMA‑type meta‑analyses, it refines them:
- in the general population: aspirin’s effect is small and “eaten up” by bleeding,
- in the high‑Lp(a) subgroup: the effect may be large.
-
Lp(a) = a potential biomarker to personalize aspirin decisions:
- if someone has:
- high Lp(a),
- other risk factors (family history of early heart attacks, atherosclerosis on imaging),
- then:
- low‑dose aspirin may make sense, because:
- the benefit (fewer heart attacks/strokes) may clearly outweigh bleeding risk.
-
But even in this group:
- aspirin does not replace:
- diet,
- exercise,
- control of blood pressure, glucose, LDL,
- it is only an add‑on.
-
From the “book” perspective (Greger, Moritz):
- still valid:
- for most people it’s better to first exhaust the potential of diet and lifestyle,
and only then consider aspirin,
- especially if:
- they haven’t had a heart attack/stroke,
- they don’t have extremely high risk (including Lp(a)).
6. One‑sentence answer to your question
The study showing ~50% risk reduction with aspirin in people with high Lp(a) is consistent with the finding that in the general population aspirin has only a minimal effect – it simply identifies a narrow, high‑risk subgroup in which the benefit‑to‑risk balance may be clearly better, but it doesn’t change the fact that for most people (average risk, normal Lp(a)) diet and lifestyle provide a much larger and safer benefit than “aspirin just in case.”
If you’d like, in a next post I can lay out a concrete “thinking algorithm”:
– when to test Lp(a),
– how to interpret the result,
– in which scenarios aspirin makes sense according to the data, and in which it’s better to avoid it.
