The mutation that protects against malaria does not protect against its cousin — and the spleen that would clear it has usually stopped working by age five.
Filed under ConditionConstellation Minerals & ironStatus Upcoming
Not yet investigated
What we have so far
The mutation that protects against malaria does not protect against its cousin — and the spleen that would clear it has usually stopped working by age five.
This star is on the map because the show intends to take the question apart properly — the trials, how it is actually tested, whether the thing sold is the thing studied. That work is not done yet, and nothing here should be read as a conclusion. When the investigation is published it will appear on this page.
What we are reading
Gathered for the investigation and not yet written up. Each note says what the paper does and does not show.
Beri D, Rodriguez M, Singh M, McLaughlin D, Liu Y, Zhong H, Mendelson A, An X, Manwani D, Yazdanbakhsh K, Lobo CA. Babesiosis and sickle red blood cells: loss of deformability, altered osmotic fragility, and hypervesiculation.Blood · 2025 · 145(19):2202–221310.1182/blood.2024027602 · PMID 39869831
Read from the sickle cell side this is a paper about membranes. The SS red cell is already rigid, already fragile, already shedding vesicles; a parasite that remodels the membrane to get in and out lands on a cell with no reserve. Pair it with the transfusion cases: both the route in and the tissue it lands on are worse in sickle cell disease than anywhere else.
Cursino-Santos JR, Singh M, Senaldi E, Manwani D, Yazdanbakhsh K, Lobo CA. Altered parasite life-cycle processes characterize Babesia infection in human sickle cell anemia.Haematologica · 2019 · 104(11):2189–219910.3324/haematol.2018.214304 · PMID 30923098
The evolutionary frame for the sickle cell node: haemoglobin S is the textbook case of balanced polymorphism — one copy protects against malaria, two copies cause disease. This paper tests whether that protection generalises to Babesia and finds it does not transfer to the trait. Explain balanced polymorphism plainly when this runs; it is the single most elegant idea in human genetics and it is usually taught badly.
