Cardiometabolic
Raised homocysteine tracks clots and strokes. Whether it CAUSES them, or just marks the damage, is still the open question.
Not yet investigated
Raised homocysteine tracks clots and strokes. Whether it CAUSES them, or just marks the damage, is still the open question.
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.
Review, and admirably direct about the thing most coverage skips: raised homocysteine is a risk factor for cardiovascular disease, stroke and VENOUS THROMBOEMBOLISM, but 'it is still uncertain whether hyperhomocysteinemia is a causative factor or a marker of vascular disease'. The causal evidence is strongest in ANIMAL models. The mechanism, where it has been worked out, is endothelial: less bioavailable nitric oxide, either through oxidative inactivation or through inhibition of NO synthase by ADMA, plus thiolation of plasma and endothelial proteins and endoplasmic-reticulum stress driving inflammation and apoptosis. Read alongside the B12 node, where LOWERING homocysteine did not lower events — the two together are the whole argument.
Connected on the map
Also in Cardiometabolic
The letter
The full citation list for each investigation, the studies that didn't make the episode, and any corrections — sent the morning it publishes.
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