Pillar 01
Inflammation that never resolves. Implicated in cardiovascular disease, diabetes, autoimmune conditions, several cancers, and cognitive decline.
| Test | What it measures | The number | What it misses |
|---|---|---|---|
| hs-CRP | C-reactive protein, which the liver makes when inflammatory signals reach it. The "hs" means the assay can read the low end, where a healthy person sits. | The CDC and the American Heart Association set three bands in 2003, in milligrams per litre of blood: under 1 is low, 1 to 3 is average, over 3 is high (PMID 12551878). | A single reading is close to uninterpretable. Measured repeatedly in the same healthy person it swings by roughly half its own value. A cold, a dental filling or a hard session in the gym all move it. |
| Interleukin 6 | One of the signals that tells the liver to make CRP, so it sits a step further upstream. | No threshold. I could not find a guideline body that has set one for people without a diagnosed disease. | Same day-to-day swing as CRP, and no agreed range to compare a result against. |
| ESR | How fast red blood cells settle out in a tube. Old, cheap, still ordered. | Normal rises with age, so the rule of thumb adjusts for it: age divided by two for men, age plus ten then divided by two for women, in millimetres per hour (PMID 6402065). | It is a rule of thumb rather than a guideline. Anaemia and pregnancy move it for reasons that have nothing to do with inflammation. |
| Fibrinogen, GlycA, neutrophil to lymphocyte ratio | Assorted proteins and cell counts that rise and fall alongside inflammation. | None of the three has a risk threshold set by any guideline body that I could find. | These are what pads an inflammation panel. They track CRP closely enough that they add very little once you already have it. |
CRP is the dashboard light, not the engine. If a high CRP were itself causing heart disease, then people born with gene variants that keep their CRP high for life should get more heart disease. Studies built around exactly that question find they do not. Interleukin 6, one step upstream, does behave like a cause (PMID 22421340). CRP looks like the readout rather than the mechanism, which matters because it is the number everybody tries to push down.
"Lowering inflammation" is not one thing, and the trials split. Six large trials have tried it in people with existing heart disease, three succeeded and three did not. Canakinumab, which blocks a signal called interleukin 1 beta, cut events in 10,061 people, a hazard ratio of 0.85, meaning about a 15 percent lower rate in the treated group (PMID 28845751). Two colchicine trials also worked. Low-dose methotrexate did not, and neither did two later trials, including one aimed squarely at interleukin 6. Which pathway you block turns out to matter more than whether the CRP number moves.
Everything above was measured in people who already had cardiovascular disease. I could not find a trial showing that driving down a healthy person's CRP, as a target in itself, changes what happens to them.
7 compounds covered here are marketed or taken on this rationale. Each entry says where its dose came from and what the published record supports, which is usually less than the pitch.
The identity check comes back clean, which is rare here. The only marketing authorisation I found is an injection into the penis, combined with a second drug, and the 50 microgram spray traces to a lung study in eight patients.
Its sequence does not appear in erythropoietin at all, which is the interesting part. Across a 1 mg to 8 mg range the response did not rise with the dose, the skin biopsy that diagnoses the disease did not move, and I found no trial registered anywhere after the 2017 announcement of progress.
KPV is the last three building blocks of a natural body signal, and almost every claim made for it borrows that signal's reputation. One lab put the two side by side and the borrowing did not hold.
The copper peptide has a credible human research record. All of it was rubbed on skin, two of the three controlled trials found nothing, and I could not find a published study injecting it into a person.
The two peptides recommended together more than any others. Neither has a completed human trial, and I could not find a single study of the pair.
The research everyone cites was run on thymosin beta-4. What is sold as TB-500 is seven amino acids cut out of it, and the FDA could not find a single published case of anyone giving it to a human.
The most popular recovery peptide has no published human trial, no known receptor, and a standard dose that looks like vial math.
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