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Each routine lab reads one layer. Your inflammation system has many.

hs-CRP, blood counts, A1c and ApoB each measure something real, and your prescriber relies on them. Here is what each one measures during GLP-1 therapy, what it can’t show, and what the Inflammation Compass adds by reading which genes your immune cells are using.

Reserve your spot The routine labs

A response starts and then ends.
Routine labs don’t read how it ends.

When your body meets a virus, an injury or a hard workout, one set of signals starts a response: they raise the alarm and call in immune cells. A second set ends it: they calm the alarm, clear away spent cells and begin repair.

GLP-1 medicines such as semaglutide and tirzepatide lower common inflammation markers. The routine tests that show it are well established and inexpensive, and each reads one layer: a protein the liver releases, a count of cells, or something circulating that feeds inflammation. None of them directly reports the signals that end a response.

Activation starts a response
Immune cells sense a trigger, send alarm signals and call in more cells. hs-CRP is a protein the liver releases further downstream of those signals, and a blood count tallies the cells that arrive.
Resolution ends it
Calming signals stop more cells arriving, regulatory cells hold the response down, and spent cells are cleared so repair can begin. Routine labs don’t read this half, and blood shows some of it only in part.

The labs often ordered with GLP-1 therapy,
and what each one can’t show.

Labs and online testing services often sell these markers together as GLP-1 panels. Which ones you need is your prescriber’s call; this is what each measures.

Proteins the liver releases

hs-CRP, ESR and ferritin rise when inflammation signals reach the liver. They are the most common inflammation tests.

  • hs-CRP

    How much C-reactive protein is in your blood. The liver releases it when signals such as IL-6 reach it. It rises about 6 hours after a trigger and peaks around 48 hours.3

    On GLP-1 therapy. In the STEP 1–3 trials, semaglutide lowered hs-CRP by 39–48% compared with placebo.1 In the European subpopulation of SELECT, hs-CRP fell by about 12% by week 4 and 19% by week 8, before major weight loss, and fell even in participants who lost little weight.2

    What it can’t show. It shows how much of one protein is in your blood. It wasn’t designed to show which parts of your inflammation system changed, or whether the signals that end a response are at work.

  • ESR

    How fast red blood cells settle in a tube. Fibrinogen and other proteins speed the settling.

    On GLP-1 therapy. Fibrinogen falls slowly with long-term weight loss, and because it lasts about four days in the blood, ESR takes weeks to change.

    What it can’t show. Red cell shape, mild anemia, antibodies and sex all affect it, so it moves too slowly and for too many reasons to show what changed early in therapy.

  • Ferritin

    An iron-storage protein that also rises with inflammation, in response to IL-1β, TNF and IL-6.

    On GLP-1 therapy. It is often raised at baseline in people with obesity and fatty liver, and tends to fall as liver fat clears.

    What it can’t show. A raised ferritin is more often due to inflammation, liver disease or metabolic syndrome than to iron overload, and inflammation can hide iron deficiency, so a result within the lab’s reference range can’t rule it out.4

Blood counts and ratios

A complete blood count is a headcount: how many of each kind of white blood cell are circulating. Ratios divide one count by another.

  • CBC differential

    Counts of neutrophils, lymphocytes, monocytes, eosinophils and basophils.

    On GLP-1 therapy. Obesity is linked with slightly raised white cell counts, and weight loss often brings total white count and neutrophil share down a little.

    What it can’t show. A count gives cell numbers without describing their activity. Exercise and dehydration can shift counts within minutes.

  • NLR

    Neutrophils divided by lymphocytes, the neutrophil-to-lymphocyte ratio.

    On GLP-1 therapy. Stress hormones raise it, so a fast dose increase, a large calorie deficit, nausea or dehydration can move it for a while.

    What it can’t show. It shifts with sleep, hydration and time of day. A meta-analysis of observational studies linked a higher NLR with cardiovascular disease risk across populations.5

  • SII and MHR

    Two composite ratios: platelets × neutrophils ÷ lymphocytes (SII), and monocytes ÷ HDL cholesterol (MHR).

    On GLP-1 therapy. In laboratory studies, GLP-1 receptor activation reduced platelet aggregation.6 Lipid changes on therapy also move the HDL side of MHR.

    What it can’t show. Like the counts they are built from, these ratios describe how many cells there are, not what they are doing.

Metabolic and cardiovascular labs

These labs measure what is circulating that can drive inflammation in blood vessels and tissue, such as sugar and fat particles.

  • ApoB

    The number of circulating particles that can carry cholesterol into artery walls (LDL, VLDL and IDL).

    On GLP-1 therapy. It tends to fall as the liver releases less VLDL and liver fat clears.

    What it can’t show. It counts particles. It doesn’t show whether immune cells are responding to them in the artery wall.

  • HbA1c and HOMA-IR

    Average blood sugar over roughly the past 2–3 months (HbA1c), and fasting insulin and glucose together (HOMA-IR).

    On GLP-1 therapy. Both usually fall on GLP-1 therapy, which increases insulin release when blood sugar is high and lowers glucagon.

    What it can’t show. High blood sugar feeds inflammation, so lowering it removes one input. These tests don’t measure what the inflammation system is doing.

  • Homocysteine

    An amino acid from protein breakdown, cleared with the help of vitamins B12, folate and B6.

    On GLP-1 therapy. Eating less on a GLP-1 medication can lower B12 and folate intake, which can raise homocysteine.

    What it can’t show. In the HOPE-2 and NORVIT trials, lowering homocysteine with B vitamins did not reduce cardiovascular events.7,8 A marker can move without the outcome it stands for moving with it.

Specialty tests

Some clinicians order direct cytokine tests or an omega-3 index.

  • Serum cytokines (IL-6, TNF-α)

    The signaling proteins themselves. In mice, GLP-1 receptor activation in the brain lowered TNF-α released in response to an immune trigger.9

    On GLP-1 therapy. IL-6 is cleared from the blood within minutes to an hour, and working muscle releases it during hard exercise.

    What it can’t show. A single sample catches a signal that rises and falls quickly, so two samples a day apart can differ widely.

  • Omega-3 index

    The share of EPA and DHA in red blood cell membranes, averaged over the cells’ 120-day life.

    On GLP-1 therapy. EPA and DHA are the raw materials for pro-resolving mediators, signals that help end a response.10

    What it can’t show. It shows the supply of raw materials, not whether immune cells are using them to end a response.

What routine labs do better
is worth saying plainly.

The Inflammation Compass adds to the labs your prescriber orders and doesn’t replace them.

Cost and coverage
Routine chemistry is inexpensive and usually covered by insurance. RNA sequencing costs more and is paid for directly.
Outcome evidence
hs-CRP, A1c and lipids have decades of large trials behind them, including SELECT and STEP. The six readings come from pathways drawn from published research, and how they move in people on GLP-1 therapy is still being studied.
Clinical cutoffs
Labs such as HbA1c have guideline thresholds used for diagnosis. The six readings have no cutoffs: each is placed against a reference group, people whose blood was measured the same way, and against your own earlier samples.
Turnaround
Routine results often come back within a day or two. Inflammation Compass results are expected about one month after the laboratory receives your sample.
Intended use
Many routine tests are cleared to help diagnose disease and guide prescribing. The Inflammation Compass is a wellness test run in a CLIA-certified laboratory. It isn’t FDA cleared or approved, and it doesn’t diagnose disease.

Six readings show
which part of your inflammation system is doing what.

The Inflammation Compass reads which genes your immune cells are using, from the signals that start a response to the signals that end it. Your report groups 38 pathways, groups of genes that work together on one job, into six readings: three for each half.

Activation starts a response

Activation Level
The fast, built-in alarm: signals that raise fever and call in immune cells.
Targeted Defense
Signals that show a threat to T cells and power up cells that kill targets.
Where the Fast Response Is Working
Mainly in the blood, or moving cells out into tissue. This one is a balance, not a level.

Resolution ends it

Resolution Level
Early feedback and calming signals that keep a response from running on.
Regulatory Cells & Repair Signals
Regulatory T cells and repair signals that hold a response down over time.
Clean-up & Rebuilding
Spent immune cells are cleared away and the body shifts toward repair.

Each reading sits within its reference range, at its edge, below it or above it. From your second sample, each is also marked as moved or about the same. A result is a position, never a grade, and lower isn’t better: the aim is a response that fits the situation and ends when its work is done.

Your report also estimates your immune cell mix, the share of each kind of immune cell in your sample, from the same RNA. It is an estimate and doesn’t replace a blood count, but because it comes from the same sample, you can see whether the mix shifted alongside a reading.

See what the report includes

What it
can't tell you.

The Inflammation Compass shows what changed and by how much. It can’t show why, because many things move these readings, and it doesn’t show whether a medication is working or is safe. It doesn’t diagnose, rule out or predict any disease, measure drug levels, or show where in your body inflammation is taking place.

A reading within its range means you are similar to the reference group at that sample, which is not a statement about your health. What a change means is for you and your clinician to weigh.

Read more
about GLP-1 therapy.

Bring your clinician a read across your inflammation system.

Your first sample starts your personal baseline, to read beside the labs your prescriber already orders.

Reserve your spot For clinical practices
Sources and further reading

References

1. Verma S, et al. (2023) — Effects of once-weekly semaglutide 2.4 mg on C-reactive protein in adults with overweight or obesity (STEP 1, 2, and 3): exploratory analyses of three randomised, double-blind, placebo-controlled, phase 3 trials. EClinicalMedicine. 55:101737. doi:10.1016/j.eclinm.2022.101737. PMID 36467859.
2. Plutzky J, et al. (2026) — Effect of semaglutide on the inflammatory biomarker high-sensitivity CRP in patients with established cardiovascular disease and overweight or obesity in SELECT: a prespecified secondary analysis. Circulation. 154(11):976–991. doi:10.1161/CIRCULATIONAHA.125.074482. PMID 42610271.
3. Pepys MB, Hirschfield GM. (2003) — C-reactive protein: a critical update. J Clin Invest. 111(12):1805–1812. doi:10.1172/JCI18921. PMID 12813013.
4. Cullis JO, et al. (2018) — Investigation and management of a raised serum ferritin. Br J Haematol. 181(3):331–340. doi:10.1111/bjh.15166. PMID 29672840.
5. Angkananard T, et al. (2018) — Neutrophil lymphocyte ratio and cardiovascular disease risk: a systematic review and meta-analysis. Biomed Res Int. 2018:2703518. doi:10.1155/2018/2703518. PMID 30534554.
6. Cameron-Vendrig A, et al. (2016) — Glucagon-like peptide 1 receptor activation attenuates platelet aggregation and thrombosis. Diabetes. 65(6):1714–1723. doi:10.2337/db15-1141. PMID 26936963.
7. Lonn E, et al. (2006) — Homocysteine lowering with folic acid and B vitamins in vascular disease (HOPE-2). N Engl J Med. 354(15):1567–1577. doi:10.1056/NEJMoa060900. PMID 16531613.
8. Bønaa KH, et al. (2006) — Homocysteine lowering and cardiovascular events after acute myocardial infarction (NORVIT). N Engl J Med. 354(15):1578–1588. doi:10.1056/NEJMoa055227. PMID 16531614.
9. Wong CK, et al. (2024) — Central glucagon-like peptide 1 receptor activation inhibits Toll-like receptor agonist-induced inflammation. Cell Metab. 36(1):130–143.e5. doi:10.1016/j.cmet.2023.11.009. PMID 38113888.
10. Serhan CN. (2014) — Pro-resolving lipid mediators are leads for resolution physiology. Nature. 510(7503):92–101. doi:10.1038/nature13479. PMID 24899309.