You go to your GP. You ask for a blood test. The results come back. A line at the bottom says "results reviewed — within normal limits." You're none the wiser.
Or you order a comprehensive private panel from Medichecks or Forth. Sixty markers. The report flags three things. The rest gets a green tick. You stare at the numbers and don't know what to do with them.
The problem isn't the test. The problem is that standard blood chemistry reporting is designed to identify disease — not to optimise health, identify early dysfunction, or explain why you feel the way you do. Here are five things your blood chemistry panel is telling you that the report almost certainly isn't.
1. Whether your insulin resistance began years ago
Fasting glucose is the standard metabolic marker. In the UK, NICE counts a fasting glucose of 5.5–6.9 mmol/L (about 99–124 mg/dL) as high risk of type 2 diabetes; the ADA 2025 starts at 5.6 (100 mg/dL). But insulin resistance — the underlying metabolic dysfunction that eventually produces elevated glucose — typically develops years before fasting glucose becomes abnormal.
The reason: as cells become less responsive to insulin, the pancreas compensates by producing more of it. Glucose stays controlled. Insulin climbs. This is why fasting insulin is the earlier and more sensitive marker — it captures the compensatory phase that glucose misses entirely. Fasting insulin above my working band of 18–48 pmol/L (3–8 µIU/mL) suggests the pancreas is working harder than it should, even when fasting glucose is 4.8 mmol/L (86 mg/dL) and the report says "normal metabolic function." There’s no standardised insulin assay, so the band is my judgement, not a validated range.
The calculated HOMA-IR score (glucose × insulin ÷ 22.5) gives a single insulin resistance index. There’s no agreed cut-off, so I watch the trend over repeat tests rather than one number (Wallace 2004). Most standard lab reports don't calculate this — or test fasting insulin at all.
2. Whether your thyroid is actually converting
The standard thyroid test is TSH. The functional thyroid picture requires TSH, Free T4, and Free T3 — and the story usually lives in the relationship between Free T4 and Free T3.
Free T4 is the storage form of thyroid hormone. Free T3 is the active form that enters cells and drives metabolism. The conversion requires selenium, iron, and a healthy gut microbiome. It's directly impaired by elevated cortisol, systemic inflammation, and low ferritin.
A TSH of 2.2 and Free T4 of 14 look acceptable on a standard report. Free T3 of 4.0 pmol/L (2.6 pg/mL) — below the 5.0–6.5 pmol/L I aim for — is worth investigating alongside the symptoms. It isn’t a diagnosis on its own. Without Free T3 on the panel, this pattern is invisible.
3. The real picture of your cardiovascular risk
Total cholesterol is the number your GP discusses. The TG:HDL ratio is the number that tells you whether you actually have a metabolic problem.
High triglycerides combined with low HDL produces the small dense LDL pattern — the genuinely atherogenic form of LDL that standard lipid testing doesn't distinguish from the large buoyant form. The Atherogenic Index of Plasma (AIP — log10 of TG divided by HDL) quantifies this with more precision than total cholesterol ever could. Neither calculation appears on a standard lab report.
4. Whether your methylation cycle is working
Homocysteine is on most comprehensive blood panels. It is almost never discussed in the GP consultation that follows.
Homocysteine is an intermediate in the methylation cycle — the one-carbon metabolic pathway that underpins DNA synthesis, neurotransmitter production, oestrogen clearance, and cellular repair. When methylation is impaired, homocysteine accumulates.
The conventional upper reference is 15 µmol/L. I flag it at about 11 µmol/L, a clinical judgement rather than a validated cut-off. Higher levels within the range go with cardiovascular and dementia risk in observational studies. In the VITACOG trial, B vitamins slowed brain shrinkage in older people with memory problems, and the benefit was in those starting above 13 µmol/L (Smith 2010). The most common drivers are low B12 and low folate; MTHFR variants play a part in some people.
5. Whether your inflammation is driving everything else
hs-CRP is the high-sensitivity inflammation marker. Many reports only flag CRP above 5 mg/L. For heart risk, the CDC/AHA tiers are below 1 mg/L low, 1–3 average and above 3 high (Pearson 2003). So an hs-CRP of 2.4 mg/L passes a standard report unremarked, though it sits in the average-risk tier for the heart. Whether it’s also driving thyroid, insulin or stress-hormone problems is a reasonable question to investigate, not an established finding.
Chronic low-grade inflammation at the 1–3 mg/L level is one of the most common findings in clients presenting with persistent, multi-system symptoms. It's the connective thread between a thyroid problem, a gut problem, a hormonal problem, and a fatigue problem. Address the inflammation and the other markers often begin to improve without direct intervention.
"The most important number on your blood panel is often not the one that's flagged. It's the one sitting in the lower portion of the reference range — technically normal, functionally insufficient, and quietly driving the symptoms you've been investigating for years."
The patterns described in this article are supported by peer-reviewed research. For the evidence behind these markers, including homocysteine, HOMA-IR and the TG:HDL ratio, see the evidence base page:
Read the TDG Evidence Base →Comprehensive blood chemistry is one of the most powerful and accessible investigative tools in functional medicine. The test itself is not the limitation. What you do with the numbers — and whether you're interpreting them against the right standards — is everything.
Sources
- NICE Quality Standard QS209, statement 1: high risk of type 2 diabetes = fasting plasma glucose 5.5–6.9 mmol/L or HbA1c 42–47 mmol/mol (6.0–6.4%). nice.org.uk/guidance/qs209
- American Diabetes Association. Standards of Care in Diabetes—2025: Diagnosis and classification. Diabetes Care 2025. PMID 39651986.
- Wallace TM, Levy JC, Matthews DR. Use and abuse of HOMA modeling. Diabetes Care 2004. PMID 15161807. doi:10.2337/diacare.27.6.1487
- Smith AD et al. Homocysteine-lowering by B vitamins slows brain atrophy in mild cognitive impairment (VITACOG). PLoS One 2010. PMID 20838622. doi:10.1371/journal.pone.0012244
- Pearson TA et al. Markers of inflammation and cardiovascular disease (CDC/AHA statement). Circulation 2003. PMID 12551878. doi:10.1161/01.cir.0000052939.59093.45