Diagnostics
CardioMetabolic Testing — Insulin, Leptin and the Lipid Picture Behind Hormonal Symptoms
A normal fasting glucose is one of the most reassuring results in medicine, and one of the least informative. Glucose is a regulated variable: the body defends it, and it will hold inside the reference range for years while the amount of insulin required to keep it there quietly doubles. By the time glucose moves, the regulation has already been failing for a long time. This panel measures the regulation rather than the regulated number.
Contents
Why insulin and not glucose · What is measured · What the extra markers add · When I use this panel · How I read these results · What to expect · Key takeaways · FAQ · References
Why insulin and not glucose
Insulin is the instruction; glucose is the outcome. Measuring only the outcome tells you whether the system is still winning, not how hard it is working to win. Fasting insulin measured alongside fasting glucose gives the ratio between effort and result, which is what the homeostatic model assessment expresses as a single number.1 [Established]
That distinction matters here rather than in a diabetes clinic, because insulin is not only a fuel-handling hormone. It acts directly on the ovary, it changes hepatic production of sex hormone-binding globulin and therefore how much testosterone circulates unbound, and it is upstream of a large part of what presents as an ovulatory or androgenic problem. This page is about measuring it.
What is measured
Twenty-one measured and calculated analytes, plus six derived ratios — twenty-seven reported values in all, in five groups. The panel is wide because reading one group without the others produces a confident answer to the wrong question.
Metabolic regulation
| Marker | What it shows |
|---|---|
| Insulin (fasting) | How much signal is required to hold glucose where it is |
| Glucose (fasting) | The regulated variable, read against insulin rather than alone |
| Leptin | Adipose tissue reporting stored energy to the brain |
| Adiponectin | The adipose signal that moves with insulin sensitivity, not against it |
| 1,5-anhydroglucitol | Glycaemic excursions over roughly the preceding one to two weeks |
Lipid transport
| Marker | What it shows |
|---|---|
| Total cholesterol, LDL (calculated), HDL, non-HDL, VLDL, triglycerides | The standard picture, as the baseline for everything below |
| Apolipoprotein B | A count of atherogenic particles rather than the cholesterol inside them |
| Apolipoprotein A1 | The corresponding count for HDL particles |
| Lipoprotein(a) | A largely inherited, life-long concentration that a standard panel does not report |
| Small dense LDL (calculated) | The particle subset that tracks with triglyceride and insulin status |
| Oxidised LDL | Modified LDL, reported as a research-grade marker |
Inflammation and one-carbon status
| Marker | What it shows |
|---|---|
| C-reactive protein | Systemic inflammatory load |
| Lp-PLA2 activity | An enzyme carried on lipoproteins, associated with vascular inflammation |
| Homocysteine | One-carbon metabolism, dependent on folate, B12 and B6 status |
Filtration
| Marker | What it shows |
|---|---|
| Creatinine with eGFR | Standard estimate of kidney filtration |
| Cystatin C | A second, independent filtration estimate, less affected by muscle mass than creatinine6 |
Derived ratios
Six ratios are reported alongside the analytes. A ratio is often the more informative number, because it describes a relationship between two things that each vary widely between people.
| Ratio | What it describes |
|---|---|
| Leptin : adiponectin | The two adipose signals read as one number |
| Total cholesterol : HDL-C | The conventional summary of the standard profile |
| LDL-C : HDL-C | The conventional distribution measure |
| Oxidised LDL : HDL-C | Modified LDL scaled to HDL |
| Small dense LDL-C : LDL-C | What proportion of the LDL is in the small dense subset |
| Apolipoprotein B : apolipoprotein A1 | Atherogenic particle count against HDL particle count |
What the extra markers add
A routine lipid profile reduces lipid transport to two words, good and bad. That vocabulary is not wrong so much as too coarse to answer a clinical question, and it is the reason people whose standard profile reads as unremarkable can still be carrying a picture worth understanding. The markers below are where the resolution comes from.
1,5-anhydroglucitol reports the spikes, not the average. HbA1c describes mean glucose over roughly three months and is not on this panel. 1,5-anhydroglucitol works differently: it is reabsorbed by the kidney in competition with glucose, so it falls when glucose repeatedly rises above the renal threshold. A low value indicates that excursions have been happening over the preceding one to two weeks, in someone whose fasting glucose and HbA1c may both read as normal.7 [Established — human observational]
Leptin and adiponectin describe the tissue, not the meal. Leptin rises with stored fat and, when the brain stops responding to it, keeps rising while the signal it carries stops arriving. Adiponectin does the opposite: it falls as adipose tissue becomes insulin-resistant. Read as a ratio, the two track insulin resistance in people whose glucose is entirely normal.2 [Established — human observational] I read the ratio against body composition and history rather than against a threshold, because the useful information is usually in how far the two markers have moved apart in a particular person. [Clinical Heuristic]
Apolipoprotein B counts particles. Every atherogenic lipoprotein carries exactly one apoB molecule, so apoB is a count where LDL cholesterol is a mass. The two diverge in precisely the group this clinic sees most — people with raised triglycerides and insulin resistance, whose LDL cholesterol can look unremarkable while the particle count is high.3 [Established]
Lipoprotein(a) is measured once in a lifetime. Its concentration is largely genetically determined and changes little with diet, weight or exercise, which is why it is worth knowing and why it is not a treatment target here.4 [Established — consensus statement] It is on the panel because it is information a standard lipid profile does not give, and because a person is entitled to know it.
Homocysteine is measured, and the trial evidence is stated with it. Raised homocysteine is a real observation and reflects folate, B12 and B6 status. Lowering it with B vitamins was tested against cardiovascular events across many thousands of participants and did not reduce them.5 [Established — systematic review, null] I therefore read homocysteine as a nutritional-status marker, which is what it reliably is, and not as a target in itself.
On the research-grade markers
Oxidised LDL and Lp-PLA2 activity are reported by the laboratory and are included here for completeness. Their place in clinical decision-making is not settled.
When I use this panel
Where the presenting picture is metabolic and the standard bloods have been normal: irregular or absent ovulation, the PMOS pattern (polyendocrine metabolic ovarian syndrome, renamed from PCOS in 2026), weight that behaves as though the set point has moved, fatigue with a normal thyroid panel, a family history of type 2 diabetes or early cardiovascular disease, or a normal-BMI presentation with a strongly metabolic history. In men it is used where testosterone is low and the question is whether the cause sits upstream in metabolism rather than in the testis.
It is frequently ordered alongside Thyroid Testing or Steroid Hormone Testing, because the three axes constrain each other. The reasoning for reading them together is on Hormone Optimisation. It is also ordered in midlife, by people with no specific complaint who want a closer look at how their metabolic regulation is holding up.
How I read these results, and what happens next
Results come back to a consultation. I read the panel as one picture: how much insulin the system is spending, what the adipose signals say about where that is coming from, and how the lipid transport picture fits the rest of the history. What follows is a plan for the parts that are modifiable — nutritional pattern, training load and type, sleep and light exposure, inflammatory burden — with a repeat interval chosen to match the marker rather than the calendar.
Where a result needs a doctor’s attention, I say so plainly and write to your GP with the report.
What to expect
One venous blood draw, taken at the clinic or at a phlebotomy service. The draw is arranged fasted — insulin, glucose, triglycerides and the calculated LDL all require it, and fasting is what makes a repeat panel comparable with the first. Water is fine; take regular medication as normal unless I have said otherwise. Supplements belong in your intake form, B vitamins especially, since they change the homocysteine reading.
Fee: £450, inclusive of VAT. That covers the laboratory work and the interpretation consultation — 45 minutes, in person in Wimbledon or online. Fees for every other panel are on the functional lab testing page.
Key takeaways
- Glucose is defended and stays in range for years; insulin is what moves first, and this panel measures insulin.
- Insulin acts directly on the ovary and changes how much testosterone circulates unbound, which is why a metabolic panel belongs in a fertility workup.
- Leptin and adiponectin describe the state of adipose tissue, and read together they track insulin resistance in people whose glucose is normal.
- Apolipoprotein B counts atherogenic particles where LDL cholesterol measures their contents; the two diverge most in insulin-resistant people.
- Lipoprotein(a) is largely inherited and worth knowing once; it is not a target of anything offered here.
- Homocysteine is read as nutritional status, because lowering it with B vitamins did not reduce cardiovascular events in trials.
- One fasted blood draw, twenty-one analytes and six derived ratios, with the interpretation consultation included in the fee.
Frequently Asked Questions
Is this a heart test?
No. Several markers on it are cardiovascular in origin, and the panel will show them, but it is used here to describe metabolic regulation upstream of a hormonal or fertility question. Cardiovascular risk assessment and any decision about lipid-lowering treatment belong to your GP, and where something on the panel needs their attention I write to them with the report.
My GP already checked my cholesterol and it was fine. What does this add?
A standard NHS lipid profile reports total cholesterol, HDL, non-HDL and triglycerides, which is the right test for the question it is asked. This panel adds the particle counts, lipoprotein(a), and — the part that usually changes the picture — fasting insulin, leptin and adiponectin, none of which are on a routine profile. It is common for the standard panel to be unremarkable and the insulin picture not to be.
Can I have this without the initial consultation?
No. Testing is selected after an evaluation, because the value of a wide panel is in choosing the right one for a specific question. The same clinical context is what makes the interpretation of the results, and the recommendations that follow, reliable.
Do I need to fast?
Yes — the draw is arranged fasted, for insulin, glucose, triglycerides and the calculated LDL. Water is fine.
How often would it be repeated?
Where something is being actively changed, three to four months is usually the shortest interval at which a repeat says anything, because that is roughly how long the markers take to settle at a new level. Lipoprotein(a) is not repeated; it does not meaningfully change.
References
-
Matthews DR, Hosker JP, Rudenski AS, et al. Homeostasis model assessment: insulin resistance and β-cell function from fasting plasma glucose and insulin concentrations in man. Diabetologia. 1985;28(7):412–419. doi:10.1007/BF00280883 [Established] ↩︎
-
Finucane FM, Luan J, Wareham NJ, et al. Correlation of the leptin:adiponectin ratio with measures of insulin resistance in non-diabetic individuals. Diabetologia. 2009;52(11):2345–2349. doi:10.1007/s00125-009-1508-3 [Established — human observational] ↩︎
-
Sniderman AD, Williams K, Contois JH, et al. A meta-analysis of low-density lipoprotein cholesterol, non-high-density lipoprotein cholesterol, and apolipoprotein B as markers of cardiovascular risk. Circ Cardiovasc Qual Outcomes. 2011;4(3):337–345. doi:10.1161/CIRCOUTCOMES.110.959247 [Established — meta-analysis] ↩︎
-
Kronenberg F, Mora S, Stroes ESG, et al. Lipoprotein(a) in atherosclerotic cardiovascular disease and aortic stenosis: a European Atherosclerosis Society consensus statement. Eur Heart J. 2022;43(39):3925–3946. doi:10.1093/eurheartj/ehac361 [Established — consensus statement] ↩︎
-
Martí-Carvajal AJ, Solà I, Lathyris D, Dayer M. Homocysteine-lowering interventions for preventing cardiovascular events. Cochrane Database Syst Rev. 2017;8:CD006612. doi:10.1002/14651858.CD006612.pub5 [Established — systematic review, null] ↩︎
-
Inker LA, Schmid CH, Tighiouart H, et al. Estimating glomerular filtration rate from serum creatinine and cystatin C. N Engl J Med. 2012;367(1):20–29. doi:10.1056/NEJMoa1114248 [Established] ↩︎
-
Dungan KM, Buse JB, Largay J, et al. 1,5-anhydroglucitol and postprandial hyperglycemia as measured by continuous glucose monitoring system in moderately controlled patients with diabetes. Diabetes Care. 2006;29(6):1214–1219. PMID: 16731998 [Established — human observational] ↩︎
Related reading
- Thyroid Testing — the thyroid panel also reports lipids, but reads them as evidence of what the gland has been doing.
- Hormone Optimisation — how the metabolic, thyroid and steroid pictures are read together.
Book a consultation
Testing is selected after an evaluation, never ordered from a list. The starting point is an initial consultation at the clinic in Wimbledon. Book a consultation.
Agnes Ryu, OMD, MATCM is the founder of Dr Ryu Natural Medicine in Wimbledon, South West London. She qualified as a Licensed Oriental Medicine Physician in Korea in 1995 — a six-year medical degree — and holds an MSc in Human Physiology. She worked as a clinician and as a research biochemist at the Natural Products Research Institute, Seoul National University, and lectured in physiology and diagnostics at the Asante Academy of Chinese Medicine, Middlesex University, before moving into private practice. Her clinical focus has been on endocrine regulation, energy metabolism and fertility. She has over 30 years in clinical medicine and close to two decades focused on fertility. Member, Association of Traditional Chinese Medicine and Acupuncture UK (ATCM) — FM0200004.