Lab result explainedHormonesLast updated November 10, 2026

C-peptide test: normal range, what high and low levels mean, and type 1 vs type 2

C-peptide · Ordered on its own or with glucose and insulin (diabetes classification, hypoglycemia work-up) · reported in ng/mL (SI: nmol/L; ng/mL x 0.331 = nmol/L)

C-peptide (connecting peptide) is a short protein chain that the pancreas releases in equal amounts with insulin, so measuring it tells you how much insulin your own body is making. A fasting C-peptide of roughly 0.5 to 2.0 ng/mL is normal (some labs print 0.8 to 3.1 or 1.1 to 4.4; use the range on your report). The test is mainly used to answer two questions: is this diabetes type 1 or type 2, and, in someone with low blood sugar, is the insulin coming from the pancreas or from somewhere else.

In the pancreas, insulin is first made as proinsulin, which is split into insulin and C-peptide; both leave the beta cell together. Insulin is cleared by the liver within minutes, but C-peptide lasts about 30 minutes and is cleared by the kidneys, so it gives a steadier readout of pancreatic output. Crucially, injected insulin contains no C-peptide, which is why the test can tell your own insulin from a prescribed dose and why it is the standard way to check whether a person with diabetes still has working beta cells.

The result only makes sense next to a glucose taken at the same time. A C-peptide of 0.4 ng/mL during a glucose of 250 mg/dL means the pancreas cannot respond and points to type 1 diabetes or advanced type 2; the same 0.4 during a fasting glucose of 80 is simply a quiet, healthy pancreas. A high C-peptide with a high glucose means insulin resistance; a high C-peptide with a glucose under 55 mg/dL is the signature of an insulin-producing tumor or a sulfonylurea drug.

C-peptide at a glance

  • What it is: a by-product released one-for-one with insulin, so it measures your own insulin production; injected insulin does not contain it.
  • Fasting normal: about 0.5-2.0 ng/mL (0.17-0.66 nmol/L); some labs print 0.8-3.1 or 1.1-4.4 ng/mL. Labs differ; 1 ng/mL = 0.33 nmol/L.
  • Low (under 0.6 ng/mL with a glucose over 144 mg/dL): severe insulin deficiency, typical of type 1 diabetes or long-standing type 2; these people need insulin.
  • High (above the lab's upper limit): insulin resistance, obesity, early type 2 diabetes, kidney disease, sulfonylurea drugs or, with low glucose, an insulinoma.
  • Type 1 vs type 2: a random C-peptide above 1.8 ng/mL (0.6 nmol/L) 3 or more years after diagnosis makes type 1 unlikely; under 0.6 ng/mL (0.2 nmol/L) makes it likely.
  • Next step: always read it with the paired glucose; repeat after a meal (stimulated C-peptide) if the fasting result is borderline.

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What C-peptide measures

Beta cells in the pancreas make a single long molecule, proinsulin, and enzymes cut it into insulin and C-peptide just before release. Every molecule of insulin that enters the blood is matched by one molecule of C-peptide, so the C-peptide concentration mirrors insulin secretion. The two differ in what happens next: about half of the insulin is removed on its first pass through the liver and the rest has a half-life of 3 to 5 minutes, while C-peptide bypasses the liver and is cleared by the kidneys with a half-life of about 30 minutes. C-peptide levels are therefore about five times higher than insulin levels in molar terms and fluctuate less.

The lab measures C-peptide by immunoassay on a blood sample, usually fasting; results are given in ng/mL in the US and nmol/L elsewhere (ng/mL x 0.331 = nmol/L). A stimulated C-peptide, drawn 90 minutes to 2 hours after a standard mixed meal or a glucagon injection, tests the pancreas's reserve and is more informative than a fasting level when the fasting value is in the low-normal range. A urine C-peptide-to-creatinine ratio on a sample passed 2 hours after a meal is a non-invasive alternative used in some clinics.

Several things shift the number without any change in the pancreas. Kidney impairment slows clearance, so C-peptide is raised in chronic kidney disease (eGFR under 60) and must be interpreted cautiously. The level is lowest after an overnight fast and highest 30 to 90 minutes after eating, so timing matters. Hypoglycemia itself suppresses secretion, which is why a C-peptide taken at a glucose under 55 mg/dL should be low: a value that is not low during hypoglycemia is the abnormal finding.

Normal range for C-peptide

Reference ranges vary between labs and by age, sex and pregnancy. Use the range printed on your own report.

GroupTypical range (ng/mL (SI: nmol/L; ng/mL x 0.331 = nmol/L))Notes
Fasting adult, typical reference rangeAbout 0.5-2.0 ng/mL (0.17-0.66 nmol/L)Labs differ widely: 0.8-3.1, 0.9-1.8 and 1.1-4.4 ng/mL are all in use; read against the range printed on your report.
Non-fasting / after a mealRises 2-5 fold, commonly 2-8 ng/mLPeak at 30-90 minutes. A random value is only interpretable with the paired glucose.
Stimulated (mixed-meal or glucagon) peakAbove 1.8 ng/mL (0.6 nmol/L)Substantial endogenous insulin production; type 2 diabetes or a non-insulin-requiring state is likely.
Stimulated peak, intermediate0.6-1.8 ng/mL (0.2-0.6 nmol/L)Reduced reserve; seen in early type 1, LADA and long-standing type 2. Repeat in 6-12 months if the classification is uncertain.
Severe insulin deficiencyBelow 0.6 ng/mL (0.2 nmol/L) with glucose above 144 mg/dLTypical of established type 1 diabetes and pancreatic diabetes. Below 0.24 ng/mL (0.08 nmol/L) is absolute deficiency; these people are at risk of ketoacidosis without insulin.
Insulinoma criteria (during hypoglycemia, glucose under 55 mg/dL)C-peptide 0.6 ng/mL or above with insulin 3 uIU/mL or aboveEndocrine Society criteria, with proinsulin 5 pmol/L or above and a negative sulfonylurea screen. A normal pancreas suppresses C-peptide below 0.6 at this glucose.
Exogenous (injected) insulin as cause of hypoglycemiaHigh insulin with C-peptide below 0.6 ng/mLInjected insulin contains no C-peptide, so the mismatch identifies it.
Chronic kidney diseaseOften 1.5-3 times higher than expectedThe kidney clears C-peptide; reduced eGFR raises the level without more insulin being made.

High C-peptide

A high C-peptide means the pancreas is secreting more insulin than usual, or clearing it more slowly. By far the most common reason is insulin resistance: when muscle, liver and fat respond poorly to insulin, the pancreas compensates by producing more, and fasting C-peptide rises to 2 to 4 ng/mL or beyond, often with a normal or mildly raised glucose. This is the picture of prediabetes, early type 2 diabetes, obesity, PCOS and fatty liver, and it means the beta cells are still working, which is good news for how the diabetes can be treated.

A high C-peptide is also what distinguishes type 2 from type 1 diabetes. In type 1 the beta cells are destroyed and C-peptide is low; in type 2 it is normal or high, at least in the first decade. A random C-peptide above 1.8 ng/mL (0.6 nmol/L) in someone diagnosed more than three years ago makes type 1 very unlikely and suggests that insulin, if being used, might be replaced by other drugs under supervision.

The one setting where a high C-peptide is dangerous is during hypoglycemia. When blood glucose is under 55 mg/dL the pancreas should switch insulin off and C-peptide should fall below 0.6 ng/mL. A C-peptide that stays at or above 0.6 with an insulin at or above 3 uIU/mL at that glucose means insulin is being produced inappropriately: an insulinoma (a usually benign insulin-secreting tumor of the pancreas), a sulfonylurea or meglitinide drug, or rarely an autoimmune insulin syndrome. This combination needs specialist investigation.

Common causes

  1. Insulin resistance, obesity and metabolic syndrome

    The pancreas raises insulin output to overcome resistance; fasting C-peptide of 2 to 5 ng/mL with a normal or slightly raised glucose is typical. Weight loss lowers it in parallel with fasting insulin.

  2. Type 2 diabetes (early to mid-course)

    C-peptide is normal or high for years after diagnosis, confirming residual beta-cell function. It drifts down over 10 to 20 years as beta cells fail, which is when insulin becomes necessary.

  3. Chronic kidney disease

    C-peptide is cleared by the kidneys, so levels rise as eGFR falls, by 50 to 200 percent in advanced disease, without any increase in insulin secretion. Results in CKD are interpreted with this in mind.

  4. Sulfonylureas and meglitinides

    Glipizide, glimepiride, glyburide, repaglinide and nateglinide stimulate the pancreas directly, raising both insulin and C-peptide, and can cause hypoglycemia with a high C-peptide that mimics an insulinoma; a drug screen separates the two.

  5. Insulinoma

    A small tumor of the beta cells that secretes insulin regardless of glucose. The hallmark is fasting hypoglycemia (glucose under 55 mg/dL) with C-peptide of 0.6 ng/mL or more and insulin of 3 uIU/mL or more, confirmed on a supervised 72-hour fast.

  6. Cushing's syndrome, acromegaly and steroid treatment

    Excess cortisol or growth hormone, and glucocorticoid drugs such as prednisone, cause insulin resistance and raise C-peptide within days.

  7. Pregnancy and gestational diabetes

    Placental hormones increase insulin resistance in the second and third trimesters; C-peptide rises physiologically and falls after delivery.

  8. Post-meal sampling or recent glucose load

    A C-peptide drawn an hour after eating or during an oral glucose tolerance test is normally 2 to 5 times the fasting value; mislabelled timing is a common cause of an apparently high result.

  9. GLP-1 agonists, DPP-4 inhibitors and some other drugs

    Semaglutide, liraglutide, sitagliptin and related drugs enhance glucose-dependent insulin release; oral contraceptives and some antipsychotics raise C-peptide through insulin resistance.

  10. Insulin autoimmune syndrome and other rare causes

    Antibodies that bind insulin (sometimes triggered by drugs containing sulfhydryl groups) cause erratic release of bound insulin with high measured insulin and C-peptide; non-islet cell tumors and nesidioblastosis after bariatric surgery are other rare causes.

Symptoms that can go with it

  • Usually none; a high C-peptide from insulin resistance is silent
  • Weight gain around the middle, carbohydrate cravings and tiredness after meals
  • Darkened velvety skin folds (acanthosis nigricans) and skin tags with insulin resistance
  • With insulinoma or sulfonylurea excess: sweating, shaking, hunger, palpitations and confusion when fasting or hours after a meal, relieved by eating
  • Blurred vision, odd behavior, seizures or loss of consciousness from severe hypoglycemia
  • Weight gain from repeated eating to prevent low blood sugar
  • In pregnancy, a high glucose on screening tests

Low C-peptide

A low C-peptide means the pancreas is making little insulin. When the paired glucose is high (above about 144 mg/dL) a C-peptide below 0.6 ng/mL (0.2 nmol/L) indicates severe insulin deficiency: the person cannot make enough insulin to control glucose and needs insulin treatment. This is the expected finding in established type 1 diabetes, in LADA once the autoimmune process has run for a few years, in type 2 diabetes after many years, and in diabetes caused by chronic pancreatitis, pancreatic surgery, cystic fibrosis or hemochromatosis. A value under 0.24 ng/mL (0.08 nmol/L) is near-absolute deficiency and carries a risk of diabetic ketoacidosis if insulin is interrupted.

A low C-peptide with a normal or low glucose is a different story. In a healthy person who has fasted overnight, C-peptide at the bottom of the range is simply a quiet pancreas. During hypoglycemia (glucose under 55 mg/dL), a low C-peptide is the correct response, and if insulin is nonetheless high it means the insulin came from an injection, whether accidental, deliberate or, rarely, factitious. Newly diagnosed type 1 diabetes often shows a low-normal rather than very low C-peptide, and some residual secretion persists for years in many people; even small amounts (above 0.6 ng/mL stimulated) are associated with fewer severe hypoglycemic episodes and complications.

Common causes

  1. Type 1 diabetes

    Autoimmune destruction of beta cells. C-peptide is low-normal to low at diagnosis and falls to under 0.6 ng/mL in most people within 3 to 5 years, though 30 to 50 percent retain a small detectable amount for much longer. GAD, IA-2 and ZnT8 antibodies confirm the cause.

  2. Latent autoimmune diabetes in adults (LADA)

    A slower autoimmune diabetes diagnosed in adults who are often first treated as type 2. C-peptide is initially preserved and then declines; antibody-positive adults with a falling C-peptide usually need insulin within 5 years.

  3. Long-standing type 2 diabetes

    After 10 to 20 years of compensating for insulin resistance, beta cells become exhausted and C-peptide falls, which explains why tablets stop working and insulin is needed.

  4. Pancreatic disease and surgery

    Chronic pancreatitis, pancreatectomy, pancreatic cancer, cystic fibrosis and iron overload (hemochromatosis) destroy or remove beta cells; this is sometimes called type 3c diabetes and C-peptide is low with glucose high.

  5. Injected insulin causing hypoglycemia

    Insulin from a syringe or pen suppresses the pancreas and contains no C-peptide, so hypoglycemia shows a high insulin with a low C-peptide. This pattern identifies an insulin overdose, whether by error or otherwise.

  6. Prolonged fasting, very low-carbohydrate diets and severe illness

    Insulin and C-peptide fall appropriately during starvation or ketogenic eating and can be suppressed in critical illness; glucose is normal or low, so this is physiological rather than a sign of beta-cell failure.

  7. Somatostatin analogues and hypokalemia

    Octreotide and lanreotide suppress insulin release; very low potassium impairs beta-cell secretion. Both are reversible.

Symptoms that can go with it

  • Thirst, frequent urination, unintended weight loss, blurred vision and tiredness, from high glucose when insulin production fails
  • Nausea, vomiting, abdominal pain, deep rapid breathing or a fruity breath smell: diabetic ketoacidosis, which is an emergency
  • Recurrent infections or slow-healing sores
  • Unstable, swinging blood sugars on tablets alone in someone treated as type 2
  • None, when the cause is an overnight fast or a low-carbohydrate diet with normal glucose

Read it alongside

  • Glucose, drawn at the same time — a C-peptide is uninterpretable without it; the pairing (low with high glucose, high with low glucose) is what carries the diagnosis.
  • Insulin — in a hypoglycemia work-up, insulin and C-peptide together distinguish insulinoma and sulfonylurea (both high) from injected insulin (insulin high, C-peptide low).
  • A1C — shows the 3-month average glucose and whether a low C-peptide is translating into poor control.
  • GAD, IA-2 and ZnT8 antibodies — positive in type 1 and LADA; ordered when the C-peptide is low or falling in an adult labelled type 2.
  • Creatinine and eGFR — reduced kidney function raises C-peptide and must be known before calling it high.
  • Proinsulin and beta-hydroxybutyrate — part of the supervised fast for suspected insulinoma; proinsulin of 5 pmol/L or more and suppressed ketones support it.
  • Sulfonylurea and meglitinide drug screen — rules out a drug cause for high C-peptide with hypoglycemia.
  • HOMA-IR or fasting insulin — quantify insulin resistance when C-peptide is high with a normal glucose.

What usually happens next

  1. Check what the glucose was on the same sample; if none was taken, the test is usually repeated as a paired fasting glucose and C-peptide, or as a stimulated C-peptide 2 hours after a meal.
  2. If C-peptide is low and the diabetes type is in question, diabetes antibodies (GAD, IA-2, ZnT8) are ordered; a positive result changes treatment to insulin and the approach to monitoring.
  3. If C-peptide is high with a normal glucose, the question becomes insulin resistance: expect a review of weight, waist, triglycerides, HDL, ALT and blood pressure.
  4. If C-peptide was high during a documented low glucose (under 55 mg/dL), expect referral to an endocrinologist for a supervised 72-hour fast, a sulfonylurea screen and, if confirmed, pancreatic imaging.
  5. In people with type 1 diabetes, C-peptide is sometimes rechecked every year or two in research or clinical-trial settings to track residual beta-cell function; it is not needed routinely.
  6. Ask whether kidney function was taken into account if your eGFR is under 60, since this alone can raise the level.

Diet, lifestyle and natural levers with evidence

What can move C-peptide once the cause is known. Nothing here replaces finding the cause.

Weight loss when C-peptide is high (insulin resistance)

Strong evidence

Fasting C-peptide tracks fasting insulin, and both fall with fat loss. In the DiRECT trial, a structured 800-kcal/day program producing 10 to 15 kg loss put 46 percent of people with recent type 2 diabetes into remission at one year, with recovery of first-phase insulin secretion. Across weight-loss trials, each 5 percent of body weight lost reduces fasting insulin and C-peptide by roughly 10 to 20 percent.

Regular aerobic and resistance exercise

Strong evidence

Exercise lowers the insulin, and therefore the C-peptide, needed to control glucose by improving muscle insulin sensitivity. Meta-analyses of training trials in type 2 diabetes show fasting insulin falls by around 15 to 25 percent and HOMA-IR by about 1.0 after 8 to 12 weeks, with combined aerobic and strength training giving the largest effect.

Mediterranean, low-glycemic or higher-fiber eating

Moderate evidence

Replacing refined grains and sugary drinks with vegetables, legumes, whole grains, nuts and olive oil lowers post-meal insulin demand. In randomised trials, viscous fiber (psyllium, oats, beta-glucan) lowered A1C by about 0.6 percentage points and fasting insulin modestly, and Mediterranean-style diets reduced fasting insulin and C-peptide by 10 to 20 percent over 6 to 12 months.

Preserving beta cells in new type 1 diabetes: what the evidence shows

Preliminary evidence

Many supplements have been tested for protecting residual C-peptide after type 1 diagnosis. Large randomised trials of nicotinamide in high-risk relatives (ENDIT) and of omega-3 and vitamin D after diagnosis found no protective effect, and smaller vitamin D trials have been inconsistent, so no diet or supplement is known to slow the fall in C-peptide. The only intervention shown to delay progression is the immunotherapy teplizumab, prescribed by specialists. Good glucose control itself appears to help preserve residual secretion.

Do not reduce or stop insulin on the basis of a supplement; people with a low C-peptide can develop ketoacidosis within a day without it.

Time-restricted and lower-carbohydrate eating patterns

Preliminary evidence

Small trials of early time-restricted eating (eating within an 8 to 10 hour window) in people with prediabetes lowered fasting insulin by about 3 to 4 uIU/mL even without weight loss, and low-carbohydrate diets reduce fasting C-peptide within weeks. Longer-term trials are few, and the benefit beyond that from weight loss is uncertain.

People on insulin or sulfonylureas can become hypoglycemic when fasting or cutting carbohydrate; adjust only with your prescriber.

When to see a clinician promptly

  • Symptoms of hypoglycemia (sweating, shaking, confusion, fainting) with a documented glucose under 55 mg/dL, especially if not on diabetes medication: a high C-peptide at that moment suggests insulinoma and needs specialist evaluation; a severe episode with loss of consciousness is an emergency.
  • High glucose with nausea, vomiting, abdominal pain, deep rapid breathing or drowsiness in anyone with a low C-peptide: possible diabetic ketoacidosis, call emergency services.
  • A low C-peptide (under 0.6 ng/mL) with a high glucose in someone treated with tablets alone, which usually means insulin is needed.
  • An adult diagnosed with type 2 diabetes who is slim, lost weight at diagnosis, has autoimmune disease or whose tablets have stopped working, to check C-peptide and antibodies for LADA.
  • A high C-peptide with a raised ALT, large waist or high triglycerides, to assess fatty liver and metabolic syndrome.
  • A high C-peptide or insulin level after bariatric surgery with post-meal faintness, which can indicate post-bariatric hypoglycemia.

Frequently asked questions

What is a normal C-peptide level?

A fasting C-peptide of roughly 0.5 to 2.0 ng/mL is normal in most US labs, though reference ranges vary considerably (0.8 to 3.1 and 1.1 to 4.4 ng/mL are also common) because the assays differ. In SI units, multiply ng/mL by 0.331 to get nmol/L: 1.5 ng/mL is about 0.5 nmol/L. After a meal the level rises two to five fold. Whatever the range, the number must be read next to the glucose from the same sample.

How does a C-peptide test tell type 1 from type 2 diabetes?

Type 1 destroys the insulin-producing cells, so C-peptide is low; type 2 is insulin resistance with a working pancreas, so C-peptide is normal or high. Three or more years after diagnosis, a random C-peptide below 0.6 ng/mL (0.2 nmol/L) with a glucose over 144 mg/dL strongly suggests type 1, while a value above 1.8 ng/mL (0.6 nmol/L) makes type 1 very unlikely. In the first years the overlap is large, so diabetes antibodies are used alongside it.

What does a high C-peptide mean?

Most often insulin resistance: the pancreas is making extra insulin to overcome poor response in the muscles and liver, as in obesity, prediabetes, PCOS, fatty liver and early type 2 diabetes. Kidney disease raises it by slowing clearance, and sulfonylurea tablets raise it directly. A high C-peptide at a time when glucose is under 55 mg/dL is the one alarming version, because it points to an insulinoma or a drug effect.

What does a low C-peptide mean?

That the pancreas is producing little insulin. With a high glucose it indicates insulin deficiency, as in type 1 diabetes, LADA, long-standing type 2 or pancreatic damage, and means insulin treatment is needed. With a normal glucose after an overnight fast it is simply a resting pancreas, and with a low glucose it is the correct response unless insulin is also high, which identifies injected insulin.

Is C-peptide used to diagnose insulinoma?

Yes, it is central. During a supervised fast, when glucose falls under 55 mg/dL, a C-peptide of 0.6 ng/mL or more together with an insulin of 3 uIU/mL or more, a proinsulin of 5 pmol/L or more and a negative sulfonylurea screen meets Endocrine Society criteria for endogenous hyperinsulinism. Imaging of the pancreas (CT, MRI or endoscopic ultrasound) then locates the tumor, which is benign in over 90 percent of cases and usually removed surgically.

Do I need to fast for a C-peptide test?

Usually yes, 8 to 12 hours with water only, because reference ranges are for fasting samples and eating raises the level several fold. Some tests are deliberately done after a meal or a glucagon injection to measure pancreatic reserve; your clinician will tell you which. Take your usual medicines unless told otherwise, and mention insulin, sulfonylureas and any steroid treatment, all of which change the result.

Can C-peptide come back in type 1 diabetes?

Residual production often persists at low levels for years, and a temporary partial recovery (the honeymoon phase) is common in the months after diagnosis as glucose control improves, but destroyed beta cells do not regrow in any clinically meaningful way with current treatment. Immunotherapies such as teplizumab can slow the decline in people at high risk or newly diagnosed. Even a small residual C-peptide is worth having, since it is linked to fewer severe lows and complications.

Does kidney disease affect C-peptide?

Yes, significantly. C-peptide is removed by the kidneys, so when eGFR is below about 60 mL/min the level rises even though the pancreas is not making more insulin; in advanced kidney disease it can be two to three times what it would otherwise be. A high C-peptide in someone with kidney disease should not be taken as proof of insulin resistance, and a low value in that setting is more worrying than it looks.

References

  1. C-peptide test. MedlinePlus, US National Library of Medicine (2023)View source
  2. Jones AG, Hattersley AT. The clinical utility of C-peptide measurement in the care of patients with diabetes. Diabetic Medicine (2013)View source
  3. Leighton E, Sainsbury CA, Jones GC. A practical review of C-peptide testing in diabetes. Diabetes Therapy (2017)View source
  4. Cryer PE, Axelrod L, Grossman AB, et al.. Evaluation and management of adult hypoglycemic disorders: an Endocrine Society clinical practice guideline. Journal of Clinical Endocrinology and Metabolism (2009)View source
  5. American Diabetes Association Professional Practice Committee. Diagnosis and classification of diabetes: Standards of Care in Diabetes - 2025. Diabetes Care (2025)
  6. Shields BM, McDonald TJ, Oram R, et al.. C-peptide decline in type 1 diabetes has two phases: an initial exponential fall and a subsequent stable phase. Diabetes Care (2018)
  7. Lachin JM, McGee P, Palmer JP; DCCT/EDIC Research Group. Residual insulin secretion and the Diabetes Control and Complications Trial: C-peptide and complications. Diabetes (2014)
  8. Lean MEJ, Leslie WS, Barnes AC, et al.. Primary care-led weight management for remission of type 2 diabetes (DiRECT): an open-label, cluster-randomised trial. The Lancet (2018)View source
  9. Diabetes mellitus (DM). Merck Manual Professional Version (2024)
  10. Insulinoma. Merck Manual Professional Version (2024)
  11. Gale EA, Bingley PJ, Emmett CL, Collier T; ENDIT Group. European Nicotinamide Diabetes Intervention Trial (ENDIT): a randomised controlled trial of intervention before the onset of type 1 diabetes. The Lancet (2004)
  12. Type 1 diabetes. National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) (2023)View source

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This page is educational and is not medical advice or a diagnosis. Lab results have to be interpreted together with your history, symptoms and other results by a clinician who knows you. Do not start or stop a supplement to change a lab value before the cause is known.