Lab result explainedMetabolic panelLast updated November 10, 2026

CK blood test: what creatine kinase is, the normal range and what high CPK levels mean

Creatine kinase (CK) · Ordered on its own or added to a metabolic panel; CK-MB and troponin when the heart is the question · reported in U/L (units per liter); some labs report IU/L, which is the same

Creatine kinase (CK), also called creatine phosphokinase (CPK), is an enzyme inside muscle cells that keeps their energy supply topped up, and a CK blood test measures how much of it has leaked into the bloodstream. Because skeletal muscle holds by far the most CK, the test is mainly a gauge of muscle injury. Normal is roughly 30 to 200 U/L in most adults, higher in men, in people with a lot of muscle and in people of African ancestry, and almost everyone who has done a hard, unfamiliar workout in the previous three days will be above it.

The size of the rise is what matters. Values up to 2 or 3 times the upper limit are common after exercise, a fall, an intramuscular injection or a viral illness and settle within days. Values above 5 times the upper limit (roughly 1,000 U/L) define rhabdomyolysis, a breakdown of muscle that can injure the kidneys once CK climbs into the many thousands. Persistently high CK without an obvious trigger raises the possibility of a statin side effect, an underactive thyroid, an inflammatory muscle disease or an inherited muscle condition.

CK used to be the main blood test for a heart attack, through its heart-specific fraction CK-MB, but troponin has largely replaced it for that purpose. Today CK is ordered for muscle pain, weakness or dark urine, before and during statin treatment when symptoms arise, after seizures, falls, heat illness or prolonged immobilisation, and as part of the work-up of unexplained fatigue or high liver enzymes (AST and ALT also come from muscle). A low CK is rarely significant.

CK at a glance

What it is: an enzyme inside muscle cells (skeletal muscle, heart and brain); it enters the blood when muscle cells are damaged.
Normal: roughly 30–200 U/L, with typical lab ranges of about 39–308 U/L for men and 26–192 U/L for women. People of African ancestry and people with large muscle mass run higher. Labs differ; use the printed range.
After exercise: CK peaks 24–72 hours after a hard or unfamiliar workout and can reach 1,000–10,000 U/L or more in extreme cases, then falls by about half every 36 hours.
Rhabdomyolysis: CK above 5 times the upper limit (about 1,000 U/L); the risk of kidney injury rises steeply above 5,000 U/L, and values over 15,000–20,000 U/L are an emergency.
Statins: muscle symptoms with CK over 10 times the upper limit mean the statin is stopped; mild rises (under 3 to 4 times) with no symptoms are usually tolerated.
Low CK is uncommon and usually reflects low muscle mass, inactivity, older age or an inflammatory condition such as rheumatoid arthritis; it is not a disease in itself.

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What CK measures

Creatine kinase sits inside muscle cells, where it converts creatine and ATP into phosphocreatine, the quick-release energy store that powers the first seconds of any contraction. It does not belong in the blood. When a muscle cell membrane is stretched, torn, inflamed or starved of oxygen, CK leaks out, and the blood level rises in proportion to how much muscle was injured. The enzyme is cleared by the liver and reticuloendothelial system with a half-life of about 36 hours, so a single injury produces a peak at 1 to 3 days and a return to normal over a week or so.

CK exists as three isoenzymes: CK-MM from skeletal muscle (over 95 percent of the normal total), CK-MB mostly from heart muscle, and CK-BB from brain and smooth muscle. A total CK test measures all three. When heart injury is the question, labs can measure CK-MB separately; a CK-MB that makes up more than about 3 to 5 percent of total CK (the relative index) points to the heart, but troponin is more sensitive and specific and has replaced CK-MB in most emergency departments. Macro-CK, a harmless complex of CK with an antibody, occasionally produces a persistently high total CK in healthy older people.

The normal range depends heavily on who is being tested. Men have more muscle and higher CK than women, and the 97.5th percentile in Black adults is about 1.5 to 2 times that in white adults, which is why some laboratories publish ancestry-specific ranges. Muscle mass, recent exercise, intramuscular injections, alcohol and muscle-relaxant drugs all push the value up. For a meaningful baseline, the test is best drawn after at least 3 days without strenuous exercise, and it does not require fasting.

Normal range for CK

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

Group	Typical range (U/L (units per liter); some labs report IU/L, which is the same)	Notes
Adult men	About 39–308 U/L	Mayo Clinic reference interval; many labs use 30–200 or 50–325 U/L. Labs differ; use the printed range.
Adult women	About 26–192 U/L	Lower muscle mass; falls further after menopause.
Adults of African ancestry	Upper limit roughly 1.5–2 times higher (up to about 500 U/L in men)	A normal variant, not a sign of disease; some labs publish separate ranges.
Newborns	Up to about 3–5 times adult values in the first days	From the muscle stress of birth; settles within a week.
Mild elevation	Up to 3 times the upper limit (about 200–600 U/L)	Recent exercise, viral illness, injections, falls, hypothyroidism, statin use, idiopathic hyperCKemia. Repeated after a week of rest.
Moderate elevation	3–10 times the upper limit (about 600–2,000 U/L)	Heavy unaccustomed exercise, inflammatory myopathy, statin myopathy, seizures, heat illness, muscular dystrophy carriers.
Rhabdomyolysis	Above 5 times the upper limit (about 1,000 U/L), often tens of thousands	Risk of acute kidney injury rises above about 5,000 U/L; values over 15,000–20,000 U/L need intravenous fluids in hospital.
Inherited muscle disease	10–100 times the upper limit	Duchenne and Becker muscular dystrophy produce values of 10,000–50,000 U/L in childhood, before weakness is obvious.

High CK (creatine kinase)

A high CK means muscle cells have been damaged, and the first job is to decide which muscle and why. In the great majority of people searching for their result, the answer is recent exercise: an unfamiliar or eccentric workout (downhill running, heavy squats, a first CrossFit session) raises CK to 2 to 20 times normal with a peak at 1 to 3 days, and it returns to baseline within a week. Minor bumps and knocks, a viral illness such as influenza or COVID-19, an intramuscular injection and a long lie on a hard floor do the same on a smaller scale.

Once exercise is excluded by repeating the test after 5 to 7 days of rest, a CK that stays above the upper limit is grouped by size. Mild persistent rises (under 3 times normal) are most often explained by statins, hypothyroidism, ancestry, large muscle mass, alcohol or idiopathic hyperCKemia, which is a benign finding in about 1 in 100 adults. Moderate rises with muscle pain or weakness raise the possibility of an inflammatory myopathy such as polymyositis or dermatomyositis, a statin-induced immune myopathy, or a metabolic or inherited muscle disease, and a neurology or rheumatology referral follows.

Very high values are a different problem. CK above 5 times normal with muscle pain, weakness or cola-colored urine is rhabdomyolysis, in which the contents of broken muscle cells, particularly myoglobin and potassium, flood the blood and can clog the kidney tubules and disturb the heart rhythm. The kidney risk climbs once CK exceeds about 5,000 U/L and is substantial above 15,000 to 20,000 U/L; this is managed in hospital with large volumes of intravenous fluid and monitoring of potassium and creatinine. Heart attacks also raise total CK, usually to 2 to 10 times normal, but troponin is now the test used to detect them.

Common causes

Strenuous or unaccustomed exercise
Eccentric, high-volume or novel exercise causes micro-tears in muscle fibers; CK rises from 24 hours, peaks at 24 to 72 hours and can reach 1,000 to 30,000 U/L after extreme sessions (exertional rhabdomyolysis). Trained people release much less for the same work, the repeated-bout effect.
Rhabdomyolysis from crush injury, immobility, heat or drugs
Trauma, a long lie after a fall, heat stroke, seizures, cocaine or amphetamine use and some medications break down large volumes of muscle; CK often exceeds 10,000 U/L and myoglobin can injure the kidneys. Dark urine is the warning sign.
Statins and other medications
Statins cause muscle symptoms in 5 to 10 percent of users; most have a normal or mildly raised CK, and CK above 10 times normal with symptoms is the usual threshold for stopping. Fibrates, colchicine, daptomycin, antipsychotics (neuroleptic malignant syndrome), corticosteroids, hydroxychloroquine and zidovudine also raise CK.
Hypothyroidism
Low thyroid hormone slows muscle metabolism and membrane repair; CK is raised in roughly half of people with overt hypothyroidism, usually to 2 to 10 times normal, and returns to normal within weeks of thyroid replacement. Always check TSH for an unexplained CK.
Inflammatory myopathies
Polymyositis, dermatomyositis, immune-mediated necrotising myopathy (including the statin-triggered anti-HMGCR form) and inclusion-body myositis raise CK to 5 to 50 times normal with progressive weakness of the shoulders and hips. Diagnosed with myositis antibodies, EMG, MRI and muscle biopsy.
Inherited muscle disease
Duchenne and Becker muscular dystrophy produce CK of 10 to 100 times normal from infancy; female carriers often have 2 to 10 times normal. Limb-girdle dystrophies, McArdle disease, carnitine palmitoyltransferase II deficiency and malignant hyperthermia susceptibility cause exercise-triggered rises.
Heart attack and heart-muscle injury
Infarction releases CK-MB; total CK rises within 4 to 8 hours, peaks at 12 to 24 hours (typically 2 to 10 times normal) and normalizes in 2 to 3 days. Myocarditis and cardiac surgery do the same. Troponin is more specific and is the test now used.
Infections
Influenza, COVID-19, Epstein-Barr virus, HIV seroconversion, legionella and some bacterial infections cause viral or bacterial myositis with CK of 2 to 20 times normal; benign acute childhood myositis after influenza B classically causes calf pain and CK in the thousands that resolves in a week.
Ancestry, muscle mass and idiopathic hyperCKemia
Black adults and heavily muscled people have higher normal CK. About 1 percent of the population has a persistently raised CK (usually under 5 times normal) with no symptoms and no disease found on full investigation; it is followed rather than treated.
Seizures, surgery, injections and alcohol
A generalised seizure can raise CK to several thousand U/L for 2 to 3 days. Surgery, intramuscular injections, electrical injury and binge drinking (alcoholic myopathy) each produce transient rises; chronic heavy drinking causes a persistent mild elevation.

Symptoms that can go with it

Muscle soreness, stiffness or swelling 1 to 3 days after exercise (delayed-onset muscle soreness)
Muscle pain or tenderness, particularly in the thighs, calves, shoulders or lower back
Weakness climbing stairs, rising from a chair or lifting the arms overhead, which points to myopathy rather than exercise
Dark brown, tea- or cola-colored urine, the sign of myoglobin from rhabdomyolysis
Passing very little urine, nausea or confusion with a very high CK, which suggests kidney injury
Muscle cramps or intolerance of exercise since childhood with inherited metabolic myopathies
A rash over the knuckles, eyelids or chest with weakness, in dermatomyositis
Fatigue, cold intolerance, weight gain and constipation when hypothyroidism is the cause
No symptoms at all, in idiopathic hyperCKemia and most statin-related mild rises

Low CK (creatine kinase)

A CK below the lab's lower limit (usually under about 20 to 30 U/L) is uncommon and almost never a problem in its own right. The commonest reasons are simply having less muscle: older age, a small frame, prolonged bed rest, frailty or a sedentary lifestyle. It is also seen in early pregnancy, in people taking corticosteroids and in some connective tissue diseases, most consistently rheumatoid arthritis and systemic lupus, where low CK has been reported in up to a third of patients and is thought to reflect reduced muscle mass and the effects of inflammation on muscle metabolism.

Clinically the main relevance of a low CK is interpretation. In someone with little muscle mass, a CK that sits in the normal range may actually represent a meaningful rise from their own low baseline, and a myopathy or statin side effect can be missed if the value is read only against the population range. A low CK does not cause symptoms and needs no treatment; if there is weakness, it is investigated on its own merits with thyroid function, electrolytes and a neurological examination.

Common causes

Low muscle mass
Older adults, small or frail people, those with sarcopenia or long illness and anyone on prolonged bed rest have less muscle to release CK; the value tracks lean body mass closely.
Sedentary lifestyle
Regular activity raises resting CK slightly through normal fiber turnover; complete inactivity keeps it at the bottom of the range. This is the mirror image of the post-exercise rise.
Rheumatoid arthritis, lupus and other connective tissue diseases
Low CK is a recognized laboratory finding in active rheumatoid arthritis and systemic lupus, independent of steroid use, possibly through cytokine effects on muscle. It is not harmful.
Corticosteroids and hyperthyroidism
Both accelerate muscle protein breakdown and reduce muscle mass over time; an overactive thyroid also speeds CK clearance. The low CK can mask a steroid myopathy, which characteristically has normal or low CK despite weakness.
Pregnancy and liver disease
CK falls in the first half of pregnancy through plasma expansion. Advanced liver disease with muscle wasting, and alcohol-related malnutrition, also lower it.

Symptoms that can go with it

None; a low CK does not cause symptoms
Weakness in someone with a low or normal CK still needs assessment, since steroid myopathy, thyroid disease and many neurological causes of weakness do not raise CK

Read it alongside

Troponin — the test for heart-muscle injury; a high CK with a normal troponin means the source is skeletal muscle.
Creatinine, potassium and eGFR — checked with any CK above about 5,000 U/L, since rhabdomyolysis can injure the kidneys and release dangerous amounts of potassium.
AST and ALT — both enzymes are also present in muscle, so a high CK explains mildly raised liver enzymes with normal GGT and bilirubin.
LDH — rises with muscle injury alongside CK and can help time it; stays raised longer.
TSH and free T4 — hypothyroidism is one of the commonest treatable causes of a persistently raised CK.
CRP and ESR — raised in inflammatory myopathies and infections, usually normal in exercise-related and statin-related rises.
Aldolase and myositis antibodies — ordered when CK stays high with weakness, to look for polymyositis, dermatomyositis or necrotising myopathy.
Urine dipstick for blood — a dipstick positive for blood with no red cells on microscopy means myoglobin, the hallmark of rhabdomyolysis.

What usually happens next

If you exercised hard in the 3 days before the test, the first step is simply to repeat the CK after 5 to 7 days without strenuous activity; most mild rises normalize.
A CK that stays above the upper limit is paired with TSH, creatinine, electrolytes, liver enzymes and a review of medications (statins, fibrates, antipsychotics, colchicine) and alcohol intake.
On a statin, muscle symptoms with a CK under 4 times normal are usually managed by a short pause and rechallenge or a switch; CK over 10 times normal, or any CK rise with dark urine, means the drug is stopped and kidney function checked.
A CK persistently over 3 to 5 times normal, or any rise with weakness, leads to a neurology or rheumatology referral for myositis antibodies, EMG, muscle MRI and sometimes a muscle biopsy or genetic testing.
A CK in the thousands with dark urine or after a crush injury, seizure, heat illness or prolonged immobilisation is treated in hospital with intravenous fluids until CK falls below about 5,000 U/L and kidney function is stable.
Ask your lab whether its reference range is sex-specific or ancestry-specific, since a value just above a generic upper limit may be normal for you.

Diet, lifestyle and natural levers with evidence

What can move CK once the cause is known. Nothing here replaces finding the cause.

Progressive training and the repeated-bout effect

Strong evidence

A single bout of unfamiliar eccentric exercise raises CK to 1,000 to 10,000 U/L or more, but repeating the same exercise 1 to 2 weeks later produces a rise that is 50 to 80 percent smaller, an adaptation that lasts for months. Increasing training volume gradually (no more than about 10 percent a week) and keeping to familiar movement patterns in the days before a blood test are the most effective ways to keep CK in range.

Severe pain, swelling or dark urine after a workout is exertional rhabdomyolysis and needs same-day medical assessment, not more training.

Hydration and heat management during hard exercise

Moderate evidence

Exertional rhabdomyolysis clusters around hot conditions, dehydration, extreme novel workouts and stimulant use (including high-dose caffeine and pre-workout products). Military and athletic cohort studies show that acclimatisation over 1 to 2 weeks, drinking to thirst with electrolytes during prolonged exertion and avoiding maximal efforts in the first sessions of a new program reduce cases substantially; the kidney risk of rhabdomyolysis is driven by low urine flow, which fluids counter.

Correct hypothyroidism and review statin dose

Strong evidence

In people with overt hypothyroidism, CK is raised in about half and falls to normal within 4 to 8 weeks of adequate thyroid hormone replacement. For statin-related rises, a lower dose, an alternate-day regimen or a switch to a hydrophilic statin (rosuvastatin, pravastatin) resolves symptoms in most people while keeping most of the LDL benefit; the European Atherosclerosis Society consensus found 70 to 90 percent of people with statin muscle symptoms can tolerate some statin regimen.

Do not stop a statin on your own after a heart attack or stroke; the risk of stopping usually exceeds the risk of mild muscle symptoms. Discuss any change with your clinician.

Omega-3 fatty acids for exercise-induced muscle damage

Preliminary evidence

A 2021 meta-analysis of randomised trials found that omega-3 supplementation (typically 1 to 3 g of EPA plus DHA a day for 1 to 8 weeks) lowered post-exercise CK at 24 and 48 hours by a small to moderate amount and reduced muscle soreness, with the largest effect after eccentric exercise in untrained people. The trials are small and the effect on resting CK is nil; this is a recovery aid, not a treatment for a high CK.

Doses above 3 g a day can increase bleeding tendency; discuss if you take anticoagulants.

Curcumin for post-exercise soreness and CK

Preliminary evidence

A 2021 meta-analysis of 11 randomised trials found curcumin (150 to 1,500 mg a day of an enhanced-absorption form, taken around the exercise session) reduced delayed-onset muscle soreness and lowered CK at 24 to 72 hours after damaging exercise compared with placebo. Effects were modest and trial quality mixed. No evidence supports curcumin for CK rises from statins, thyroid disease or myopathy.

Curcumin can increase bleeding with anticoagulants and has rare reports of liver injury with high-dose supplements; avoid in gallbladder disease.

Coenzyme Q10 for statin muscle symptoms

Preliminary evidence

Statins lower blood CoQ10, which prompted trials of supplementation. A 2018 meta-analysis of 12 randomised trials (575 people) found CoQ10 at 100 to 600 mg a day reduced statin-associated muscle pain, weakness, cramps and tiredness, but it did not significantly change CK. Earlier meta-analyses found no benefit for symptoms either, so the evidence is mixed; it is a reasonable low-risk trial for symptoms, not a way to lower CK.

May reduce the effect of warfarin; check INR if you start or stop it.

When to see a clinician promptly

Dark brown, tea- or cola-colored urine, severe muscle pain or swelling, or passing very little urine after intense exercise, a fall, a seizure, heat exposure or a long period lying immobile: possible rhabdomyolysis, needs same-day emergency assessment.
A CK above 5,000 U/L on any test, or above 1,000 U/L with muscle symptoms, which needs kidney function and potassium checked promptly.
Muscle pain, weakness or dark urine while taking a statin, fibrate, colchicine or an antipsychotic; the drug may need to be paused and CK checked.
High fever, muscle rigidity, confusion and sweating in someone on antipsychotic medication, which can be neuroleptic malignant syndrome and is an emergency.
Progressive weakness climbing stairs, rising from a chair or lifting the arms, with a persistently raised CK, which needs referral for myopathy.
A raised CK with chest pain or breathlessness, since the heart may be the source; this is assessed as a possible heart attack with an ECG and troponin.

Frequently asked questions

What is CK in a blood test?

CK stands for creatine kinase, an enzyme inside muscle cells that recycles energy for contraction. It is also called CPK (creatine phosphokinase); the two names mean the same test. CK is measured in the blood because it leaks out when muscle fibers are injured, so the test shows whether muscle has been damaged and, roughly, how much. Most of the CK in blood comes from skeletal muscle, a small fraction from the heart and a trace from the brain.

What is a normal creatine kinase level?

Typical adult reference ranges are about 39 to 308 U/L for men and 26 to 192 U/L for women, though many labs simply quote 30 to 200 U/L. Men, people with a lot of muscle and people of African ancestry run higher, and the upper limit in Black men can be around 500 U/L. Labs differ in their method and range, so compare your result with the range printed on your report, and remember that any hard exercise in the previous 3 days will raise it.

How high is CK after exercise?

A moderate familiar workout may raise CK by 50 to 100 percent. An unfamiliar, prolonged or eccentric session (a first marathon, heavy squats, downhill running, a bootcamp class) commonly produces 500 to 5,000 U/L, with a peak 24 to 72 hours later, and extreme efforts can push it above 10,000 or even 30,000 U/L. Values fall by about half every 36 hours and are usually back to baseline within a week. A CK drawn within 3 days of hard exercise is best repeated after rest before any other conclusion is drawn.

What CK level is rhabdomyolysis?

Rhabdomyolysis is usually defined as a CK more than 5 times the upper limit of normal, roughly 1,000 U/L, together with muscle pain, weakness or dark urine. Most cases run from a few thousand to over 100,000 U/L. The risk of acute kidney injury becomes significant once CK exceeds about 5,000 U/L and rises steeply above 15,000 to 20,000 U/L, which is why those values are managed in hospital with intravenous fluids and monitoring of creatinine and potassium.

Can statins cause high CPK levels?

Yes. Statins cause muscle aches in about 5 to 10 percent of users, and a minority of those have a raised CK. Mild rises under 3 to 4 times normal without symptoms are usually tolerated and monitored. Symptoms with a CK above 10 times normal, or any rise with dark urine, mean the statin is stopped and kidney function checked; rhabdomyolysis occurs in roughly 1 in 10,000 users a year. A rare immune-mediated necrotising myopathy with CK in the thousands can persist after stopping and needs a rheumatology referral.

Does hypothyroidism raise CK?

Yes, and it is one of the easiest causes to miss. About half of people with overt hypothyroidism have a raised CK, typically 2 to 10 times normal, sometimes with muscle aches, cramps and stiffness that can be mistaken for a statin side effect. The CK returns to normal within 4 to 8 weeks of adequate thyroid hormone replacement. A TSH is part of the standard work-up of any unexplained CK elevation.

Is a CK of 300, 500 or 1,000 high?

A CK of 300 U/L is at or just above the upper limit for most labs and is normal for many men, people with large muscle mass and people of African ancestry; after a workout it means nothing. A CK of 500 is a mild rise that is almost always exercise, a viral illness, a medication or thyroid-related and is repeated after a week of rest. A CK of 1,000 is 5 times most upper limits: without exercise or symptoms it needs investigation, and with muscle pain or dark urine it meets the definition of rhabdomyolysis and needs prompt kidney function testing.

What does a low CK level mean?

A CK below the lower limit (around 20 to 30 U/L) is uncommon and rarely matters. It usually reflects low muscle mass from age, small build, inactivity or long illness, and it is also seen in pregnancy, with corticosteroid use, in hyperthyroidism and in rheumatoid arthritis or lupus. It does not cause symptoms and needs no treatment. The one practical point is that in someone with a naturally low CK, a value in the normal range can still be a real rise from their own baseline.

References

Creatine kinase (CK) test. MedlinePlus, US National Library of Medicine (2022)View source
Rhabdomyolysis. Merck Manual Professional Version (2024)
Bosch X, Poch E, Grau JM. Rhabdomyolysis and acute kidney injury. New England Journal of Medicine (2009)
Torres PA, Helmstetter JA, Kaye AM, Kaye AD. Rhabdomyolysis: pathogenesis, diagnosis, and treatment. Ochsner Journal (2015)
Kyriakides T, Angelini C, Schaefer J, et al.. EFNS guidelines on the diagnostic approach to pauci- or asymptomatic hyperCKemia. European Journal of Neurology (2010)
Brancaccio P, Maffulli N, Limongelli FM. Creatine kinase monitoring in sport medicine. British Medical Bulletin (2007)
Clarkson PM, Hubal MJ. Exercise-induced muscle damage in humans. American Journal of Physical Medicine and Rehabilitation (2002)
Brewster LM, Mairuhu G, Sturk A, van Montfrans GA. Distribution of creatine kinase in the general population: relations with race and body size. American Heart Journal (2007)
Stroes ES, Thompson PD, Corsini A, et al.. Statin-associated muscle symptoms: impact on statin therapy. European Atherosclerosis Society Consensus Panel statement on assessment, aetiology and management. European Heart Journal (2015)
Hekimsoy Z, Oktem IK. Serum creatine kinase levels in overt and subclinical hypothyroidism. Endocrine Research (2005)
Qu H, Guo M, Chai H, Wang WT, Gao ZY, Shi DZ. Effects of coenzyme Q10 on statin-induced myopathy: an updated meta-analysis of randomized controlled trials. Journal of the American Heart Association (2018)
Fang W, Nasir Y. The effect of curcumin supplementation on recovery following exercise-induced muscle damage and delayed-onset muscle soreness: a systematic review and meta-analysis of randomized controlled trials. Phytotherapy Research (2021)

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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.