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Nutrient Name: Carnitine.
Synonyms:L-Carnitine, levocarnitine; vitamin BT.
Forms: Acetyl-L-carnitine (ALC),L-acetylcarnatine (LAC); propionyl-L-caritine (PLC),L-propionylcarnitine (LPC).
Related Substance:D-Carnitine (synthetic isomer).

Summary Table
nutrient description

Chemistry and Forms

Carnitine (3-hydroxy-4N-trimethylammoniumbutanoate) is a naturally occurring quaternary amine. Forms include acetyl-L-carnitine (ALC;L-acetylcarnitine, LAC) and propionyl-L-carnitine (PLC;L-propionylcarnitine, LPC).

Physiology and Function

Carnitine (levocarnitine,L-carnitine) is considered to be a nonessential amino acid, although in certain situations it is considered conditionally essential (e.g., dialysis patients, premature and very-low-birth-weight infants, coronary artery disease). The highest concentrations of carnitine are found in the heart, muscles, liver, and kidney. The major biochemical function of carnitine is to act as a transmembrane carrier of long-chain fatty acids to the interior of mitochondria. It plays a major role in the utilization of fats in energy production at the mitochondrial level through the beta-oxidation of branched-chain amino acids and ketoacids. Carnitine also participates in transportation of acyl-coenzyme A (CoA) compounds. The activated long-chain fatty acyl-CoA esters in the cytosol are able to be transported to the mitochondrial matrix only by combining with carnitine. Beta-oxidation, the primary metabolic process by which fatty acids, branched-chain amino acids, and ketoacids (as acyl-coA esters) are used as fuel for cellular energy, occurs in the mitochondria. Thus, carnitine functions as an important physiological mediator of fatty acid and protein metabolism. Carnitine also enables hepatic detoxification and excretion of chemicals, including drugs, and improves glucose disposal and may reduce insulin resistance. Carnitine is instrumental in the production and release of acetylcholine.

Carnitine from dietary sources is rapidly absorbed from the intestinal tract by both passive and active transport. Although it exhibits vitamin-like properties, carnitine is a small amino acid derivative that can be synthesized de novo in the liver, brain, and kidneys using lysine and methionine in a process requiring vitamins C, B6, and niacin. Exogenous intake may be necessary during periods of increased demand or increased loss. Acetyl-L-carnitine (ALC), the acetylated derivative ofL-carnitine, is particularly localized in muscles, brain, and testicles.

nutrient in clinical practice

Known or Potential Therapeutic Uses

Carnitine's central role in muscle function and fat metabolism has drawn the attention of clinicians and researchers to clinical applications related to these roles. Carnitine is proposed for increasing endurance and improving cardiac performance based on its known action of enhancing the efficiency of energy production in muscle tissue in general and the myocardium in particular. Human research has focused on therapeutic application of carnitine, especially as propionyl-L-carnitine (PLC), in the treatment of angina, myocardial insufficiency, peripheral claudication, and other conditions related to arterial insufficiency. CardiacL-carnitine content, essential for mitochondrial fatty acid transport and adenosine triphosphate (ATP)–diphosphate (ADP) exchange, decreases during ischemia. Furthermore, acetyl-L-carnitine (ALC) has been administered for slowing, and even partially reversing, nerve and brain deterioration associated with the aging process. Thus, the primary potential clinical uses for carnitine include claudication, Alzheimer's disease, myocardial insufficiency, and renal dialysis. Hyperlipidemia, male infertility, athletic performance, and weight loss have also been the subjects of therapeutic claims and evolving investigations, although results have been more mixed.

During pregnancy, infancy, and breastfeeding (i.e., situations of high energy demands), the physiological need forL-carnitine can exceed the capacity for endogenous synthesis. Consequently,L-carnitine is often used as a supplement with breast milk or infant formula for low-birth-weight (LBW) infants (either preterm or full term).

Possible Uses

Attention deficit–hyperactivity disorder (ADHD), alcohol dependence, Alzheimer's disease, angina pectoris, anorexia nervosa, arrhythmias, atherosclerosis, athletic performance (enhancement), cardiac ischemia, cardiac surgery (recovery), cataracts, chronic fatigue syndrome, chronic obstructive pulmonary disease (COPD), congestive heart failure (CHF; propionyl-L-carnitine), dementia, depression in elderly (acetyl-L-carnitine), diabetes mellitus, diabetic cardiac autonomic neuropathy, erectile dysfunction, human immunodeficiency virus (HIV) infection, hyperactivity in fragile X syndrome, hypercholesterolemia, hyperthyroidism, hypertriglyceridemia, infertility (male), intermittent claudication, myocardial infarction, myocardial insufficiency (e.g., CHF or cardiomyopathy), Peyronie's disease, Raynaud's disease, renal dialysis, seizure disorders, weight loss.

Deficiency Symptoms

Carnitine deficiency is characterized by inadequate tissue levels, resulting in impaired tissue fatty acid oxidation. Other symptoms of a relative deficiency may include elevated blood lipids, abnormal liver function, chronic muscle weakness, reduced energy, impaired glucose control, cardiomyopathy, encephalopathy, and recurrent episodes of coma. 1

Absolute carnitine deficiency is unlikely because of endogenous synthesis. Primary systemic carnitine deficiency is caused by a defect in the specific high-affinity carnitine transporter, which is expressed in most tissues and is responsible for bringing carnitine into the cytosol. This carnitine uptake defect is rare and is characterized by progressive infantile-onset carnitine-responsive cardiomyopathy, weakness, recurrent hypoglycemic hypoketotic encephalopathy, and failure to thrive. 2 Several inherited metabolic disorders, especially organic acidurias and disorders of beta-oxidation, can cause secondary carnitine deficiency. 3,4

Carnitine deficiency can result from numerous factors, independently or in combination, and will contribute to further sequelae and increased risk factors. Deficiency can result from high fat diets and insufficient supply of precursors for synthesis (methionine, lysine, niacin, vitamins C and B6). Individuals who have a limited intake of meat and dairy products tend to have lowerL-carnitine intakes. However, even long-term vegans usually do not display signs of carnitine deficiency. Seizure disorders, diabetes mellitus, cirrhosis, illness, and infection (e.g., HIV), strenuous exercise, trauma, pregnancy and lactation, and other conditions characterized by increased physiological stress are associated with decreased carnitine levels. A carnitine deficiency can also result from oxygen deprivation, which can occur in some cardiac conditions. 5 Carnitine deficiency may play a role in the development of retinopathy, hyperlipidemia, neuropathy, or complications of diabetes. 6 Many prescription medications may also have an adverse effect on carnitine levels and functions.

Dietary Sources

As implied by its name, carnitine is primarily found in foods of animal origin, and to a lesser extent, in foods of plant origin. Meat, milk, eggs, and dairy products are the richest sources of dietary carnitine intake, with beef being the most abundant. Generally, the redder the meat, the higher is the carnitine content. Cereals, fruit, and vegetables are relatively poor dietary sources.

Nutrient Preparations Available

Carnitine is administered as one of three salts ofL-carnitine:L-carnitine (for heart and other conditions), propionyl-L-carnitine (for heart conditions), and acetyl-L-carnitine (for Alzheimer's disease). The dosage is the same for all three forms, typically 500 mg to 1 g three times daily.

  • Note:   Only pureL-carnitine should be used as a supplement or therapeutic agent.

Dextrocarnitine (D-carnitine), or theDL-mixture, may interfere with the normal function of the levo (L-) isomer and produce signs of deficiency.

Dosage Forms Available

Capsule, powder, tablet.

Source Materials for Nutrient Preparations


Dosage Range


  • Dietary:   No dietary reference intake (DRI) or recommended dietary allowance (RDA) has been established for carnitine. The average omnivorous diet provides approximately 100 to 300 mg of carnitine per day.
  • Supplemental/Maintenance:   1500 to 4000 mg per day in divided doses, when supplementation is indicated. Optimal levels of intake have not been established.
  • Pharmacological/Therapeutic:   150 mg to 1 g three times daily.
  • Toxic:   No toxicities have been reported or suspected as being associated with carnitine.

Pediatric (<18 Years)

  • Dietary:   No DRI or RDA has been established for carnitine.
  • Supplemental/Maintenance:   Usually not necessary, although often administered to LBW infants (preterm or full term) with breast milk or infant formula and in children receiving long-term total parenteral nutrition (TPN). Optimal levels of intake have not been established.
  • Pharmacological/Therapeutic:   50 mg to 1 g three times daily. One clinical trial involving children diagnosed with ADHD used 50 mg/kg twice daily, up to a maximum of 4 g daily. 7
  • Toxic:   No reported adverse effects have been specifically related to children.

safety profile


L-Carnitine is quite safe, with no significant adverse effects reported, even at high doses.

Nutrient Adverse Effects

General Adverse Effects

Rarely, gastrointestinal (GI) complaints such as nausea and vomiting have been reported with the use ofL-carnitine. 8 Sleeplessness may occur if taken before bed.

Pregnancy and Nursing

Adverse effects are not predicted, and reports are lacking. However, the lack of controlled studies involving pregnant or lactating women prevents any claims of safety and suggests that supplementation should be avoided during such life stages.

Infants and Children

Adverse effects are not predicted, and reports are lacking. Supplementation is not recommended unless otherwise indicated as essential.


Individuals with low or borderline-low thyroid levels should avoid carnitine supplementation because it may impair the action of thyroid hormone. 9,10This proposed effect is primarily extrapolated from research involving patients being treated for goiter with exogenous hormone.

Precautions and Warnings

DL-Carnitine may produce muscle weakness; theDisomer should be avoided because it may interfere with the activity ofL-carnitine and thus is potentially toxic.

interactions review

Strategic Considerations

The activity of carnitine suggests significant potential in preventing and treating many conditions, particularly in supporting healthy cardiovascular function. Combination therapy with a statin drug can be particularly effective in reducing lipoprotein(a) levels, especially in patients with type 2 diabetes. However, several common medications and drug classes can increase carnitine excretion or interfere with its activity. Continued development of carnitine therapy in treatment of ischemic disease is probable given its potential to limit anoxic damage while simultaneously reducing peripheral arterial resistance. 11 Furthermore, it may inhibit platelet-activating factor (PAF), thus potentially contributing an antithrombotic effect. Arterial insufficiency can decrease carnitine content of heart muscle cells. Carnitine is used conventionally in critical care and cancer surgery and has been found to benefit elderly and other high-risk patients undergoing elective cardiac surgery. 12

In regard to neurological conditions and carnitine, emerging evidence supports further research into its value in treating individuals with Alzheimer's disease. 13 Anticonvulsant medications tend to increase carnitine excretion, thus suggesting a potential role for coadministration in seizure disorders. Its immune-enhancing activity and potential efficacy during infections is countered by the adverse effects exerted on it by some chemotherapeutic agents and antiviral drugs, especially antiretroviral nucleoside analogs. Carnitine inhibits entry of thyroid hormone into certain cells and can be used to prevent adverse effects of thyroid therapy for goiter. 9,10

nutrient-drug interactions
Doxorubicin and Related Anthracycline Chemotherapy
Isotretinoin and Related Retinoids
Levothyroxine and Related Thyroid Hormones
Nitroglycerin and Related Nitrates
Pivalate Prodrugs
Simvastatin and Related HMG-COA Reductase Inhibitors (Statins)
Evidence: Simvastatin (Zocor). Atorvastatin (Lipitor), fluvastatin (Lescol, Lescol XL), lovastatin (Altocor, Altoprev, Mevacor); combination drug: lovastatin and niacin (Advicor); pravastatin (Pravachol), rosuvastatin (Crestor); simvastatin combination drug: simvastatin and extended-release nicotinic acid (Niaspan).
Beneficial or Supportive Interaction, with Professional Management
Prevention or Reduction of Drug Adverse Effect

Probability: 3. Possible or 2. Probable
Evidence Base: Emerging

Effect and Mechanism of Action

Interventions to reduce lipoprotein(a) [Lp(a)] concentration are important given its atherogenic/prothrombotic properties and associations with both coronary artery and cerebrovascular disease. Statin therapy, as well as fibrates and resins, are generally considered incapable of reducing Lp(a) levels and may in many cases contribute to an increase in Lp(a) levels, even while lowering total cholesterol and low-density lipoprotein (LDL) cholesterol levels. Among conventional pharmaceutical interventions, only nicotinic acid (2-4 g/day) is known to reduce Lp(a). However, L-carnitine can lower plasma Lp(a) levels.


A series of clinical trials conducted by Italian researchers have demonstrated the efficacy of L-carnitine in lowering Lp(a) and a synergistic interaction between L-carnitine and statin therapy in lipid-lowering strategies, especially in individuals with type 2 diabetes. In a double-blind, placebo controlled study, Sirtori et al. 55 found that L-carnitine (2 g/day) significantly reduced Lp(a) levels in subjects with hyper-Lp(a) (i.e., serum Lp(a) levels of 40-80 mg/dL). Two years later, in a study involving patients with type 2 diabetes and hyperlipidemia, Brescia et al. 56 reported that combined therapy with simvastatin (20 mg/day) and L-carnitine (2 g/day) demonstrated greater lipid-lowering efficacy than simvastatin alone, particularly in lowering triglyceride levels. Subsequently, in a trial involving 94 subjects newly diagnosed with type 2 diabetes mellitus being managed through dietary restriction alone, Derosa et al. 57 observed significantly lower plasma Lp(a) levels, compared with placebo, after 3 and 6 months of L-carnitine (2 g/day). Based on these findings, Solfrizzi et al. 58 conducted an open, randomized, parallel-group study involving 52 patients with type 2 diabetes mellitus, triglyceride serum levels less than 400 mg/dL (<4.5 mmol/L), and Lp(a) serum levels greater than 20 mg/dL (>0.71 mmol/L). Subjects were randomized into two groups of equal size and administered either simvastatin alone (20 mg/day) or simvastatin plus L-carnitine (2 g/day) orally for 60 days. The investigators reported that “Lp(a) serum levels increase[d] from baseline to 60 days in the simvastatin group alone versus a significant decrease in the combination group.” No differences between the two groups were observed regarding LDL cholesterol, non-HDL cholesterol, and apoB serum levels. The consistent pattern of evidence from these trials indicates that the combination of L-carnitine with statin therapy can enhance therapeutic management of hyperlipidemia, particularly in individuals with type 2 diabetes.

Nutritional Therapeutics, Clinical Concerns, and Adaptations

Physicians treating individuals with hyperlipidemia characterized by elevated Lp(a), particularly the context of type 2 diabetes, are advised to consider a comprehensive approach founded on regular exercise and a healthy diet and combining L-carnitine, as well as fish oil, chromium, and niacin (as inositol hexaniacinate), with conventional lipoid management interventions such as statin therapy. As previously noted, L-carnitine is unlikely to produce any adverse effects on the therapeutic action of a statin drug and may in fact mitigate potential adverse effects on Lp(a) status. Enthusiastic support for improved diet, invigorating exercise, and other healthy lifestyle changes are fundamental to an effective integrative strategy for optimizing healthy function, reversing patterns of dyslipidemia and dysglycemia, and reducing risk of cardiovascular disease.

Valproic Acid and Related Anticonvulsant Medications
Zidovudine (AZT) and Related Antiretroviral Agents, Reverse-Transcriptase Inhibitor (Nucleoside)
theoretical, speculative, and preliminary interactions research, including overstated interactions claims
Calcium Channel Blockers
Cisplatin, Ifosfamide, and Related Chemotherapy
Propranolol and Related Beta-1-Adrenoceptor Antagonists (Beta-1-Adrenergic Blocking Agents)
nutrient-nutrient interactions
Alpha-Lipoic Acid
Coenzyme Q10, Fish Oil, Magnesium, and Taurine
herb-nutrient interactions
Citations and Reference Literature
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