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The body needs about 15 mg/day of carnitine from a combination of dietary sources and endogenous synthesis [7]. Foods of animal origin provide most of the carnitine in American diets. A typical omnivorous diet provides about 24 to 145 mg carnitine daily for a person weighing 165 pounds. In contrast, a vegan diet provides about 1.2 mg carnitine [1].

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Endogenous carnitine synthesis does not appear to be affected by dietary carnitine intake or carnitine excretion and is sufficient to meet the carnitine needs of healthy people [1]. A person weighing 165 lb who follows a strict vegetarian diet, for example, synthesizes approximately 14.4 mg/day carnitine [1].

Carnitine status is not routinely assessed in clinical practice, but it can be determined by measuring circulating carnitine. A plasma free carnitine concentration of 20 mcmol/L or less, or a total carnitine concentration of 30 mcmol/L or less, is abnormally low [1]. The ratio of acyl-L-carnitine ester to free L-carnitine can also be used to assess carnitine status because under normal conditions most carnitine is in the free unesterified form. A ratio of 0.4 or greater in plasma or serum indicates abnormal carnitine metabolism and suggests carnitine insufficiency [1,8,9].

Healthy children and adults do not need to consume carnitine from food or supplements because the liver and kidneys synthesize sufficient amounts to meet daily needs [10,11,12]. In 1989, the Food and Nutrition Board (FNB) of the National Academies of Sciences, Engineering, and Medicine concluded that carnitine is not an essential nutrient [12]. Therefore, the FNB did not establish Dietary Reference Intakes (DRIs) for carnitine [13].

FoodCarnitine is present in animal products, especially red meat [1]. Poultry, fish, and dairy foods also provide some carnitine, but vegetables, fruits, and grains provide negligible amounts [1,12,14].

Dietary supplementsCarnitine is available in dietary supplements containing only carnitine or a combination of carnitine and other ingredients [17]. The two main forms of carnitine in dietary supplements are L-carnitine and acetyl-L-carnitine, and amounts range from about 3 mg to 5,000 mg [17].

Two types of carnitine deficiency states exist. Primary carnitine deficiency is a genetic disorder of the cellular carnitine transporter system that causes a shortage of carnitine within cells. Primary carnitine deficiency usually presents during infancy or early childhood. It can result in epilepsy and encephalopathy in infants; seizures, irregular heartbeat, and breathing problems in adolescents and young adults; and myopathy, rhabdomyolysis, cardiomyopathy, or sudden death in older people. Although some individuals with primary carnitine deficiency do not have symptoms, all affected people have an increased risk of heart failure, hepatic disorders, and coma [18].

Secondary carnitine deficiency results from certain disorders (such as chronic renal failure) that reduce endogenous carnitine synthesis or increase its excretion, or from chronic use of pivalate-containing medications that reduce carnitine absorption or increase its excretion [10,19]. Signs and symptoms of secondary carnitine deficiency include hyperammonemic encephalopathy (malaise, seizures, and decreased consciousness caused by elevated ammonia levels), hypoglycemia, hypoketonemia (low level of ketones in the blood), dicarboxylic aciduria (increased concentrations of dicarboxylic acids in the urine), hyperuricemia (excess uric acid in the blood), muscle weakness, myoglobinuria (excess myoglobin in the urine), cardiomyopathy, and sudden death [20].

Premature infantsBabies born prematurely have high growth demands but have low carnitine stores and an inadequate ability to synthesize this nutrient [24]. Premature infants may require supplemental carnitine in addition to that supplied in breast milk and fortified infant formula [1]. Many enteral and parenteral formulas for premature infants are fortified with L-carnitine to improve lipid metabolism and promote weight gain [1]. However, a Cochrane review of six randomized clinical trials in newborns requiring parenteral nutrition (many of whom were premature) did not support the use of parenteral carnitine to improve lipid utilization or weight gain [25].

Individuals with secondary carnitine deficiency due to end-stage renal disease, hemodialysis, or bothCarnitine homeostasis in individuals with renal diseases can be impaired by reduced synthesis and increased elimination of carnitine by the kidneys. Renal diseases can also reduce carnitine intake from food because patients often have poor appetite and consume fewer animal products [20]. Many patients with end-stage renal disease, particularly those on hemodialysis, become carnitine insufficient.

Low levels of carnitine in blood and muscle stores can contribute to anemia, muscle weakness, fatigue, altered levels of blood fats, and heart disorders. Numerous studies suggest that high doses of supplemental carnitine (often injected) administered to patients on maintenance hemodialysis can correct some or all of these symptoms [26]. However, most of these studies had small numbers of participants and were not double-blind clinical trials. The authors of a meta-analysis of these studies concluded that carnitine supplements might help patients manage their anemia, but not their blood-lipid profiles, and that the effects of these supplements on exercise capacity and heart disorders were inconclusive [26].

In contrast, a 2003 Cochrane review of 15 clinical trials (including 13 of those in the meta-analysis described above) had somewhat different findings [29]. The clinical trials assessed the effectiveness of 1 to 3 g/day acetyl-L-carnitine supplementation or placebo over 12 to 52 weeks in participants with mild to moderate dementia or cognitive decline. The results showed that the supplementation decreased symptom severity at 12 and 24 weeks but not at 52 weeks. Similarly, acetyl-L-carnitine supplements improved scores on the Mini Mental State Examination at 24 weeks but not at 12 or 52 weeks and had no effect on the severity of dementia, functional ability, or overall clinical global impression scores. The authors of the Cochrane review noted that results from studies conducted more recently were less positive than those from earlier studies; they concluded that the routine clinical use of acetyl-L-carnitine supplements to treat the signs and symptoms of dementia was not justified.

Cardiovascular disease (CVD) and peripheral artery diseaseCarnitine plays a role in transporting long-chain fatty acids in the myocardial mitochondria, where they are metabolized via oxidation for energy. It is also involved in moderating oxidative stress [33,34] and might decrease markers of inflammation [35]. During ischemic events, carnitine prevents fatty acid ester accumulation, which can lead to fatal ventricular arrhythmias [34]. For these reasons, researchers are examining whether carnitine affects cardiovascular health.

Clinical trials examining the effects of carnitine supplements on CVD have had mixed results. A meta-analysis of 13 clinical trials included a total of 3,629 adults with acute myocardial infarction who took either L-carnitine (from 2.7 g/day for 5 days to 6 g/day for 12 months) or placebo. The study found that L-carnitine significantly reduced rates of all-cause mortality, ventricular arrhythmias, and new-onset angina but did not affect risk of heart failure or myocardial reinfarction [34,36]. The carnitine dose and duration of the clinical trial did not appear to affect outcomes.

Another meta-analysis of 17 clinical trials that included a total of 1,625 adults with chronic heart failure found that 1 g/day to 6 g/day for 7 days to 3 years L-carnitine supplements improved left ventricular ejection fraction by 4.14%, stroke volume by 8.21 mL and cardiac output by 0.88 L/min compared to routine/conventional treatment [37]. These benefits did not vary by supplement dose or study duration. However, L-carnitine did not affect rates of all-cause mortality or performance on a timed walking test.

A 2022 clinical trial also found potentially deleterious outcomes in 157 individuals aged 58 to 75 years with metabolic syndrome who received 1 g supplemental L-carnitine or placebo twice a day for 6 months [39]. Although the results showed no differences in total plaque volume between groups, total cholesterol and low-density lipoprotein cholesterol levels were higher in participants taking L-carnitine. L-carnitine supplementation was also associated with 9.3% greater carotid arterial plaque stenosis in males who ate less red meat and had lower baseline stenosis and total plaque volume than other participants.

Peripheral artery disease is a vascular disorder usually caused by atherosclerosis and its resulting arterial stenosis and occlusion. It is prevalent among older adults, although it is often underdiagnosed [40,41]. Researchers have examined whether propionyl-L-carnitine, an acyl derivative of L-carnitine, mitigates the cramping leg pain of intermittent claudication, the main symptom of peripheral artery disease, but findings from studies have been mixed. A systematic review of three randomized clinical trials compared 234 participants who took 2 g/day oral propionyl-L-carnitine for 4 to 6 months with 222 patients who took placebo [42]. In one trial, participants supplemented with propionyl-L-carnitine had improved peak walking times (walking until pain could not be tolerated), self-reported improvements in walking distance and speed, and decreased pain. The other two trials showed no benefit of propionyl-L-carnitine on peak walking time compared with placebo.

Insulin resistance and diabetesInsulin resistance plays an important role in the development of type 2 diabetes. Because insulin resistance may be associated with mitochondrial dysfunction and a defect in fatty-acid oxidation in muscle [43,44,45,46], carnitine supplementation has been studied for its possible effects on insulin resistance and diabetes. 041b061a72