L-carnitine and nutrient absorption -
The main dietary sources of L-carnitine are meat and some other animal products, such as milk. A healthy individual can also produce sufficient amounts within the body.
For this reason, L-carnitine levels are often lower in vegetarians and vegans since they restrict or avoid animal products Therefore, vegetarians and vegans may want to consider L-carnitine supplements, which can help normalize carnitine levels in the blood and muscles In fact, one study found that taking 1.
On the other hand, another study showed that L-carnitine supplementation had no effect on muscle strength or markers of inflammation in older women The risk of deficiency is also higher for those with diseases like cirrhosis and kidney disease.
If you have one of these conditions, a supplement may be beneficial 40 , Specific populations may benefit from L-carnitine supplements. This includes older adults and people who rarely or never eat meat. Although dosage varies from study to study, here is an overview of the use and dose for each form 13 , 19 , 33 :.
Although the recommended dose varies, around —4, mg 0. Studies also support its use for health, brain function, and disease prevention. Supplements may also benefit those with lower levels, such as older adults, vegans, and vegetarians.
Of the different forms, acetyl-L-carnitine and L-carnitine are the most popular and seem to be the most effective. Our experts continually monitor the health and wellness space, and we update our articles when new information becomes available.
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Miguel-Carrasco et al. In opposition to the reported beneficial effects of carnitine overload, Diaz et al. In addition, carnitine supplementation increased contracture of the heart shortly after reperfusion.
Diaz and colleagues concluded that in conditions where it does not increase glucose oxidation, carnitine supplementation worsens both injury and recovery of contractile function after transient ischemia in perfused rat heart [ ]. L-carnitine has been shown to have favorable effects in patients with severe cardiovascular disorders, such as coronary heart disease, chronic heart failure and peripheral vascular disease [ — ].
In patients with chronic heart disease, administration of L-carnitine over 12 months led to attenuation of left ventricular dilatation and prevented ventricular remodeling while reducing incidence of chronic heart failure and death [ ].
In ischemia, L-carnitine reduces myocardial injury mainly through improving carbohydrate metabolism and by reducing the toxicity of high free fatty acid levels [ ]. The protective effect of L-carnitine on ST-elevation myocardial infarction has been documented.
Following an acute myocardial infarction prompt L-carnitine administration and subsequent maintenance therapy attenuates progressive left ventricular dilatation [ ].
L-carnitine reduces early mortality but not overall risk of death or heart failure at 6 months [ ]. L-carnitine supplementation also prevents ventricular enlargement and dysfunction, reduces the infarct size and cardiac biomarkers, and diminishes the total number of cardiac events including cardiac deaths and nonfatal infarction [ , ].
Xue and colleagues suggest that the beneficial effects of L-carnitine in cardiovascular disease are due to the resumption of normal oxidative metabolism and restoration of myocardial energy reserves [ , ].
Carnitine has been widely recommended as a supplement in cardiovascular disease. However, it should be noted as mentioned previously, in conditions where it does not increase glucose oxidation, carnitine supplementation worsens both injury and recovery of contractile function after transient ischemia in the perfused rat heart [ ].
Myopathy can be seen with biochemically defined defects in mitochondrial substrate transport or utilization, including the myopathic form of carnitine deficiency; CPT II deficiency which most often presents with exercise intolerance and myoglobinuria and is discussed below [ ].
Patients with Duchenne dystrophy and Becker dystrophy showed lower carnitine levels in muscle biopsies than controls [ ] though these levels were higher than in patients suffering primary carnitine deficiency as a result of severe muscle damage [ 1 ].
CPT II Type 1 "muscle" phenotype, which is the most frequent clinical presentation, is characterized by recurrent episodes of muscle pain, rhabdomyolysis a potentially fatal disease that occurs suddenly and with great force destroying skeletal muscle and myoglobinuria.
Cyclosporin A induced nephrotoxicity has been discussed above. Valproic acid VPA is a broad-spectrum anti-epileptic drug [ ]. It is usually well tolerated, but rare serious complications such as VPA-induced hepatotoxicity VHT and VPA-induced hyperammonaemic encephalopathy VHE may occur in some patients who receive VPA chronically [ ].
It has been suggested that VHT and VHE may be promoted by carnitine deficiency, either pre-existing or deficiency induced by VPA [ ]. VPA is used to treat psychiatric disorders and as such there is an association with accidental or deliberate overdose, the incidence of which is increasing [ , ].
Benefits of oral L-carnitine in relation to VPA-associated deficiency and related adverse effects have been reported [ — ]. Carnitine supplementation during VPA therapy in high-risk patients is now recommended by some, especially by pediatricians [ ]. L-carnitine therapy could also be valuable in those patients who develop VPA-induced hepatotoxicity or VPA-induced hyperammonaemic encephalopathy [ ].
Al-Majed and colleagues [ ] found that carnitine deficiency and oxidative stress are risk factors during development of cisplatin CDDP -induced cardiomyopathy and that carnitine supplementation, using propionyl-l-carnitine, prevents the progression of CDDP-induced cardiotoxicity.
Adverse effects of aging are, in part, attributed to decreases in mitochondrial function and increases mitochondrial oxidant production [ ].
L -carnitine levels in tissues have been found to decline with age [ ]. Acetyl- L -carnitine ALCA fed to aged rats was shown to reverse age-related declines in tissue L -carnitine levels and also reversed a number of age-related changes in liver mitochondrial function; however, high doses of ALCA increased liver mitochondrial oxidant production [ ].
Liu et al. ALCA, together with alpha-lipoic acid, was shown to improve mitochondrial energy metabolism and decrease oxidative stress leading to improved memory in aged rats [ , ].
Several studies have reported that supplementing rats with both L -carnitine and alpha-lipoic acid halts age-related increases in reactive oxygen species ROS , lipid peroxidation, protein carbonylation, and DNA strand breaks in heart, skeletal muscle and brain, concomitant with improvement in mitochondrial enzyme and respiratory chain activities [ — ].
In a clinical trial of Levocarnitine-treated elderly patients [ ], there was significant improvement in total fat mass, total muscle mass, total cholesterol, LDL-C, HDL-C, triglycerides, apoA1, and apoB with concomitant decreases in physical and mental fatigue.
These data suggest that administration of levocarnitine to healthy elderly subjects may result in reduction of total fat mass, and increase of total muscle mass, may be reduce fatigue and serum lipids. Carnitine levels decrease with age [ ].
Patano and colleagues suggest that this decrease in energy availability might compromise osteoblast activity and bone remodeling in an age-related manner [ ].
Patano et al. Using an aging ovariectomized rat model they found supplementation of L-carnitine can influence bone density and slow the rate of bone turnover by slowing bone loss and improving bone microstructural properties through decreasing bone turnover [ ].
The study reported that benefits of carnitine are comparable with other drugs of choice in terms of effectiveness in preventing BMD loss due to aging.
Colluci and colleagues [ ] used an in vitro model to suggest that carnitine supplementation in the elderly may stimulate osteoblast activity and decrease age-related bone loss.
Dry eye is a common disease of the ocular surface that is associated with corneal surface irregularity and blurred vision [ — ]. In artificial tear formulations, L-carnitine is considered a "compatible solute". Use of carnitine in artificial tears has demonstrated rapid and consistent improvements in signs and symptoms in patients with dry eye [ ] suggesting an intrinsic homeostatic role for carnitine in the eye [ ].
Recently, Pescosolido and colleagues [ ] evaluated the presence of carnitine in tears of dry eye patients and suggested that the damage incurred on the ocular surface of dry eye patients may, in part, be due to a lack of carnitine in the tear film of these patients relative to the ocular surface cells and suggested use of solutions containing carnitine to reduce this damage.
Increased tear osmolarity in dry eye disease has been found to stimulate production of inflammatory cytokines and matrix metalloproteinases by ocular surface epithelial cells [ ].
Tears of patients with dry eye show significantly increased osmolarity, with a mean value of mOsm compared with mOsm in healthy controls [ ].
Corrales and colleagues [ ] showed that osmoprotectants such as L-carnitine reduce activation of mitogen-activated protein MAP kinases, the phosphorylation of which leads to an increased expression of cytokines, chemokines and matrix metalloproteases [ ]. These factors mediate and control immune and inflammatory responses.
Dysregulation of these factors in the eye can lead to corneal melting and scarring with deleterious consequences. Under hyperosmolar conditions, L-carnitine was found to protect against stress activation of corneal epithelial cells by reducing levels of kinase [ ].
that otherwise bring about the painful sunburn. Peluso et al. Mitochondrial trifunctional protein MTP defects are disorders of mitochondrial fatty acid β-oxidation pathway of which progressive pigment chorioretinopathy is a long-term complication [ ]. Chorioretinopathy emerges during early childhood as granular pigmentation of the central fundus with or without pigment clumping which may progress to chorioretinal atrophy, high myopia, posterior staphyloma and low vision [ ].
Current treatment includes a low fat, high carbohydrate diet and avoidance of fasting which dramatically improves prognosis allowing long term survival. However the dietary impact is controversial [ ]. Roomets et al. examined the expression of CPT-1 isoforms in photoreceptor cells and retinal pigment epithelial cells that are known to be affected morphologically and functionally in complete MTP deficiency and deficiency of long-chain 3-hydroxyacyl-CoA hydratase LCHAD [ ].
They concluded that the mitochondrial fatty acid β-oxidation pathway probably plays an active metabolic role in retinal pigment epithelium and other neuroretinal cell types. They further suggest that accumulation of 3-hydroxylated intermediates of long-chain fatty acids may contribute to the pathogenesis of retinopathy in MTP deficiencies [ ].
Carnitine as a nutritional supplement has, since the s, been promoted as beneficial in a number of disorders of human carnitine deficiency of impaired fatty acid oxidation, suggesting that nutritional or pharmacologic supplements of carnitine might be beneficial in some disorders [ ].
However it should be noted that according to Stanley [ ], over the past 40 years, there have been only two clear examples of disorders directly due carnitine deficiency that have provided evidence of unequivocal benefit from carnitine treatment.
Most healthy people, including vegetarians, produce and gain sufficient carnitine from their diets. Carnitine is thus considered a "conditionally essential" nutrient since individuals' requirements might exceed dietary intake during specific disease states.
The increase of L-carnitine in plasma via oral administration, even up to and exceeding 2 mg, is limited, since L-carnitine has a very poor absorption and bioavailability, a very high renal clearance, and active uptake into tissues.
Despite this, in a number of disease states much work has been done regarding the effects of prophylactic levels of carnitine though some controversy and misconceptions relating to its use in general nutrition need to be addressed. Carnitine is a natural compound, free from toxicity when given in oral doses up to several grams and thus supplements are often recommended in primary and secondary deficiencies.
Since carnitine is readily excreted, supplemental ingestion is well tolerated. Evidence from both rodent and human studies supports health-related benefits when used as a therapeutic agent. Kendler BS: Carnitine: an overview of its role in preventive medicine.
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The conundrum posed by the novel concept of supplemental l -carnitine as a source of atherosclerosis-promoting TMAO was recently reviewed [ 29 ]. The pro-atherogenic effect of TMAO may be related to upregulation of macrophage scavenger receptors linked to atherosclerosis, promoting foam cell differentiation [ 27 ] or to reduced reverse cholesterol transport and reduced expression of Cyp7a1 , the rate limiting step in the catabolism of cholesterol [ 21 ].
The intimate molecular mechanisms of TMAO actions is yet unknown, but TMAO may stabilize the folded state of diverse proteins, functioning as a chemical chaperone [ 32 ]. Plasma l -carnitine levels predicted incident major adverse cardiac events in a large cohort only among subjects with concurrently high TMAO levels [ 21 ].
While the relationship between serum TMAO and adverse cardiovascular events was established in the general population, TMAO metabolism in CKD has not been completely clarified. In this regard, high circulating TMAO levels in haemodialysis patients are efficiently removed during a single haemodialysis session [ 25 ] while increased urinary TMAO levels were observed in CKD patients [ 33 ].
These increased urinary levels may represent local renal TMAO synthesis or renal excretion of circulating TMAO. In summary, complex interactions between diet, genetics and the microbiota may impact on processing of oral l -carnitine into pro-atherogenic metabolites such as TMAO that regulate lipid metabolism.
The differential effect of oral versus intravenous l -carnitine supplementation observed by Fukami et al. If Fukami et al. have biobanked serum from their study, it would be interesting to analyse the impact of switching from oral to intravenous l -carnitine on serum TMAO levels and the relationship between TMAO and the observed changes in free fatty acid and HDL levels.
See related article by Fukami et al. Effects of switching from oral administration to intravenous injection of l -carnitine on lipid metabolism in hemodialysis patients. Clin Kidney J ; 7: — Evans A Dialysis-related carnitine disorder and levocarnitine pharmacology Am J Kidney Dis 41 Suppl 4 S13 S Google Scholar.
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Lipid-lowering effect of carnitine in chronically uremic patients treated with maintenance hemodialysis Am J Clin Nutr 33 Lacour B Di Giulio S Chanard J et al.
Carnitine improves lipid anomalies in haemodialysis patients Lancet 2 Eknoyan G Latos DL Lindberg J Practice recommendations for the use of l -carnitine in dialysis-related carnitine disorder.
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Identification of a urine metabolomics signature in patients with advanced-stage chronic kidney disease Kidney Int 85 Oxford University Press is a department of the University of Oxford. It furthers the University's objective of excellence in research, scholarship, and education by publishing worldwide.
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L-Carnitine β-hydroxy-γ-N-trimethylaminobutyric acid is a L-carntine of the amino acidlysine Figure 1. It was first isolated from wnd carnus in Vitamins and minerals for athletes in absorptoin Only the L- isomer of Weight loss pills for stubborn fat is Weight loss pills for stubborn fat active 1. L-Carnitine appeared to act as a vitamin in the mealworm Tenebrio molitor and was therefore termed vitamin B T 2. Vitamin B Thowever, is a misnomer because humans and other higher organisms can synthesize L-carnitine see Metabolism and Bioavailability. Under certain conditions, the demand for L-carnitine may exceed an individual's capacity to synthesize it, making it a conditionally essential nutrient 3, 4.
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