Acetyl L-Carnitine

Plain Language Summary

Acetyl-L-Carnitine reduces the production of harmful oxidants and preserves cellular energy throughout the body after drinking alcohol.


Acetyl-L-Carnitine’s main target is the liver and CNS where it stabilizes mitochondrial function leading to fewer reactive side products of ethanol oxidation. Since L-carnitine is so intimately involved in energy homeostasis, many other interactions exist.

Author’s Conclusions

Acetyl-L-Carnitine is included in V1.0.


Acetyl-L-Carnitine (ALCAR) is a conditionally essential micronutrient for humans and is present in regular foodstuffs such as meat and dairy products. [zotpressInText item=”{EHWP7425}” etal=”yes”]

ALCAR contributes acyl and carnitine (CAR) groups; both of which are biologically active. [zotpressInText item=”{J46EUDDI}” etal=”yes”]

D-carnitine does exist synthetically but appears to be physiologically inactive and absent in nature. D-carnitine can become toxic due to its competitive binding for L-carnitine transport systems. [zotpressInText item=”{EHWP7425}” etal=”yes”]



Significant discrepancies exist in the literature for ALCAR pharmacokinetics. Kwong and Chung noted quite large differences if baseline ALCAR determinations were not accounted for. [zotpressInText item=”{J46EUDDI}” etal=”yes”] Rebouche et al. determined absorption of supplementary CAR at 14-18%. Dietary CAR absorption is significantly higher (as high as 86%) and varies only moderately (~10%) with physiological need. Supplementary ALCAR absorption is expected to be higher than CAR, but it has not been directly evaluated. The remainder of CAR not absorbed is degraded by the bacterial flora. [zotpressInText item=”{H53WDP4B}” etal=”yes”]


More than 90% of the CAR pool in humans resides in skeletal and myocardial muscle cells. The remainder is in circulation, kidneys, liver, and brain. [zotpressInText item=”{EHWP7425}” etal=”yes”] Intracellular CAR accounts for 99% of all body stores. [zotpressInText item=”{I2MKF6BC}” etal=”yes”]

Variations exists in distribution, but the majority of total carnitine in the body exists as the free form carnitine. [zotpressInText item=”{J46EUDDI}” etal=”yes”]

Supplemental CAR does not appear able to influence muscle CAR concentrations. [zotpressInText item=”{B225HEJ9}” etal=”yes”]


The level of circulating CAR is regulated primarily by excretion and reabsorption kinetics in the kidney. [zotpressInText item=”{H53WDP4B}” etal=”yes”] The elimination half-life (t1/2) is approximately 4.2 hours with a time to maximal concentration (Cmax) of approximately 3.1 hours in humans. [zotpressInText item=”{J46EUDDI}” etal=”yes”] Rapid uptake from the lumen is seen in perfused rat intestinal cells, but the absorbed CAR is only slowly released to circulation resulting in this uncommonly similar t1/2 and Cmax. [zotpressInText item=”{H53WDP4B}” etal=”yes”]



CAR’s primary physiological function is to transfer long chain fatty acid acyl groups as CAR esters to the mitochondria for β-oxidation. [zotpressInText item=”{EHWP7425}” etal=”yes”] CAR can also facilitate the transfer of short and medium chain fatty acids out of the mitochondria. [zotpressInText item=”{I2MKF6BC}” etal=”yes”]

Disease States

Under certain physiological states, such as advanced training regimes in athletes, endogenous synthesis of CAR may be insufficient. [zotpressInText item=”{EHWP7425}” etal=”yes”]

ALCAR increased the complete oxidation of alcohol to CO2 and H2O by reducing side products by 40% in isolated rat hepatocytes. Most notable is a small but consistent decrease in acetaldehyde accumulation. The authors suggest that an inhibition of ADH could result in fewer down stream side products by maintaining ALDH homeostasis. [zotpressInText item=”{6R53HJIR}” etal=”yes”] Besides the inherent limitations in using in-vitro models like this, limited conclusions may be drawn from this study due to their choice of incubation media:

Because shuttle intermediates were not replaced in the incubation mixture of these studies, their impact on the carnitine/acetylcarnitine inhibition cannot be evaluated in a direct manner. [zotpressInText item=”{6R53HJIR}” etal=”yes”]

ALCAR (1g, 3g per day) was able to reduce cravings in anhedonic alcoholics and improve liver function panels with 1g showing slightly better outcomes. ALCAR treatment was not associated with any adverse effects. [zotpressInText item=”{BH4R6PV8}” etal=”yes”]

A recent review on hepatic encephalopathy determined that ALCAR’s primary effect in this disease is to reduce systemic ammonia levels. Furthermore, ALCAR is able to interact with glutamate receptors to reduce the toxic effects of hyperammonemia. The authors also comment on ALCAR’s more general functions:

In fact [ALCAR] enhances the mitochondrial function, improves cerebral energy levels, protects against neurotoxic insults, improves thrombocytopoiesis, erythropoiesis, leucopoiesis and immune functions, plays major roles in the metabolism of carbohydrates and lipids, leading to an increase in ATP generation and in cell energy. [zotpressInText item=”{JX4Z9UU8}” etal=”yes”]

In isolated rat myoblast cells, ALCAR was able to dose-dependently ameliorate the insulin resistance seen with TNF-α exposure by activating AMPK signaling. [zotpressInText item=”{2FB3DKWH}” etal=”yes”] Binge drinking has been shown to increase circulating TNF-α in healthy human volunteers [zotpressInText item=”{6R53HJIR}” etal=”yes”], therefore, ALCAR could mitigate some of the same insulin effects in these subjects.

ALCAR administered to a mouse model of chronic alcohol feeding was able to mitigate oxidative damage in the brain. Specifically, ethanol increases the activity of CYP2E1 and upregulates iNOS and NOX activity leading to increased ROS and RNS generation. These active species lead to cell degeneration by adduct formation and neuroinflammation. The authors suggest that ALCAR stabilizes mitochondrial function thereby preventing the excessive production of ROS and RNS. [zotpressInText item=”{XSQG27MB}” etal=”yes”]

In a chronic alcohol rat model, ALCAR was able to mitigate GSH depletion and increase GSH reductase activity leading to reduced accumulation of peroxidated lipids. [zotpressInText item=”{PQV69E24}” etal=”yes”]

In a double blind, placebo controlled study of patients with hepatic encephalopathy, ALCAR was able to significantly reduce serum ammonia concentrations and reduce both physical and mental fatigue. [zotpressInText item=”{I2MKF6BC}” etal=”yes”]


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