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Plasma acetyl-l-carnitine and l-carnitine in major depressive episodes: a case-control study before and after treatment
Plain-language summary
Paraphrased from the published abstract below — not a verdict on whether anything works.
In this human case-control study, researchers measured plasma acetyl-l-carnitine (ALC), l-carnitine, and the l-carnitine/ALC ratio in 460 patients with a current major depressive episode (MDE) and 893 healthy controls (HCs), and re-assessed depressed patients after 3 and 6 months of antidepressant treatment. Compared to HCs, depressed patients had lower ALC levels, higher l-carnitine levels, and higher l-carnitine/ALC ratios (all p<0.00001). ALC levels increased and l-carnitine levels and l-carnitine/ALC ratios decreased after treatment, with these parameters reported as restored after 6 months. The baseline l-carnitine/ALC ratio was associated with remission after 3 months of treatment (odds ratio=1.14; 95% CI 1.03-1.27; p=0.015). The authors suggest decreased mitochondrial metabolism of l-carnitine to ALC during MDE.
Abstract
Major depressive disorder (MDD) is the main cause of disability worldwide, its outcome is poor, and its underlying mechanisms deserve a better understanding. Recently, peripheral acetyl-l-carnitine (ALC) has been shown to be lower in patients with major depressive episodes (MDEs) than in controls. l-Carnitine is involved in mitochondrial function and ALC is its short-chain acetyl-ester. Our first aim was to compare the plasma levels of l-carnitine and ALC, and the l-carnitine/ALC ratio in patients with a current MDE and healthy controls (HCs). Our second aim was to assess their changes after antidepressant treatment. l-Carnitine and ALC levels and the carnitine/ALC ratio were measured in 460 patients with an MDE in a context of MDD and in 893 HCs. Depressed patients were re-assessed after 3 and 6 months of antidepressant treatment for biology and clinical outcome. As compared to HC, depressed patients had lower ALC levels (p < 0.00001), higher l-carnitine levels (p < 0.00001) and higher l-carnitine/ALC ratios (p < 0.00001). ALC levels increased [coefficient: 0.18; 95% confidence interval (CI) 0.12-0.24; p < 0.00001], and l-carnitine levels (coefficient: -0.58; 95% CI -0.75 to -0.41; p < 0.00001) and l-carnitine/ALC ratios (coefficient: -0.41; 95% CI -0.47 to -0.34; p < 0.00001), decreased after treatment. These parameters were completely restored after 6 months of antidepressant. Moreover, the baseline l-carnitine/ALC ratio predicted remission after 3 months of treatment (odds ratio = 1.14; 95% CI 1.03-1.27; p = 0.015). Our data suggest a decreased mitochondrial metabolism of l-carnitine into ALC during MDE. This decreased mitochondrial metabolism is restored after a 6-month antidepressant treatment. Moreover, the magnitude of mitochondrial dysfunction may predict remission after 3 months of antidepressant treatment. New strategies targeting mitochondria should be explored to improve treatments of MDD.
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