Summary:
Childhood stress or chronic childhood unhappiness can alter the gene expression resulting in chronic, severe, and treatment resistant forms of depression, as well as chronic mild depression, known as dythymia.People with this disorder cannot manufacture acetyl-l-carnitine properly, but amazingly, supplementing with Acetyl-l-carnitine not only relieves the depression (and often within days), it can also repair the faulty gene expression leading to a lasting cure.LAC - Acetyl-l-carnitine
That LAC treatment might reverse some of the epigenetic-based vulnerability could have enormous clinical implications. In the defeat-stress model, the low BDNF in the hippocampus is related to trimethylation of H3K27 (H3K27me3) that is not reversed by traditional ADs (even though they do reverse the BDNF
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Childhood stress or chronic childhood unhappiness can alter the gene expression resulting in chronic, severe, and treatment resistant forms of depression, as well as chronic mild depression, known as dythymia.
People with this disorder cannot manufacture acetyl-l-carnitine properly, but amazingly, supplementing with Acetyl-l-carnitine not only relieves the depression (and often within days), it can also repair the faulty gene expression leading to a lasting cure.
LAC - Acetyl-l-carnitine
That LAC treatment might reverse some of the epigenetic-based vulnerability could have enormous clinical implications. In the defeat-stress model, the low BDNF in the hippocampus is related to trimethylation of H3K27 (H3K27me3) that is not reversed by traditional ADs (even though they do reverse the BDNF changes and the behavioral deficits) (17, 18). Since LAC increases acetylation of H3K27, it raises the possibility of more permanent elimination of vulnerability to defeat-stress depression-like behaviors. This proposition could readily be tested in animals and pursued clinically.
To the extent that some vulnerability to depression is based on these early childhood experiences, LAC treatment could theoretically reverse that vulnerability in the long term in a fashion different from traditional ADs, which require continued prophylactic treatment to prevent recurrent depressions (6, 14). This clinical possibility is further bolstered by the findings that LAC can induce resilience in an animal model by increasing astroglial cysteine-glutamate exchangers and glutamate transporters in the ventral hippocampus (9). LAC can also increase the structural plasticity in the medial amygdala and reverse depressive-like behaviors in a chronic restraint-stress model (19). It also has positive effects on energy balance and insulin/glucose levels, suggesting positive effects on aspects of the metabolic syndrome (20), which is so prominent in many psychiatric disorders and may be a key driver of early mortality related to cardiovascular disease (6, 14). Bigio et al. (20) concluded that “agents such as LAC that regulate metabolic factors and reduce glutamate overflow could rapidly ameliorate depression and could also be considered for treatment of insulin resistance in depressed subjects.”
PNAS
Myriad of implications of acetyl-l-carnitine deficits in depression
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