The need for viable augmentation strategies to assist in the pharmacological management of treatment-resistant depression has become so dire that clinicians seem to perk up to any option nowadays – regardless of how fly-by-night, “here today gone tomorrow” it may be. This is happening, at least in part, due to the ever-growing problem of suboptimum response to traditional antidepressant therapies.
The genesis of treatment-resistant depressions is linked to how neurotransmitters are born. Cell bodies manufacture their own messenger molecules – more typically referred to as neurotransmitters. The neurotransmitters thought to play the biggest role in mood – norepinephrine, serotonin and dopamine – are generated via pathways that start with amino acids and end with the neurotransmitters just mentioned. The problem is that we humans are not all able to manufacture the same amount of neurotransmitters. The rate of development also varies and is controlled by our genotype.
SAMe and L-methylfolate aid in the synthesis and subsequent generation of neurotransmitters. A breakdown in the functioning of these substances results in neurotransmitter development impairment.
Recent, well conducted studies with both SAMe and L-methylfolate have created quite a buzz. These studies give high marks to the effectiveness and tolerability of both SAMe and L-methylfolate as augmenting agents to traditional SSRI and SNRI antidepressants when these agents as monotherapy yielded suboptimal response rates.
The robust results from these recent studies should not be a gateway to irrational exuberance; but by the same token, all potentially effective options for the ever-growing population of folks struggling to achieve symptom remission from depression via pharmacotherapy should definitely remain on the table.