L-Methylfolate in combination with SSRIs

When it comes to being resistant to SSRIs, you aren’t alone. About two-thirds of patients with depression do not get better with only antidepressant medications such as SSRIs. Their effects are either non-existent or quite temporary. Suicidal ideation and hefty medical bills are more common among depressives than in the general population. People who were resistant to therapy saw an increase in these side effects.

The good news is that many treatment-resistant persons are suffering from a nutritional deficiency that may be corrected.

Since the 1960s, there has been a relationship between low folate intake and depression. Reduced folate levels are not only associated with depression, but they also have a clear scientific basis to explain why. Nutritional folate creates L-methylfolate, which has an impact on the generation of serotonin, dopamine, and norepinephrine in the brain and body. An amino group from L-methylfolate is required by tetrahydrobiopterin (BH4). A cofactor for rate-limiting enzymes, which are required for neurotransmitter synthesis, is provided by this metabolite. Accordingly, the body’s neurotransmitter synthesis is influenced by its L-methylfolate levels.

Reduces the ability of neurotransmitters to re-absorb, allowing them to communicate for longer periods of time. Inhibitors of serotonin and norepinephrine reuptake If the brain is unable to produce enough neurotransmitters, it may be counter-productive. On the other hand, L-methylfolate may assist the process by acting as a substrate.

If you are on an SSRI or SNRI medication, L-methylfolate is generally recommended to ensure that you are getting the right nutrients. It works in conjunction with an SSRI to modulate neurotransmitter levels. If you have a nutritional shortfall that is causing you to be depressed, L-methylfolate may not be sufficient.

Folic acid (synthetic folate) supplements have been promoted in the past for women who are pregnant or breastfeeding. Folic acid is transformed to L-methylfolate before it can reach the brain and play a role in neurotransmitter synthesis or enter the brain. It is estimated that around half of the population is affected by a genetic mutation that prevents folic acid from converting into L-methylfolate. An SNP in the MTHFR gene is responsible for the condition. A single normal copy of the gene is inherited, but heterozygous individuals can only metabolise half of the folate they consume. The likelihood of developing depression is higher in those who have lower gene expression levels. Having two defective copies of the gene that metabolisesfolate increases the likelihood of developing a depressive disorder. It is possible that eating enough folic acid will not prevent folate insufficiency in some people.

There is currently a supplement that contains L-methylfolate. By substituting L-methylfolate for folic acid, the MTHFR enzyme is eliminated. Whatever one’s genetic makeup, L-methylfolate has the potential to function well in the body and to readily cross the blood-brain barrier (BBB). L-methylfolate is a B vitamin that is water-soluble. As a result, if you are deficient in folate, you should take it often. In addition, it seems to be well tolerated and to be devoid of side effects, which is encouraging.

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