In the previous post, I gave a couple of reasons why people being treated for depression have a problem passing on the “happy” neurotransmitters (Serotonin, Dopamine, Norepinephrine) from neuron to neuron in the brain:
- A lack of the necessary neurotransmitter being produced by the neuron
- Neurons that are hypersensitive to the neurotransmitter
- Neurons that are insensitive to the neurotransmitter
- The secreting neuron starts to reabsorb the neurotransmitter before it is passed on to the next neuron
The last of these reasons seems to be the one that is most targeted by antidepressants to alleviate depression symptoms. I like to think of the reabsorbing (reuptake) action of the neurotransmitter Serotonin in terms of a bucket, water and sponge.
For instance, in a healthy brain chemistry, Serotonin is naturally produced by ongoing chemical reactions in the body. The Serotonin is secreted from one neuron and passed on to a connecting neuron, building pathways throughout the brain. Don’t worry about the little hole in the bucket – the excess Serotonin is always reabsorbed properly by the secreting neuron to avoid an undesirable flood of Serotonin in the brain.
Sometimes with untreated depression, the Serotonin that is supposed to be passed on from one neuron to another is being reabsorbed too quickly by the secreting neuron. This is illustrated in the figure below through the enlarged hole in the bucket, as well as the enlarged sponge that is mopping up the Serotonin too rapidly. In this situation the receptor neuron does not receive an adequate amount of Serotonin before it is reabsorbed by the original secreting neuron.
Psychiatrists prescribe Selective Serotonin Reuptake Inhibitors (SSRI’s) to help limit the reabsorbing (reuptake) action of the secreting neuron, so that the necessary Serotonin may be passed on to the receptor neuron before it is reabsorbed too quickly. In the figure below, the SSRI is shown as a plug in the hole in the bucket. When the antidepressant is prescribed correctly, the correct amount of excess Serotonin is reabsorbed back into the secreting neuron.
We now turn our attention to depression caused by the MTHFR gene mutation. As stated before, people with the more severe types of this mutation are very limited in their ability to convert folate into L-methyfolate, the active form of folate that is able to be absorbed and utilized by the brain and body. Once absorbed by the brain, L-methyfolate is then further converted into the enzymes which are involved in the creation of Serotonin.
Since people with the MTHFR gene mutation are unable to turn folate into the form that can be utilized by the brain to create Serotonin, they typically have very little Serotonin in their neurons. SSRI’s and other antidepressants (the plug in the hole in the bucket) typically have very little effect, since the neurons in the brain have very little Serotonin to start with. This is illustrated in the figure below:
In this example, the more reasonable solution for this type of depression would be to increase the amount of Serotonin going into the “bucket” in the first place. That’s where the supplement Deplin comes in. Deplin is L-methylfolate, which is allowed to cross into the brain to complete the chemical transformation into Serotonin, Dopamine, and Norepinephrine.
(Note: It was also suggested that I continue to take my antidepressant, since it works as the “plug in the bucket” to avoid excess reabsorption by the secreting neuron.)
In reality, there are several holes in the bucket and several sponges, with each one corresponding to its own particular neurotransmitter. Some neurotransmitters have been discovered and identified for its own job in the human brain. Some neurotransmitters have been discovered, but their jobs are not fully understood. Still others have not even been discovered yet. SSRI’s (Selective Serotonin Reuptake Inhibitors) focus specifically on the neurotransmitter Serotonin. Tricyclics and SNRI’s (Serotonin Norepinephrine Reuptake Inhibitor) are antidepressants that focus on both the Serotonin and Norepinephrine neurotransmitters. MAOI’s (Monoamine Oxidase Inhibitors) focus on all of the members of the Monoamine Oxidase neurotransmitter family, including Serotonin, Norepinephrine, and Dopamine. Trycyclic and MAOI antidepressants are older antidepressants that carry with them various side effects or dietary restrictions, while SSRI’s and SNRI’s are relatively newer classes of antidepressants that generally have fewer side effects and restrictions on diet.
I personally take Nardil, which is a type of MAOI. I’m not entirely psyched about the dietary restrictions associated with this medication, and I am also unable to take any other antidepressant medication or antihistamines while on Nardil. However, I’ve been feeling great for the past 45 days on both Nardil and Deplin, so I am really uninterested in rocking the boat at this point.
Thanks for reading, and please comment me if you feel that my information is inaccurate or misleading. Happy Easter!