Billions of neurons exist in the brain. These cells share information with other nerve cells through electrical impulses, allowing for thought and communication throughout the body. Neurotransmitters inform many necessary processes like getting your stomach to digest, your heart to beat, or your lungs to breathe. While all neurotransmitters transmit information, they do not all do so in the same manner or with the same intention.

There are “inhibitory” neurotransmitters and “excitatory” neurotransmitters. Inhibitory neurotransmitters work to counterbalance excitatory neurotransmitters and are considered the “feel-good” neurotransmitters. GABA, serotonin, and dopamine are among a few. They allow the brain to calm and feel balanced. Excitatory neurotransmitters are responsible for motivation, focus, anxiety, stress, and more. Norepinephrine and epinephrine (noradrenaline and adrenaline) are classified as excitatory, stimulating the brain.

It’s not uncommon for the body to run out of inhibitory neurotransmitters when one has overactive excitatory neurotransmitters. When inhibitory and excitatory neurotransmitters are not working together and are imbalanced, moods like anger, agitation, anxiety, depression can occur. Change in weight, sleep issues, and poor concentration can also be a byproduct. An estimated 86% of Americans have an imbalance between inhibitory and excitatory neurotransmitters.

Depression is not genetically inherited, but the potential for depression in each person is epigenetically modified by environment, stress, genetic makeup and nutritional health. In the nutrigenomic world, the depression risk factors are associated with two genes that are associated with a higher risk of developing depression. These genes do not guarantee any person will get depression. The specific genes are the MAO and COMT. Both of these genes affect the speed at which neurotransmitters are broken down and cleared from the post synaptic receptor. In both MAO A and B homozygous and COMT homozygous, the mono-amines are cleared from the receptor site in a sluggish manner. This makes the post synaptic neuron less adaptable to changes in neurotransmitter status and leads to a higher likelihood of depression and/or anxiety in that patient. By assisting these mutations with methyl donors (ie taurine, methionine, choline, inositol), the practitioner can speed the clearance of the neurotransmitters and lessen the likelihood of developing depression.*

The issues that accompany an imbalance of inhibitory and excitatory neurotransmitters can be exacerbated by specific genetic SNPs in neurotransmitter markers like COMT, MAO-A, MAO-B, GAB 12. Drugs (recreational and/or prescription), neurotoxins, stress, alcohol, poor diet, and caffeine can also fuel symptoms by encouraging these SNPs to further express themselves.