Homocysteine and Depression: What You Need To Know

Ask your psychiatrist if Homocysteine could be contributing to your depression…

What is HCY?

Homocysteine (HCY) is an amino acid that is destructive to cell integrity and DNA, and is a risk factor for the development of vascular and neuropsychiatric pathologies.

HCY has been linked to cardiovascular diseases, but when it passes the blood-brain barrier, it contributes to other chronic disorders such as depression, dementia, bipolar disorder, schizophrenia, and acute events, like strokes.

Where do these amino acids come from? HCY is not obtained from the diet – it’s not present in a naturally occurring protein. An amino acid found in a normal diet, called methionine, is broken down to either cysteine (a ‘good’) amino acid or homocysteine (the ‘bad’ form).

What causes HCY Toxicity?

The mostly commonly suggested mechanisms are oxidative injury, direct vascular damage, impaired methylation and impaired DNA synthesis. Another possible mechanism is the possibility of a heightened the inflammatory process, which is associated with depression.

Causes for elevated HCY can be genetic, epigenetic, and environmental and lifestyle-related.

The most common causes of elevated HCY:

• smoking
• excessive alcohol consumption
• lack of exercise
• obesity
• some medications
• psychological stress

Exercise helps distribute the HCY more evenly throughout the body, facilitating metabolism. Poor vitamin intake makes it impossible for the metabolism of homocysteine to a ‘good’ form (cysteine). Decreased magnesium levels also slows down the metabolism of HCY. Lipid lowering medications or anticonvulsants impair the HCY metabolism as well. Genetic predisposition, like a mutation in the MTHFR enzyme can also decrease the ability of the body to metabolize HCY efficiently (TT and CT are the most variants shown to be associated with depression).

Why and how is this important for the treatment of depression?

Based on the theory of impaired metabolism of HCY, the low monoamines levels (serotonin, dopamine, norepinephrine) are related to the lack of important coenzymes that are necessary for the metabolism of HCY and the synthesis of neurotransmitters.

The coenzymes necessary for the HCY reduction are fully metabolized B vitamins. If a patient with depression is genetically predisposed to not be able to metabolize them (such in CT and TT variants of MTHFR) then they will have high levels of HCY, which may cause a higher level of inflammation and neurotoxic effects on the brain.

How can we individualize the treatment of depression?

1. Check for the MTHFR mutation. Although it is not the only etiological factor, it can suggest a polymorphism contributory to the inflammation and depression.
2. Supplement treatment with antidepressants by adding metfolate at 15 mg/day. Depression has been associated with reduced metfolate. Supplementing can help the HCY metabolism, reducing its toxic effects on the brain.
3. Supplement with complex B vitamins and other necessary micronutrients. Maximizing methylation with reduced complex B and micronutrients necessary in the metabolism of HCY. Many patients can benefit from this supplementation even in the presence of HCY and because they are safe, they should be more largely used as a routine addition to the antidepressant treatment.

If you like this article on Homocysteine and Depression, or have questions, schedule your first session by calling us at 713.426.3100.

Bibliography:

1. Homocysteine and Neuropsychiatric Disease: Angela Pana, MD, Psychiatric Ann. 2015;45(9):463-468.
2. Inadequate Homocysteine Metabolism: A theory of Depression, Andrew Farah, MD. Psychiatr. Ann. 2015;45 (9): 469-472.
3. Theory into Practice-Addressing the Homocysteine Basis of Depression. Andrew Farah, MD Psychiatr. Ann. 2015;45(9):473-477.

To learn more about Psychiatrist for Bipolar Disorder, Medical Center, TX, contact Midtown Psychiatry and TMS Center Houston at 713-426-3100.

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