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
its 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?
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.
Bibliography:
1.

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.
Summary: article about Homocysteine and Depression by Psychiatrist Daniela
White
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