Dr. Bob's Psychopharmacology Tips

Vitamin E for tardive dyskinesia prophylaxis

Date: Tue, 20 Feb 96 20:11 EST
From: Karin E Olson <kolson@traverse.com>
Subject: Vitamin E for tardive dyskinesia prophylaxis

Has anyone thought of using vitamin E prophylactically, e.g., have patients taking antipsychotics take 400 mg of vitamin E qd? I have started doing that, telling my patients there is no evidence it will help but it also will not do any harm. I explain that it is helping some with tardive dyskinesia that has already developed.

Date: Wed, 21 Feb 1996 10:56:52 -0600
From: Kevin Miller <MillerKB@wpogate.slu.edu>
Subject: Vitamin E for tardive dyskinesia prophylaxis

I have started doing this with all patients I'm expecting to be on neuroleptics longer than a few months. My rationale is based on a a few data pieces:

1. I have heard a lecture by Joseph Coyle, MD, chair at Harvard, describing the process of cell over-stimulation leading to cell death by the internal release of oxidants. Glutamate plays a role in the process. vitamin E "scavenges" the oxidants, impairing the cell death process.

2. Vitamin E has been used successfully to limit the progression of neuron cell death diseases, I believe both Huntington's Chorea and Parkinson Disease, supporting the suggested mechanism of its action. Indeed, it even seemed to produce some improvement, perhaps rescuing some near-death cells.

3. It has been said that the irreversible nature of tardive dyskinesia is due to neuronal death.

From: "Schweickert, Lori" <LSCHWEIC@npih.medsch.ucla.edu>
Subject: Vitamins C and E for tardive dyskinesia prophylaxis
Date: Thu, 04 Apr 96 09:01:00 PST

One (and probably major) mechanism by which vitamin E theoretically helps TD is by scavenging harmful intramembranous (oxygen and peroxyl) free radicals, by donating a hydrogen atom to the radicals, in turn generating a more stable vitamin E free radical.

In my biochemistry training (pre-med and medical school), I was taught that the vitamin E free radical is reduced (thus recycled back to a useful form) by ascorbic acid (vitamin C), a water-soluble vitamin which is then excreted in the urine.

Thus, in my practice, I routinely recommend that patients with early manifestations of TD consume two 16 oz glasses of vitamin C-containing fruit juice per day in conjunction with up to 1600 IU/d (as tolerated) of vitamin E. So far, the results are encouraging enough to continue doing so, but I have no way of sorting out whether the vitamin C actually adds any clinical benefit.

My recommendation is on a theoretical basis alone. I would love to see some data which looks at this issue more specifically.

Date: Sun, 29 Dec 1996 21:59:05 -0500
From: Hugues J Richard <kristof@cycor.ca>
Subject: Vitamins for tardive dyskinesia prophylaxis

Here are a few referrences:

• Goff DC, Tsai G, Beal MF, Coyle JT. Tardive dyskinesia and substrates of energy metabolism in CSF. American Journal of Psychiatry. 152 (12): 1730-6, 1995 Dec.

  Good article on free radical production due to the effects of neuroleptic on mitochondrial phosphorylation.

• Hawkins, David R. The prevention of Tardive Dyskinesia with high dosage vitamins: A study of 58,000 patients. Journal of Orthomolecular Medicine. 1 (1) 24-26, 1986.

  Incidence of TD of 0.05% over 10 years for a caseload of pts of 80 physicians, on neuroleptics plus, daily, vitamin C 3 gr, vitamin B3 3 gr, vitamin B6 600 IU, and vitamin E 600 IU.

Date: Fri, 21 Feb 1997 08:44:57 -0800
From: Charles Kuttner <ckuttner@proaxis.com>
Subject: Vitamin E for tardive dyskinesia prophylaxis

I have my patients on the non-novel [!] neuroleptics take 400 IU twice daily. I tell them there is evidence it *may* decrease the risk of TD and document that on the chart. I know of no dangers to this intervention, and it doesn't cost much.

Date: Mon, 24 Feb 1997 11:47:43 -0600
From: Kevin Miller <MillerKB@wpogate.slu.edu>
Subject: Vitamin E for tardive dyskinesia prophylaxis

Having had an interest in vitamins and written a research paper (unpublished) on vitamin E in medical school, I have followed it's medical appearance and disappearance.

The production of superoxide in dying neural cells is believed to be part of the mechanism of release of glutamate, which functions in the CNS as a "cell death messenger" (my phrase). Vitamin E inhibits the formation of superoxide and may delay neural cell death. The permanent quality to TD may be due to the death of neurons. Thus vitamin E may slow, inhibit, or partially remit that process. This would explain the positive reports of vitamin E in new onset TD, where cells are failing but not yet dead, as opposed to the negative effects in long-standing TD, where many cells may already have died.

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