Diet Enriched with Omega-3 Fatty Acids Alleviates Convulsion Symptoms in Epilepsy Patients

Authors


Address correspondence and reprint requests to Dr. M. Shinitzky at Biological Chemistry, The Weizmann Institute of Science, 76100 Rehovot, Israel. E-mail: meir.shinitzky@weizmann.ac.i

Abstract

Summary:  Purpose: We examined whether a dietary supplement containing omega-3 polyunsaturated fatty acids (n-3 PUFAs) can alleviate and/or reduce the frequency of epileptic seizures in patients with central nervous system (CNS) diseases treated with anticonvulsive drugs (ACDs).

Methods: A special spread containing 65% n-3 PUFAs was added to the daily diet. The patients consumed 5 g of this spread at every breakfast for 6 months.

Results: Five patients completed the study. In all of them, a marked reduction in both frequency and strength of the epileptic seizures was recorded.

Conclusions: Incorporation of the dietary supplement containing n-3 PUFAs may be beneficial in suppression of some cases of epileptic seizures.

Omega-3 polyunsaturated fatty acids (n-3 PUFAs) are essential for normal brain development and function (1–4). Deficiency in n-3 PUFAs can contribute to the emergence of neurologic dysfunctions (reviewed in 5). With respect to epilepsy, recent studies in animal models have shown that n-3 PUFAs can raise the threshold of epileptic seizures (6–8). In one investigation, the effect of n-3 PUFAs was tested in patients with similar results (9). In the following study, we examined the anticonvulsive effect of n-3 PUFAs on epilepsy patients.

METHODS

Twenty-one patients hospitalized in The Kalanit Institute (Rishon LeZion, Israel), participated in the study. The patients had profound mental retardation and epilepsy secondary to another primary central nervous system (CNS) disease like West syndrome, cerebral palsy, Angelman syndrome, Lennox–Gastaut syndrome, Pelizaeus–Merzbacher disease, and of unknown etiology. Their epileptic seizures were mostly of grand mal (GM), with less frequent petit mal (PM) attacks. The frequency of GM attacks was more than three to four per month. The 21 patients were treated with two or more anticonvulsive drugs (ACDs), mostly valproic acid (VPA) and carbamazepine (CBZ). The drug therapy continued during the study.

Five grams of n-3 PUFA supplement was provided daily as a semisolid bread spread of different flavors (Yamega LTD, Israel). The spread contained 65% n-3 PUFA (46% DHA, 18% EPA, 1%α-linolenic acid), and 100 IU of vitamin E. Because of severe physical limitations of the participants, the diet feeding was inspected by the institute personnel.

RESULTS

Of the 21 patients, 16 patients refused to eat the spread and were disqualified from the trial. The five remaining patients were fed the n-3 PUFA diet at breakfast, for 6 consecutive months, which was verified daily by the personnel. Their medical features, drug therapy, and frequency of seizures, before and after 6 months of n-3 PUFA consumption, are presented in Table 1. As shown in Table 1, all five patients exhibited substantial improvement and alleviation in frequency and strength of both GM and PM seizures. No adverse affects were noticed in any of them.

Table 1.  Initial and final features of the five patients who complied with the n-3 PUFA diet
Patient
(gender)
Age
(yr)
NeuropathologyDrug therapyFrequency of
Grand malPetit mal
BeforeAfterBeforeAfter
1 (F)14West syndromeTab vigabatrin500 mg × 2/d2–3/wk05/wk1/wk
   Tab clonazepam0.5 mg × 2/d    
   Tab carbamazepine500 mg × 2/d    
   Tab lamotrigine500 mg × 2/d    
2 (M)26West syndromeCap valproic acid600 mg × 3/d6–8/wk0  
   Tab vigabatrin1 gr × 2/d    
   Tab carbamazepine400 mg × 2/d    
   Tab thioridazine10 mg × 1/d    
3 (F)24Unknown etiologyTab carbamazepine500 mg × 2/d1–2/wk1/mo  
   Tab diazepam10 mg × 1/d    
4 (F)14Cerebral palsySyr sodium valproate200 mg × 3/d1–2/wk0  
5 (F)12Angelman syndromeTab topiramate125 mg × 2/d14/wk3/wk  
   Syr sodium valproate200 mg × 2/d    
   Syr d-carnitine 30%2.5 ml × 3/d    

DISCUSSION

Recent studies have shown that n-3 PUFAs can prevent cardiac arrhythmias, attributed to the reduction in excitability of cardiomyocytes (1,2). Similar inactivations have been observed in isolated hippocampal neurons, probably by raising their stimulatory threshold of action (6,7,10). It was suggested that n-3 PUFAs act as inhibitors of second messenger–regulated protein kinases (4) and as neuroprotectors (11). Epileptic anticonvulsant effects also were observed in rats treated with a mixture of n-3 and n-6 PUFAs (8).

Our study shows that n-3 PUFAs can alleviate symptoms of human epilepsy. Although the biologic mechanism of this activity remains to be elucidated, the therapeutic benefits of n-3 PUFAs on human epilepsy should be seriously considered and merit further investigation.

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