1Marotta F, 1Signorelli P, 2Sollano J, 3Naito Y, 1Lorenzetti A, 2Yoshioka M, 1Polimeni A
1ReGenera Research Group, Milano, Italy; 2Gastroenterology Dept, University of Santo Tomas, Manila, The Philippines; 3Seyukai Medical Institute & Clinic, Nagoya, Japan;
Context. Patients with chronic pancreatitis (CP) suffer from malabsorption and complex while subtle nutritional deficiencies. Few years ago, it has been shown that docosa-hexaenoic-acid (22 : 6(n-3)) (DHA) may be significantly decreased in the CP with associated diabetes mellitus. This abnormality has been advocated for by the effects of diabetes mellitus and by selenium deficiency. We have also recently shown that patients with alcohol-induced (AICP) without overt diabetes would show a DHA deficiency associated with impaired essential fatty acids index (16:1(n7)/18:2(n6)).
Aim. The aim of the present investigation was to study the effect of EPA/DHA and selenium supplementation in patients with AICP.
Methods. Sixteen clinically-stable patients with proven AICP, abstinent for at least 5 years and without major associated diseases or malnourishement were recruited. A dietary questionnaire was used at the entry and re-assessed at the end of the study using the web-based version of the National Institutes of Health Diet History Questionnaire to assess diet history over the past 3 months and along the study period. Subjects were advised not to use any multivitamin supplement, fortified food or fish oil supplement while maintaining their usual diet. A 3-week wash out period from such use was observed when present. Patients were given a 8-weeks supplementation with high quality 2cp/day of eicosapentaenoic acid-EPA/DHA (Mega EPA/DHA®: EPA 720mg/DHA480mg, LEF, Ft. Lauderdale, USA) during meals and 2tab/day of a high-bioavailability selenium (SuperSelenium Complex®: Se-methylselenocysteine, SelenoPureTM, L-selenomethionine, sodium selenate, selenodiglutathione 200mg and d-alpha tocopheryl succinate 30 IU, LEF, Ft. Lauderdale, USA).
Results. Plasma DHA and selenium were significantly low in all patients and normalized after supplementation (p<0.01). Plasma Se was inversely correlated with RBC omega6 poly-unsaturated FA (PUFAs) and positively with omega3 PUFAs. Plasma Se, RBC omega3 PUFAs, and EPA increased with supplementation (p<0.05). Plasma and 24h urinary F2-isoprostanes was within normal limits in CP patients and did not change after supplementation.
Conclusion. Given the multifactoriality of the disease and the subtle and progressing clinical deterioration, such dietary intervention seems an effective integrative therapeutic tool within the complex fatty acid profile abnormalities occurring in these subjects. Moreover, this supplementation seems safe and, probably due also to the selenium-combined schedule, does not increase lipid peroxidation markers despite the likely concomitant ongoing oxidative stress abnormalities, as we have already shown in prior studies.