Low fat dietary intervention with omega-3 fatty acid supplementation in multiple sclerosis patients.

OBJECTIVES: To determine whether a low fat diet supplemented with omega-3 positively affects quality of life (QOL) in relapsing-remitting MS (RRMS) patients. In this 1-year long double-blind, randomized trial, patients were randomized to two dietary interventions: the "Fish Oil" (FO) group received a low fat diet (15% fat) with omega-3 FOs and the "Olive Oil" (OO) group received the AHA Step I diet (fat 30%) with OO supplements. The primary outcome measure was the Physical Components Summary Scale (PCS) of the Short Health Status Questionnaire (SF-36). Additional measures using MS specific QOL questionnaires, neurological status and relapse rate were obtained. RESULTS: 31 RRMS patients were enrolled, with mean follow up over 11 +/- SD 2.9 months. Clinical benefits favoring the FO group were observed on PCS/SF-36 (P = 0.050) and MHI (P = 0.050) at 6 months. Reduced fatigue was seen on the OO diet at 6 months (P = 0.035). The relapse rate decreased in both groups relative to the rates during the 1 year preceding the study: mean change in relapse rate in the FO group: -0.79 +/- SD 1.12 relapses/year (P = 0.021) vs. -0.69 +/- SD 1.11 (P = 0.044) in the OO group. This study suggests that a low fat diet supplemented with omega-3 PUFA can have moderate benefits in RRMS patients on concurrent disease modifying therapies.

Effect of dietary fat intake and exercise on inflammatory mediators of the immune system in sedentary men and women.

OBJECTIVE: Dietary fat intake and exercise affect the immune system. This study determined the changes in inflammatory components of the immune system in response to maximal exercise with three levels of dietary fat intake: 19%, 30%, and 50% of total calories. METHODS: Five men and six women were randomly assigned to consume diets with 19% and 50% calories from fat for three weeks each, with a one-week washout. The habitual and washout diets were 30% calories from fat. At the beginning and the end of each diet, body composition and maximal exercise tests were performed. Blood samples were collected before and after exercise to determine the immunological parameters. RESULTS: The subject's energy intake was balanced to expenditure on the 30% and 50% diets, but was in negative balance on the 19% diet. Exercise led to significant increases in the concentrations of leukocytes, neutrophils, lymphocytes, monocytes, plasma tumour necrosis factor (TNF)-alpha, plasma interleukin (IL)-2, plasma soluble vascular cell adhesion molecule (sVCAM)-1, and the production of IL-1beta and IL-6 by peripheral blood mononuclear (PBMN) cells stimulated with lipopolysaccharide (LPS), irrespective of diets (p < 0.05). The 19% fat diet resulted in increased plasma soluble intercellular adhesion molecule (sICAM)-1 after exercise. Leukotriene (LT) B4 concentration released by neutrophils stimulated with LPS was higher in the 50% fat diet, compared to the lower fat diets, and the sICAM-1 production of neutrophils stimulated with LPS was significantly increased after exercise only with 30% fat diet. CONCLUSION: While a short, intense bout of exercise increased pro-inflammatory mediators of the immune system, decreasing fat intake to 19% on a caloric deficient diet caused a greater increase in plasma TNF-alpha, sVCAM-1 and sICAM-1 concentration than the 30% and 50% fat diets in male and female subjects. Increasing fat calories to 50% with caloric balance did not exacerbate pro-inflammatory mediators compared to a 30% fat diet.

Effects of dietary omega3 and omega6 lipids and vitamin E on chemokine levels in autoimmune-prone MRL/MpJ-lpr/lpr mice.

Elevated levels of chemokines, such as Regulated upon Activation, Normal T cell Expressed and Secreted (RANTES), Monocyte Chemotactic Protein-1 (MCP-1), Macrophage Inflammatory Protein-1alpha (MIP-1alpha), and Macrophage Inflammatory Protein-1beta (MIP-1beta) have been found in rheumatoid arthritis (RA) and juvenile arthritis (JA), and they may be associated with the pathogenesis of these diseases. These chemokines are implicated in the migration of specific leukocytes into the joints. Omega-3 (omega3) fatty acid rich-fish oil (FO) and vitamin E may delay the progress of certain autoimmune diseases. The present study was designed to understand the effects of dietary lipids (omega-6 and omega-3 fatty acids) and vitamin E on the production of chemokines in autoimmune-prone MRL/lpr (a mouse model for RA) and congenic control MRL/++ mice. The MRL mice were fed for 4.5 months omega-6 and omega-3 diets that varied in lipid sources (corn oil; CO and fish oil; FO) and vitamin E levels (269 I.U./kg and 694 I.U./kg diet). Spleen cells were isolated and cultured aseptically in the presence of PHA for 48 h at 37 degrees C and the levels of chemokines (RANTES, JE/MCP-1 and MIP-1alpha) were determined in the cell-free supernatants. The levels of RANTES and JE/MCP-1 were significantly higher in MRL/lpr mice compared to MRL/++ mice. The FO had differential effect on RANTES and MCP-1 production by spleen cells. The production of RANTES and JE/MCP-1 by spleen cells in mice fed the FO diets was significantly lower than in mice fed the CO diets (p < 0.0001). The levels of vitamin E did not affect the production of RANTES and JE/MCP-1. The levels of vitamin E had a significant effect on MIP-1alpha as the spleen cells of mice fed diets containing 694 IU/kg diet of vitamin E produced significantly higher levels of MIP-1alpha compared to the group of mice fed the diets containing 269 IU of vitamin E (p < 0.0001). The data obtained from this study in MRL/lpr and MRL/++ mice suggest that FO diets containing omega-3 fatty acids are beneficial in decreasing the levels of certain pro-inflammatory chemokines (RANTES and MCP-1) thereby delaying the onset of and severity of autoimmune symptoms in MRL/lpr mouse model.

Effect of dietary intake on immune function in athletes.

Athletes are exposed to acute and chronic stress that may lead to suppression of the immune system and increased oxidative species generation. In addition, the tendency to consume fewer calories than expended and to avoid fats may further compromise the immune system and antioxidant mechanisms. The exercise stress is proportional to the intensity and duration of the exercise, relative to the maximal capacity of the athlete. Muscle glycogen depletion compromises exercise performance and it also increases the stress. Glycogen stores can be protected by increased fat oxidation (glycogen sparing). The diets of athletes should be balanced so that total caloric intake equals expenditure, and so that the carbohydrates and fats utilised in exercise are replenished. Many athletes do not meet these criteria and have compromised glycogen or fat stores, have deficits in essential fats, and do not take in sufficient micronutrients to support exercise performance, immune competence and antioxidant defence. Either overtraining or under nutrition may lead to an increased risk of infections. Exercise stress leads to a proportional increase in stress hormone levels and concomitant changes in several aspects of immunity, including the following: high cortisol; neutrophilia; lymphopenia; decreases in granulocyte oxidative burst, nasal mucociliary clearance, natural killer cell activity, lymphocyte proliferation, the delayed-type sensitivity response, the production of cytokines in response to mitogens, and nasal and salivary immunoglobulin A levels; blunted major histocompatibility complex II expression in macrophages; and increases in blood granulocyte and monocyte phagocytosis, and pro- and anti-inflammatory cytokines. In addition to providing fuel for exercise, glycolysis, glutaminlysis, fat oxidation and protein degradation participate in metabolism and synthesis of the immune components. Compromising, or overusing, any of these components may lead to immunosuppression. In some cases, supplementation with micronutrients may facilitate the immune system and compensate for deficits in essential nutrients. In summary, athletes should eat adequate calories and nutrients to balance expenditure of all nutrients. Dietary insufficiencies should be compensated for by supplementation with nutrients, with care not to over compensate. By following these rules, and regulating training to avoid overtraining, the immune system can be maintained to minimise the risk of upper respiratory tract infections.