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We examined the effects of energy restriction on immune response and also compared the effects of low fat (LF, 18.6 E%) and high fat (HF, 40.7 E%) diets during energy restriction on immunological parameters. Ten overweight women were fed the HF diet for 42 days (P1) to maintain their body weights. For the next 84 days (P2), the energy intake was reduced to 50% of the intake during P1 for all the women, five of them were fed the HF diet and the other five the LF diet. For the last 35 days of the study (P3), subjects remained on their respective diets, but the energy intake was increased to maintain BW to the level reached at the end of energy restriction. Serum concentrations of IgG, IgA, IgM, C3 and C4, numbers of lymphocytes and their subsets, blastogenesis of peripheral blood mononuclear cells cultured with phytohemagglutinin, concanavalin A and protein A were determined several times during the study. Delayed hypersensitivity skin (DHS) response to seven recall antigens was determined towards the end of each study period. None of the parameters studied were different between the HF and LF dietary groups. During energy restriction the subjects lost an average of 7 kg in the LF group and 9 kg in the HF group. Energy restriction caused a significant (P < 0.005) decrease in the serum concentration of IgG, IgA, C3, and the number of circulating natural killer (NK) cells. An increase in energy intake during P3 reversed some of the decreases caused by energy restriction, but the levels did not return to pre-restriction levels during these 35 days of refeeding adequate dietary energy. The numbers of circulating lymphocytes and their subsets with the exception of NK cells, serum levels of IgM and C4, and the DHS response monitored 48 h after the application of antigens were not affected by energy restriction. Health status of the women in our study did not seem to be compromised; however, it could be compromised under more drastic restrictions or with moderate restrictions in high risk subjects.

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We examined the effect of dietary alpha-linolenic acid (ALA) on the indices of lipid and coagulation status and on the fatty acid composition of serum and peripheral blood mononuclear cell (PBMNC) lipids in ten healthy men (age 21-37 yr) who consumed all their meals at the Western Human Nutrition Research Center for 126 d. There was a stabilization period of 14 d at the start when all 10 subjects consumed the basal diet (BD) containing 23.4 energy percent (en%) fat and two intervention periods of 56 d each. During the first intervention period, 5 subjects consumed the BD containing 23.4 en% fat, and 5 subjects consumed a diet providing 6.3% calories from alpha-linolenic acid [flaxseed oil (FSO) diet containing 28.8 en% fat]. Diets were crossed over between the two groups during the second intervention period. Feeding the FSO diet did not significantly alter serum triglycerides, cholesterol, high-density lipoproteins, low-density lipoproteins, apoprotein A-I and apoprotein B when compared to the corresponding values in the subjects fed the BD, nor was there any effect of the FSO diet on the bleeding time, prothrombin time and partial prothrombin time for these subjects. Feeding the ALA-containing diet did cause a significant increase in ALA concentration in serum (P < 0.001) and PBMNC lipids (P < 0.05). It also caused a significant increase (P < 0.05) in the eicosapentaenoic and docosapentaenoic acid contents of PBMNC lipids, and a decrease (P < 0.01) in linoleic and eicosatrienoic acid contents of serum lipids.(ABSTRACT TRUNCATED AT 250 WORDS)

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We examined the effect of feeding a salmon-containing diet on the immune status of nine healthy men (age 30-65 years) who lived at the metabolic suite of the Western Human Nutrition Research Center for 100 days. During the first 20 days all nine subjects consumed a basal diet (BD). For the next 40 days, three subjects continued to consume BD, while the diet of remainder six subjects was modified to contain 500 g salmon every day. During the last 40 days, the diets of the two groups were crossed over. Feeding 500 g salmon daily for 40 days did not significantly suppress the blastogenesis of peripheral blood mononuclear cells cultured with phytohemagglutinin, Concanavalin A, protein A or pokeweed when compared to the corresponding pre-salmon diet values. It also did not significantly affect the delayed hypersensitivity skin response to seven recall antigens, serum concentrations of immunoglobulins G, M, and A, and complement fractions C3 and C4. Our results indicate that the short-term consumption of a high fish (salmon)-containing diet does not adversely affect the immune system, as has been reported with fish oil supplements.

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We examined the effect of the dietary concentration of total fat and n-6 polyunsaturated fatty acids (PUFA) on the immune status of seven healthy women (age 30-65 years) who lived at our metabolic suite. During the first 20 days all subjects consumed a stabilization diet that contained 5.2 energy percent (en%) PUFA and 41.1 en% fat. For the next 40 days, three subjects consumed a diet with 3.2 en% PUFA and 26.1 en% fat, while the remaining four subjects consumed a diet with 9.1 en% PUFA and 31.1 en% fat. For the next 40 days, the diets of the two groups were crossed over. Blastogenesis of peripheral blood mononuclear cells cultured with phytohemagglutinin, concanavalin A, protein A, and pokeweed, and the serum concentrations of complement fractions C3 and C4 were significantly increased upon the feeding of both low fat (26.1 or 31.1 en%) diets compared to the values when the high fat (41.1 en%) diet was fed. None of the indices tested were different when the high PUFA (9.1 en%) and low PUFA (3.1 en%) diets were compared. Our results indicate that low fat diets improve some of the indices of human immune status and that a moderate increase in the level of n-6 PUFA in an otherwise low fat diet does not suppress the human immune system.

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We examined the effect of dietary alpha-linolenic acid (ALA) on the indices of immunocompetence in 10 healthy free-living men (age 21-37 y) who consumed all meals at the Western Human Nutrition Research Center for 126 d. There was a stabilization period of 14 d at the start when all 10 subjects consumed basal diet (BD) and there were two intervention periods of 56 d each. Five of the subjects consumed the basal diet and the other five consumed flax-seed-oil diet (FD) during each intervention period. Feeding of FD suppressed the proliferation of peripheral blood mononuclear cells when they were cultured with phytohemagglutinin-P (P = 0.041) and concanavalin A (P = 0.054) and the delayed hypersensitivity response to seven recall antigens (NS). Concentrations of immunoglobulins in serum, C3, C4, salivary IgA, the numbers of helper cells, suppressor cells, and total T and B cells in the peripheral blood were not affected by the diets.

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We have compared the effects of dietary saturated and unsaturated fats of the n-6 and n-3 types on the immune status of male New Zealand white rabbits. Four groups of rabbits (n = 8) were fed purified diets containing one of the following fats (7.6% w/w, 23 kcal%) for 5 mo, hydrogenated soybean oil (HSO); safflower oil (SFO); linseed oil (LSO); or menhaden oil (MHO). In vitro proliferation of peripheral blood lymphocytes (PBL) cultured with T-cell mitogens was significantly higher in the LSO group than in the other three groups, and that in the HSO group was higher than in the MHO and SFO groups which were not different from each other. Proliferation of PBL in response to B-cell mitogens was significantly higher in the LSO group than in the SFO and MHO groups. In vitro proliferation of splenocytes (SPC) from the LSO group was higher than that from the other three groups only when SPC were cultured with T-cell mitogens. Serum antibody levels against bovine serum albumin were significantly higher in the LSO group than in the SFO group after second and third immunizations. Spleen weights, number of SPC or PBL, and delayed-type hypersensitivity were not different among the four dietary groups. Our data show that linseed oil diet enhanced several indices of immune status in rabbits.

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One hundred twenty-five patients with chronic urticaria were evaluated with 11 commonly recommended laboratory and radiologic procedures. Abnormal studies were obtained in 26 (20.8%) of these patients, but the majority of these abnormalities were evident from the initial history and physical examination. These results indicate that, with the possible exception of sinus roentgenograms, these laboratory studies are not likely to be helpful in the evaluation of chronic urticaria unless there are suggestive findings in the history and physical examination. The yield and equivalent charge of diagnosis for each procedure used was also analyzed.

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Heat-stable, immunoglobulin G, short-term sensitizing antibodies (IgG S-T S) were sought in serum from 149 allergic patients who had strongly positive immediate skin tests to inhalant allergens. The sera were tested by passive cutaneous anaphylaxis (PCA) in monkeys. No IgG S-T S antibodies were demonstrated in 169 tests with a variety of allergens. Antibody with the characteristics of IgE was demonstrated in 47% of monkey PCA tests and, in an additional 34% of sera. IgE antibody to the same allergen was demonstrated by radioallergosorbent testing (RAST).

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Serum IgA and IgE levels were obtained in 706 patients, 294 of whom were also tested for cutaneous delayed hypersensitivity. The results do not support the concept that a deficiency of serum IgA or of T lymphocyte function underlies the elevated serum IgE levels observed in a majority of allergic patients.

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The response to preseasonal immunotherapy with aqueous grass extract, timothy antigen D, or water-soluble timothy (WST) in alginate was compared in patients sensitive to grass pollen. Injections of antigen D in alginate produced little evidence of clinical or immunologic response. Treatment with aqueous grass extract or WST in alginate, on the other hand, significantly reduced the seasonal rise in grass-specific IgE. Aqueous extract therapy was also associated with a decline in leukocyte sensitivity during the pollen season, while WST treatment produced the greatest rise in hemagglutinating antibodies.

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Controversy exists as to the advisability of mist therapy in pulmonary disease. We studied the effects of several forms of humidity on asthmatic airways. Thirty-four children were tested over a period of 8 months as follows: (1) mist with a mean particle size of 3 mu was delivered for 30 min by an ultrasonic nebulizer to 11 children individually in a plastic tent; (2) to another 11 subjects in a tent, mist with a mean particle size of 10 mu was delivered by a jet nebulizer for 30 min;3) 15 patients in a croup room recieved for 30 min water droplets ranging from a microscopic fog to large rain particles (mean 16 mu) generated by a Melco natural fog generator; (4) 10 children were challenged with 3 solutions used commonly for the production of mist: distilled water, half-normal saline, and normal saline. Pulmonary functions were studied on each patient pre- and post-mist exposure. Approximately two thirds of the patients had a significant response, either improvement or deterioration, when challenged with the various forms of mist. No particular group trends were produced either by increasing the mean particle size of humidity, or by using solutions of increasing salinity.

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Cardiovascular and metabolic responses to exercise and consecutive epinephrine infusions 24 hours apart were measured in 7 normal individuals before and following a week's administration of ephedrine sulfate. There was evidence of less beta adrenergic response to the second control epinephrine infusion compared to the first control infusion, and the depression of the rise in blood lactate was significantly different. A week of ephedrine produced more profound depression of the beta adrenergic responses to epinephrine with significant differences in the rise in blood glucose and lactate, and the pulse and blood pressure responses. Furthermore, these same responses remained significantly altered when a second epinephrine infusion was performed 36 hours following the last dose of ephedrine. The alterations in the response to epinephrine induced by ephedrine are consistent with the concept of effector cell "subsensitivity," an adaptive response to prolonged excessive stimulation.

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