Low-grade inflammation is a characteristic of the obese state, and adipose tissue releases many inflammatory mediators. The source of these mediators within adipose tissue is not clear, but infiltrating macrophages seem to be especially important, although adipocytes themselves play a role. Obese people have higher circulating concentrations of many inflammatory markers than lean people do, and these are believed to play a role in causing insulin resistance and other metabolic disturbances. Blood concentrations of inflammatory markers are lowered following weight loss. In the hours following the consumption of a meal, there is an elevation in the concentrations of inflammatory mediators in the bloodstream, which is exaggerated in obese subjects and in type 2 diabetics. Both high-glucose and high-fat meals may induce postprandial inflammation, and this is exaggerated by a high meal content of advanced glycation end products (AGE) and partly ablated by inclusion of certain antioxidants or antioxidant-containing foods within the meal. Healthy eating patterns are associated with lower circulating concentrations of inflammatory markers. Among the components of a healthy diet, whole grains, vegetables and fruits, and fish are all associated with lower inflammation. AGE are associated with enhanced oxidative stress and inflammation. SFA and trans-MUFA are pro-inflammatory, while PUFA, especially long-chain n-3 PUFA, are anti-inflammatory. Hyperglycaemia induces both postprandial and chronic low-grade inflammation. Vitamin C, vitamin E and carotenoids decrease the circulating concentrations of inflammatory markers. Potential mechanisms are described and research gaps, which limit our understanding of the interaction between diet and postprandial and chronic low-grade inflammation, are identified.

/pdf/dietary-factors-and-low-grade-inflammation-in-relation-to-35j1dsb8lf.pdf

Dietary factors and low-grade inflammation in relation to overweight and obesity

IL-10, IL-6, and TNF-α: Central factors in the altered cytokine network of uremia—The good, the bad, and the ugly

Diet-quality scores and plasma concentrations of markers of inflammation and endothelial dysfunction

http://www.zunis.org/JACC%20SOTA%207-06%20to%208-08/Diet%20and%20Metabolic%20Syndrome%208-08.pdf

The effects of diet on inflammation: emphasis on the metabolic syndrome.

The increased risk of stroke observed in the Women's Health Initiative (WHI) trial in connection with combined estrogen/progestin hormone therapy was one reason for ending the study early. The present authors analyzed theeffects of combined hormone therapy (CHT) on ischemic and hemorrhagic stroke in the 16,608 postmenopausal women, 50 to 79 years of age, who participated in the multicenter, double-blind, placebo-controlled WHI trial and were followed up for 5.6 years on average. All women were followed for at least 3.7 years. The women were randomly assigned to receive either CHT (0.625 mg conjugated equine estrogen plus 2.5 mg medroxyprogesterone acetate) or a placebo each day. The rate of stroke was 1.8% in women given CHT and 1.3% in the placebo group. Four of 5 strokes were ischemic. Hemorrhagic stroke accounted for 11.9% of events in the CHT group and 18.6% in the placebo group. There were 23 deaths resulting from stroke, 12 in the CHT group and 11 in placebo recipients. The combined hazard ratio (hour) for all subtypes of stroke combined was 1.31 (nominal 95% confidence interval [CI], 1.02-1.68). Women who had never taken hormones had a 37% excess risk of stroke when given CHT, for a hazard ratio of 1.37 (95% CI, 1.03-1.82). On multivariate analysis, controlling for race/ethnicity and baseline systolic blood pressure did not influence stroke risk for women taking CHT. An excess risk was noted in all age groups; in women with all levels of baseline stroke risk; and in participants with and without hypertension, a history of cardiovascular disease, and statin or aspirin treatment. A number or risk factors for stroke failed to modify the effect of CHT on stroke risk. They included smoking, diabetes, biomarkers of inflammation, and a higher white blood cell count or hematocrit. These findings indicate that, independently of blood pressure, estrogen/progestin therapy augments the risk of stroke in postmenopausal women who are in good general health. Considering the increased risk of invasive breast cancer, myocardial infarction, and venous thrombosis in women participating in the WHI trial, the findings reinforce the view that the overall risk from CHT outweighs its possible benefits.

Effect of estrogen plus progestin on stroke in postmenopausal women: The Women's Health initiative: A randomized trial

Background: Atherogenesis is a complex process involving both a low-grade inflammation and a disturbed lipid profile. Although dietary fish and fish oil improve the latter of these two risk factors, their impact on the former is less clear. Objective: This study addressed the effect of supplementation with fish oil in doses achievable with diet on serum C-reactive protein (CRP), interleukin-6 (IL-6), and the lipid profile. Methods and results: Thirty healthy subjects taking HRT were randomly divided into three groups and supplemented for five weeks with 14g/day safflower oil (SO), 7g/day of both safflower oil and fish oil (LFO), or 14g/day fish oil (HFO). Measurements included serum high-sensitivity CRP, IL-6 in plasma and in cell culture supernatant collected from 24-hr lipopolysaccharide (LPS)-stimulated whole blood, and lipid profile markers. CRP and IL-6 were adjusted for body mass index (BMI). Fish oil supplementation significantly decreased CRP and IL-6 compared to SO, with a greater effect in the LFO than HFO groups. Plasma triacylglycerol (TG) and the TG/HDL-C ratio were significantly lower in the HFO compared to the SO group. Conclusions: These results suggest that dietary fish oil may decrease the risk for cardiovascular disease through the modulation of both plasma lipids and inflammatory markers in healthy postmenopausal women.

Dietary fish oil decreases C-reactive protein, interleukin-6, and triacylglycerol to HDL-cholesterol ratio in postmenopausal women on HRT.

Background: Oxidized low-density lipoprotein (oxLDL) promotes apoptosis in atherosclerotic plaques in the vascular wall, a process mediated through its oxidized lipids. 4-Hydroxynonenal (HNE) and 4-hydroxyhexenal (HHE), derived from oxidation of n-6 and n-3 fatty acids, respectively, are among the major oxidized products in oxLDL.
Hypothesis: This study hypothesized that eicosapentaenoic acid/docosahexaenoic acid (EPA/DHA)-rich versus linoleic acid-rich oxLDL obtained from postmenopausal women and HNE versus HHE differentially influence apoptosis in U937 cells.
Experimental Design: Thirty healthy postmenopausal women were supplemented with 14 g/day safflower oil (SO), 7 g/day of both fish oil and SO (low dose LFO) or 14 g/day fish oil (high dose HFO) for 5 weeks. Low-density lipoprotein, obtained after supplementation, was oxidized with 5 µM CuSO4 at 37°C for 6 h. The concentration of cholesteryl ester hydroperoxides (CEOOH) and conjugated dienes was measured in the oxidized LDL (oxLDL). U937 cells were incubated with the oxLDL, 10 µM of HHE, 7 µM of HHE plus 3 µM of HNE, 5 µM of both HHE and HNE or 10 µM of HNE and the extent of apoptosis measured three ways.
Results: The concentration of CEOOH and conjugated dienes in oxLDL did not differ among the three treatment groups. The percent of apoptotic cells was approximately 40% lower when incubated with oxLDL obtained from the HFO-supplemented group than the SO- supplemented group measured by both the Annexin V and the DNA fragmentation assays (P=.04 and .004, respectively). Apoptosis of U937 cells was significantly lower in cells incubated with 10 µM of HHE, and mixtures of HHE and HNE than the 10 µM HNE when measured by the Annexin V, DNA fragmentation and 4,6-diamidino-2-phenylindole (DAPI) staining.
Conclusions: These data suggest that the cardioprotective properties of n-3 fatty acids may derive in part from their less reactive oxidized lipid metabolites.

/pdf/reduced-effect-on-apoptosis-of-4-hydroxyhexenal-and-oxidized-4zmxwcmwne.pdf

Reduced effect on apoptosis of 4-hydroxyhexenal and oxidized LDL enriched with n-3 fatty acids from postmenopausal women

Oxidized LDL (oxLDL) may contribute to the accumulation of apoptotic cells in atherosclerotic plaques. Although it is well established in monophasic chemical systems that the highly unsaturated EPA and DHA will oxidize more readily than FA that contain fewer double bonds, our previous studies showed that enrichment of LDL, which has discrete polar and nonpolar phases, with these FA did not increase oxidation. The objective of this study was to compare the extent of apoptosis induced by EPA/DHA-rich oxLDL to that induced by EPA/DHA-non-rich oxLDL in U937 cells. LDL was obtained from one healthy subject three times before and after supplementation for 5 wk with 15 g/d of fish oil (FO), an amount easily obtainable from a diet that contains fatty fish. After supplementation, an EPA/DHA-rich LDL was obtained. Oxidative susceptibility of LDL, as determined by measuring the formation of conjugated dienes and the accumulation of cholesteryl ester hydroperoxides, was not higher in EPA/DHA-rich LDL. The oxLDL-induced cell apoptosis was detected by the activation of caspase-3, the translocation of PS to the outer surface of the plasma membrane using the Annexin V-fluorescein isothiocyanate binding assay, and the presence of chromatin condensation and nuclear fragmentation using the 4,6-diamidino-2-phenylindole staining assay. All three measures showed that after FO supplementation, EPA/DHA-rich oxLDL-induced cell apoptosis decreased. The decrease was not related to the concentration of lipid hydroperoxides. This study suggests that a possible protective effect of EPA/DHA-rich diets on atherosclerosis may be through lessening cell apoptosis in the arterial wall.

/pdf/enrichment-of-ldl-with-epa-and-dha-decreased-oxidized-ldl-52u9x7viww.pdf

Enrichment of LDL with EPA and DHA decreased oxidized LDL-induced apoptosis in U937 cells.

We disclose novel classes of alloy nanocompositions that have superior decontaminant properties which are derived from their superior immediate and residual biocidal properties. By decontaminant properties it is understood that the preferred compositions are antiseptics, disinfectants, sanitizers, and/or sterilizers. By biocidal properties it is understood that the preferred compositions are excellent antimicrobials, antivirals, antifungals, and sporicidals. The preferred compositions have superior immediate and residual biocidal properties in free or bound form and they are safe to humans and environmental friendly. The nanocomposites described herein are in two element, three element or four element combinations. The preferred compositions have additional properties such as they are magnetic and/or they have distinct natural colors. The compositions are produced in different sizes ranging from 5 nm up to 500 nm, and for some other classes above 500 nm.

Ye-Sun Lee

Papers

Dietary fish oil decreases C-reactive protein, interleukin-6, and triacylglycerol to HDL-cholesterol ratio in postmenopausal women on HRT.

Reduced effect on apoptosis of 4-hydroxyhexenal and oxidized LDL enriched with n-3 fatty acids from postmenopausal women

Enrichment of LDL with EPA and DHA decreased oxidized LDL-induced apoptosis in U937 cells.

Nanocomposites with residual biocidal and biostatic properties