BackgroundCurcumin extracts of turmeric are proposed to produce health benefits. To date, human intervention studies have focused mainly on people with existing health problems given high doses of poorly absorbed curcumin. The purpose of the current study was to check whether in healthy people, a low dose of a lipidated curcumin extract could alter wellness-related measures.MethodsThe present study was conducted in healthy middle aged people (40–60 years old) with a low dose of curcumin (80 mg/day) in a lipidated form expected to have good absorption. Subjects were given either curcumin (N = 19) or placebo (N = 19) for 4 wk. Blood and saliva samples were taken before and after the 4 weeks and analyzed for a variety of blood and saliva measures relevant to health promotion.ResultsCurcumin, but not placebo, produced the following statistically significant changes: lowering of plasma triglyceride values, lowering of salivary amylase levels, raising of salivary radical scavenging capacities, raising of plasma catalase activities, lowering of plasma beta amyloid protein concentrations, lowering of plasma sICAM readings, increased plasma myeloperoxidase without increased c-reactive protein levels, increased plasma nitric oxide, and decreased plasma alanine amino transferase activities.ConclusionCollectively, these results demonstrate that a low dose of a curcumin-lipid preparation can produce a variety of potentially health promoting effects in healthy middle aged people.

Objective-Zinc deficiency is common among populations at high risk for sepsis mortality, including elderly, alcoholic, and hospitalized patients. Zinc deficiency causes exaggerated inflammatory responses to endotoxin but has not been evaluated during bacterial sepsis. We hypothesized that subacute zinc deficiency would amplify immune responses and oxidant stress during bacterial sepsis [i.e., cecal ligation and puncture (CLP)] resulting in increased mortality and that acute nutritional repletion of zinc would be beneficial.Design-Prospective, randomized, controlled animal study. Setting-University medical center research laboratory.Subjects-Adult male C57BL/6 mice.Interventions-Ten-week-old, male, C57BL/6 mice were randomized into three dietary groups: 1) control diet, 2) zinc-deficient diet for 3 weeks, and 3) zinc-deficient diet for 3 weeks followed by oral zinc supplementation for 3 days (n = 35 per diet). Mice were then assigned to receive either CLP or sham operation (n = 15 each per diet). CLP and sham-operated treatment groups were further assigned to a 7-day survival study (n = 10 per treatment per diet) or were evaluated at 24 hours (n = 5 per treatment per diet) for signs of vital organ damage.Measurements and Main Results-Sepsis mortality was significantly increased with zinc deficiency (90% vs. 30% on control diet). Zinc-deficient animals subject to CLP had higher plasma cytokines, more severe organ injury, including increased oxidative tissue damage and cell death, particularly in the lungs and spleen. None of the sham-operated animals died or developed signs of organ damage. Zinc supplementation normalized the inflammatory response, greatly diminished tissue damage, and significantly reduced mortality.Conclusions-Subacute zinc deficiency significantly increases systemic inflammation, organ damage, and mortality in a murine polymicrobial sepsis model. Short-term zinc repletion provides significant, but incomplete protection despite normalization of inflammatory and organ damage indices.The authors have not disclosed any potential conflicts of interest. Sepsis is a major cause of morbidity, mortality, and healthcare costs in hospitalized patients and is the tenth leading cause of death overall in the United States (1). Currently, it is expected that between 20% and 50% of patients who develop sepsis will die despite receiving the current standard of appropriate therapy. The basic cellular and molecular mechanisms accounting for sepsis-related morbidity and mortality remain poorly understood. However, a number of host factors, including immunosuppression, advanced age, chronic alcoholism, and poor nutritional status, are known to increase sepsis mortality (2,3). NIH Public AccessZinc is an essential dietary micronutrient with beneficial functions that facilitate cytoprotection, improved wound healing, and tissue repair (4). Humans, in response to sepsis or endotoxin administration, experience a transient decrease in plasma zinc levels without a concomitant loss of whole body zinc content (5). ...

The alteration of zinc metabolism was more pronounced in septic patients than in noninfected critically ill patients. Specifically, sepsis was associated with lower plasma zinc concentrations and higher SLC39A8 mRNA expression, which correlated with an increased severity of illness, including cardiovascular dysfunction.

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Results demonstrate that repetitive endurance exercise in dogs is associated with lipid peroxidation and a reduction in plasma antioxidant concentrations. We interpret these results as indicating that the antioxidant mechanisms of minimally trained dogs may, in some instances, be inadequate to meet the antioxidant requirements of repetitive endurance exercise.

Background: Although soy protein may have many health benefits derived from its associated antioxidants, many male exercisers avoid soy protein. This is due partly to a popular, but untested notion that in males, soy is inferior to whey in promoting muscle weight gain. This study provided a direct comparison between a soy product and a whey product.

Theoretically, zinc can exert a number of indirect antioxidant functions. Researchers at our laboratory have found evidence to support this concept by studying mild zinc deficiency in rats. This state produces low resistance to chemically induced liver oxidant injury, and it produces high vulnerability of lipoproteins to oxidation. We are building on this work in rats to test a hypothesis in humans that increased zinc intake will protect against oxidant stress in persons with tendencies for both moderate zinc deficiency and high oxidant stress. This hypothesis has been tested in postmenopausal, type 2 diabetic women. A 3-wk supplementation with zinc (30 mg/d as glycine-chelate) raised initially low plasma zinc values to above normal values and increased plasma activities of 5'-nucleotidase. However, the latter values were still well below normal. Lipoprotein oxidation tendencies, a measure of oxidant stress, were not altered by the zinc treatment. A new project has been initiated to determine whether both a higher dose and longer duration of zinc treatment will normalize 5'-nucleotidase activities and affect the indices of oxidant stress. The latter will be considered in terms of both zinc supplementation and supplementation of zinc plus vitamin C, another problem nutrient for diabetic persons.

Doses up to 30 mg/day of zinc were safe for at least 8 weeks, but clinical effect was equivocal except for 37% reduction in amphetamine optimal dose with 30 mg/day zinc (not with 15 mg). Possible reasons for difference from mideastern reports include endemic diets, population genetics, relative rate of zinc deficiency, difference in background nutrition, insufficient dosage or absorption, or wrong anion (sulfate may be necessary for reported benefit). Dose may be especially important: All visually impressive advantages over placebo appeared only with 15 mg b.i.d. rather than once a day. Future research should use larger doses than 15 mg/day, provide a basic recommended daily allowance/intake multivitamin/mineral supplement for all to standardize background nutrition, select participants for low zinc, and consider the issue of anion interaction.