Cost-effectiveness of health risk reduction after lifestyle education in the small workplace.

INTRODUCTION: Investigations suggest that worksite health promotions in large companies decrease employer health costs and the risk for chronic disease. However, evidence of the success of such programs in small organizations is lacking. The purpose of this study was to determine whether a worksite health promotion program improves health risk and is cost-effective for a small employer. METHODS: Intervention (n = 29) and comparison (n = 31) participants from a 172-employee organization underwent health screening of risk factors for coronary heart disease at baseline (fall 2006) and at 12 months (fall 2007). The intervention group attended lifestyle education videoconferences and reported physical activity. We used the Framingham Risk Score to calculate risk of coronary heart disease. To calculate cost-effectiveness, we used direct employer costs of the program divided by either the relative reduction in low-density lipoprotein cholesterol or the absolute change in coronary heart disease risk. RESULTS: At 12 months, low-density lipoprotein cholesterol, total cholesterol, and number of metabolic syndrome markers were significantly higher in the comparison group than in the intervention group. Total cholesterol was significantly lower at 12 months than at baseline in the intervention group. Waist circumference and number of metabolic syndrome markers increased significantly from baseline in the comparison group. Cost-effectiveness of the intervention was $10.17 per percentage-point reduction of low-density lipoprotein cholesterol and $454.23 per point reduction in coronary heart disease risk. CONCLUSION: This study demonstrated the cost-effectiveness in a small organization of a worksite health promotion that improved low-density lipoproteins and coronary heart disease risk in participating employees.

Exposure of alveolar macrophages to polybrominated diphenyl ethers suppresses the release of pro-inflammatory products in vitro.

Inhalation of chemical pollutants has been associated with a reduced immune response in humans. Inhalation of dust is a major route of exposure for one endocrine-disrupting chemical and suspected xenoestrogen, polybrominated diphenyl ethers (PBDEs); however, the impact of PBDEs on immune function is unclear. The objective of this study was to investigate the action of PBDEs on cytokine and eicosanoid release by alveolar macrophages and determine whether the effects are mediated via the estrogen receptor. The production of tumor necrosis factor (TNF)-α, interleukin (IL)-6, IL-1ß, IL-10 and prostaglandin E(2) (PGE(2)) by porcine alveolar macrophages exposed to different concentrations of the pentabrominated diphenyl ether mixture, DE-71, were measured; cells were also exposed to varying concentrations of 17ß-estradiol and the selective estrogen receptor-modulating agent, tamoxifen. Cells exposed to PBDEs released significantly less pro-inflammatory cytokines (TNF-α and IL-6) and PGE(2) compared with controls; IL-1ß and IL-10 were not detected in the culture medium. Cells exposed to 17ß-estradiol released significantly less TNF-α compared with controls, an effect that was reversed by the addition of tamoxifen; tamoxifen had no effect on the inhibition of TNF-α release by PBDEs. Although the suppression of TNF-α with DE-71 was similar to that of estrogen, the inhibitory effects of DE-71 were not found to be dependent on the estrogen receptor. Findings of this study suggest that chronic exposure to PBDEs suppressed innate immunity in vitro. Whether the immunosuppressant effects of PBDEs occur in vivo, remains to be determined.

Elevated atopy in healthy obese women.

BACKGROUND: Allergic disorders, including asthma, have increased dramatically in the United States in the past 20 y. Epidemiologic studies have found body mass index (body weight in kg/height squared in m) to be a positive independent correlate of atopy in women but not in men. OBJECTIVE: We investigated the prevalence of atopy among healthy obese and nonobese women and its relation to fat mass (FM), insulin resistance, and plasma concentrations of 17beta-estradiol, interleukin 4 (IL-4), and leptin. DESIGN: A cross-sectional study of 21 obese (> or = 30% body fat) and 22 nonobese (< 30% body fat) women (18-41 y of age) was performed. The following measurements were taken: FM by plethysmography, total and specific immunoglobulin E (IgE) by automated immunosorbent analysis, and blood glucose, insulin, C-peptide, 17beta-estradiol, sex hormone-binding globulin, and IL-4. Insulin sensitivity was determined on the basis of the fasting insulin resistance index and with an oral-glucose-tolerance test. RESULTS: The frequency of specific IgE in the obese group was almost 3 times that in the nonobese group (P = 0.008). The total IgE concentration was not significantly different between groups. Plasma concentrations of 17beta-estradiol, the ratio of 17beta-estradiol to sex hormone-binding globulin, the fasting insulin resistance index, and C-peptide and leptin concentrations were higher in the obese than in the nonobese group (P < 0.05) after adjustment for oral contraceptive use. All factors correlated positively with FM. Logistic regression showed FM to be the only positive predictor of specific IgE (P = 0.01). CONCLUSION: The findings confirm a direct relation between obesity and a T helper 2 cell immune response in women.

Effects of ketamine-xylazine and isoflurane on insulin sensitivity in dehydroepiandrosterone sulfate-treated minipigs (Sus scrofa domestica).

Isoflurane and ketamine-xylazine (KX) combinations are widely used veterinary anesthetics, KX being the particularly common agent for immobilizing swine. Results of previous studies indicate that KX and xylazine suppress insulin release. The steroid hormones, dehydroepiandrosterone (DHEA) and its sulfated form, dehydroepiandrosterone-sulfate (DHEAS), have variable effects on insulin sensitivity in animals. We evaluated the effect of DHEAS on plasma glucose and insulin concentrations in female Yucatan swine under KX and isoflurane anesthesia. A 2 x 2 factorial design was used. Twenty-four 17-week-old gilts were randomly assigned to receive vehicle (placebo) or DHEAS as part of an ongoing study. The KX was given intramuscularly to all animals prior to blood sample collection at weeks two and four. At week three, all animals received isoflurane by inhalation. During KX anesthesia, mean insulin concentration in DHEAS-treated and control groups approximated half the postisoflurane values (P < 0.001). While under isoflurane, the DHEAS group had significantly higher mean plasma insulin concentration and mean insulin-to-glucose ratio, compared with values for controls (P < 0.05). These findings are consistent with changes in insulin values following DHEAS treatment observed previously in nonanesthetized swine. The effect of DHEAS treatment was absent in animals under KX anesthesia. These results suggest that KX significantly decreases plasma insulin concentration and blunts DHEAS-associated insulin resistance in female minipigs.

Flavonoid antioxidants: chemistry, metabolism and structure-activity relationships.

Flavonoids are a class of secondary plant phenolics with significant antioxidant and chelating properties. In the human diet, they are most concentrated in fruits, vegetables, wines, teas and cocoa. Their cardioprotective effects stem from the ability to inhibit lipid peroxidation, chelate redox-active metals, and attenuate other processes involving reactive oxygen species. Flavonoids occur in foods primarily as glycosides and polymers that are degraded to variable extents in the digestive tract. Although metabolism of these compounds remains elusive, enteric absorption occurs sufficiently to reduce plasma indices of oxidant status. The propensity of a flavonoid to inhibit free-radical mediated events is governed by its chemical structure. Since these compounds are based on the flavan nucleus, the number, positions, and types of substitutions influence radical scavenging and chelating activity. The diversity and multiple mechanisms of flavonoid action, together with the numerous methods of initiation, detection and measurement of oxidative processes in vitro and in vivo offer plausible explanations for existing discrepancies in structure-activity relationships. Despite some inconsistent lines of evidence, several structure-activity relationships are well established in vitro. Multiple hydroxyl groups confer upon the molecule substantial antioxidant, chelating and prooxidant activity. Methoxy groups introduce unfavorable steric effects and increase lipophilicity and membrane partitioning. A double bond and carbonyl function in the heterocycle or polymerization of the nuclear structure increases activity by affording a more stable flavonoid radical through conjugation and electron delocalization. Further investigation of the metabolism of these phytochemicals is justified to extend structure-activity relationships (SAR) to preventive and therapeutic nutritional strategies.