Preliminary evaluation of the Healthy Savings Program: a novel health insurance-based wellness programme to encourage healthy food purchases.

OBJECTIVE: To examine level of participation and satisfaction with the Healthy Savings Program (HSP), a programme that provides price discounts on healthier foods. DESIGN: For Study 1, a survey was distributed to a random sample of adults who were invited to participate in a version of the HSP that provided a discount for the purchase of fresh produce and discounts on other healthier foods. In Study 2, interviews were conducted with a convenience sample of adults invited to participate in a version of the HSP that provided price discounts on specific products only (no fresh produce discount). SETTING: The HSP is provided to all employer-based insurance plan members of a large health plan. Employers can choose to enhance the version of the HSP that their employees receive by paying for a weekly discount on fresh produce. SUBJECTS: Employees in employer groups that received the enhanced HSP (Study 1) and employees in an employer group (Study 2) that received the standard HSP. RESULTS: Among survey respondents in Study 1, 69·3 % reported using the HSP card. Most were satisfied with the fresh produce discount and ease of use of the HSP card. Satisfaction was lower for selection of participating stores, amounts of discounts and selection of discounted products. In Study 2, barriers to the use of the HSP card cited included the limited number of participating stores and the limited selection of discounted products. CONCLUSIONS: Satisfaction with some elements of the HSP was high while other elements may need improvement to increase programme use.

Trends in fatty acid intake of adults in the Minneapolis-St Paul, MN Metropolitan Area, 1980-1982 through 2007-2009.

BACKGROUND: Intake of dietary fatty acids has been linked to cardiovascular disease risk. However, data available to evaluate trends in fatty acid intake in the US population are limited, particularly with regard to trans fatty acids, docosahexaenoic acid (DHA), and eicosapentaenoic acid (EPA). METHODS AND RESULTS: The present analysis examined trends in fatty acid intake from 1980-1982 through 2007-2009 and compared levels of intake to those recommended in the 2010 Dietary Guidelines for Americans and by the American Heart Association. Twenty-four-hour dietary recalls were collected from 12 526 participants enrolled in the Minnesota Heart Survey, a series of 6 independent cross-sectional surveys designed to monitor cardiovascular risk factors in noninstitutionalized adults residing in the Minneapolis-St Paul, MN metropolitan area. Mean intake estimates were generated for each survey, and a generalized linear mixed model was used to test the null hypothesis of no difference in the age-adjusted, sex-specific means across survey years. Downward trends were observed for total, saturated, and trans fat as a percent of total energy in both men and women. However, mean intakes were still above recommended levels for both trans and saturated fatty acids. Mean intakes of DHA and EPA were also below recommended levels. CONCLUSIONS: Despite promising trends, mean intakes of trans and saturated fatty acids do not meet current recommendations. Additional public health strategies are needed to promote recommended intakes of dietary fats.

Diet-induced obesity and insulin resistance spur tumor growth and cancer cachexia in rats bearing the Yoshida sarcoma.

Obesity and insulin resistance are associated with increased risk of cancer and cancer mortality. However, it is currently unknown whether they contribute to the development of cancer cachexia, a syndrome that contributes significantly to morbidity and mortality in individuals with cancer. The present experiment addresses the question of whether preexisting obesity and insulin resistance alter tumor growth and cancer cachexia symptoms in Yoshida sarcoma bearing male rats. Obesity and insulin resistance were induced through 5 weeks of high-fat (HF) diet feeding and insulin resistance was confirmed by intraperitoneal glucose tolerance testing. Chow-fed animals were used as a control group. Following the establishment of insulin resistance, HF- and chow-fed animals were implanted with fragments of the Yoshida sarcoma or received a sham surgery. Tumor growth rate was greater in HF-fed animals, resulting in larger tumors. In addition, cancer cachexia symptoms developed in HF-fed animals but not chow-fed animals during the 18-day experiment. These results support a stimulatory effect of obesity and insulin resistance on tumor growth and cancer cachexia development in Yoshida sarcoma-bearing rats. Future research should investigate the relationship between obesity, insulin resistance, and cancer cachexia in human subjects.

Chronic exendin-4 treatment prevents the development of cancer cachexia symptoms in male rats bearing the Yoshida sarcoma.

Cancer cachexia is the syndrome of weight loss, loss of appetite, and wasting of skeletal muscle and adipose tissue experienced by many individuals with cancer. Currently, few effective treatment and prevention strategies are available for these patients, due in part to a poor understanding of the mechanisms contributing to cachexia. Insulin resistance has been associated with cancer cachexia in epidemiological, human, and animal research. The present experiment was designed to examine the ability of Exendin-4, a GLP-1 agonist and insulin sensitizing agent, to prevent the development of cachexia symptoms in male Sprague Dawley rats bearing the Yoshida sarcoma. Following tumor implantation or sham surgery, rats were treated daily with saline or Exendin-4 (3 µg/kg body weight/day) and were monitored for tumor growth and cachexia symptoms for 21-23 days. As a result of large variability in treatment effects, data were analyzed separately for animals with large and small tumors. Exendin-4 treatment reduced tumor growth and prevented the development of cancer cachexia symptoms in animals with small, but not large, tumors. In addition, insulin levels were preserved in Exendin-4-treated tumor-bearing animals. The results of this experiment demonstrate a novel preventative therapy for cancer cachexia and a novel use of Exendin-4. Further research is necessary to determine the mechanisms through which Exendin-4 exerts these potent effects.

Characterization of the Yoshida sarcoma: a model of cancer cachexia.

PURPOSE: Cancer cachexia contributes significantly to morbidity and mortality in individuals with cancer. Currently, the mechanisms contributing to the development of cachexia are largely unknown, leading to a paucity of treatment and prevention options. Animal models are necessary in determining causal mechanisms and in testing potential treatments. While the Yoshida sarcoma has been utilized for more than 50 years, the cachexia syndrome produced by this model has not been well characterized in the literature. METHODS: Tumor allografts were subcutaneously implanted in male Sprague Dawley rats (n = 16) and allowed to grow for 23 days. Control animals (n = 16) received a sham surgery. All rats were monitored daily for the presence of hallmark cachexia symptoms. RESULTS: The results demonstrate the presence of decreased body weight gain, as well as lower levels of body adiposity and skeletal muscle mass, in tumor-bearing animals, as compared to controls. CONCLUSIONS: While a large tumor burden was reached, the extent of cachexia was similar to that which is observed in many individuals with cancer cachexia. Future experiments utilizing this model are encouraged to identify mechanisms and effective treatment and prevention strategies.

Sensitivity to the anorectic effects of leptin is retained in rats maintained on a ketogenic diet despite increased adiposity.

BACKGROUND: Rats maintained on a ketogenic diet (KD; 80% fat, 15% protein, 5% carbohydrate) have increased adiposity and leptin as compared to chow-fed controls (CH; 16% fat, 19% protein, 65% carbohydrate), although body weights and daily caloric intakes do not differ. METHODS: Rats maintained on a KD or CH were assessed for responsivity to intraperitoneal (i.p.) or intracerebroventricular (i.c.v.) leptin. Hypothalamic gene expression was evaluated to determine the effects of KD on proopiomelanocortin (POMC) mRNA expression and components of the leptin-signaling system. RESULTS: Caloric intake by KD rats was decreased at a lower dose of i.p. leptin (100 microg) than was required to reduce intake by CH rats (leptin, caloric intake was reduced in KD rats as compared to intake following i.p. saline; p < 0.05). In a separate experiment to evaluate responsivity to i.c.v. leptin, the minimal dose of leptin required to significantly reduce 24-hour caloric intake did not differ between the groups. In the arcuate nucleus, POMC mRNA was elevated after a lower dose of i.c.v. leptin in KD rats (5 microg) than was required to increase POMC mRNA expression in CH rats (15 microg) or reduce caloric intake in either group. Finally, evaluation of the level of phosphorylated STAT3 (pSTAT3) in the arcuate and SOCS3 mRNA in the hypothalamus revealed significantly more pSTAT3-positive cells and increased SOCS3 mRNA expression at baseline for KD rats, compared to CH, neither of which was further increased following i.p. leptin administration. CONCLUSION: These data demonstrate that despite increased adiposity, leptin and markers of leptin resistance, responsivity to the anorectic effects of exogenous leptin is retainable during maintenance on a KD.

Insulin sensitivity and glucose tolerance are altered by maintenance on a ketogenic diet.

Low-carbohydrate, ketogenic diets (KD) are frequently implemented in efforts to reduce or maintain body weight, although the metabolic effects of long-term exposure to this type of diet remain controversial. This study assessed the responsivity to peripheral and central insulin, glucose tolerance, and meal-induced effects of consuming a KD in the rat. After 8 wk of consuming chow or KD, caloric intake after peripheral or central insulin and insulin and glucose levels after a glucose challenge were assessed. In a separate group of rats, glucose and insulin responses to either a low- or high-carbohydrate test meal were measured. Finally, rats maintained on KD were switched back to a chow diet, and insulin sensitivity and glucose tolerance were evaluated to determine whether the effects of KD were reversible. Maintenance on KD resulted in decreased sensitivity to peripheral insulin and impaired glucose tolerance. Furthermore, consumption of a high-carbohydrate meal in rats that habitually consumed KD induced significantly greater insulin and glucose levels for an extended period of time, as compared with chow-fed controls. Responsivity to central insulin was heightened in KD rats and associated with increased expression levels of insulin receptor mRNA. Finally, returning to a chow diet rapidly reversed the effects of KD on insulin sensitivity and glucose tolerance. These data suggest that maintenance on KD negatively affects glucose homeostasis, an effect that is rapidly reversed upon cessation of the diet.

Effects of consuming a high carbohydrate diet after eight weeks of exposure to a ketogenic diet.

BACKGROUND: Ketogenic diets have been utilized for weight loss and improvement in metabolic parameters. The present experiments examined the effects of returning to a chow diet after prolonged ingestion of a ketogenic diet. METHODS: Rats were maintained on chow (CH) or a ketogenic diet (KD) for 8 weeks, after which the KD rats were given access to chow only (KD:CH) for 8 additional weeks. Caloric intake, body weight, and plasma leptin, insulin and ghrelin were measured before and after the dietary switch. RESULTS: After 8 weeks of consuming a ketogenic diet, KD rats had increased adiposity and plasma leptin levels, and reduced insulin, as compared to CH controls. One week after the diet switch, fat pad weight and leptin levels remained elevated, and were normalized to CH controls within 8 weeks of the dietary switch. Switching from KD to chow induced a transient hypophagia, such that KD:CH rats consumed significantly fewer calories during the first week after the dietary switch, as compared to calories consumed by CH rats. This hypophagia was despite significantly increased plasma ghrelin in KD:CH rats. Finally, KD:CH rats developed hyperphagia over time, and during weeks 6-8 after the diet switch consumed significantly more calories per day than did CH-fed controls and gained more weight than CH-fed controls. CONCLUSION: Collectively, these data demonstrate that returning to a carbohydrate-based diet after a period of consuming a ketogenic diet has post-diet effects on caloric intake, body weight gain, and insulin levels.

Binge-type eating attenuates corticosterone and hypophagic responses to restraint stress.

Binge eating has been associated with stress responses. Data in rats suggest that activation of the hypothalamic-pituitary-adrenal (HPA) axis is suppressed by consumption of a high sucrose diet, and is increased with exposure to a high fat diet. Additionally, the choice to consume a highly palatable food following exposure to a stressor results in reduced corticosterone levels. To test the effects of intermittent access to a high sugar/high fat food on stress hormone levels, rats were given either unrestricted (UR) access to a sucrose-vegetable shortening mixture (SVS) or 2 hour SVS access 7 days (7D) or 3 days (3D) per week for 4 weeks. Rats on the UR and 3D schedules consumed significantly more calories per day than did controls with no access to SVS, and the 7D and 3D rats consumed as many SVS calories in the 2 hour access period as did the UR rats with 24 hour access to SVS. After 4 weeks of access to SVS (UR, 7D, and 3D), rats were briefly restrained. Control and UR rats had elevated corticosterone during and following restraint, whereas there were no differences in corticosterone levels of 7D and 3D rats in response to restraint, as compared to baseline. Post-restraint consumption of chow was significantly decreased in all groups, and consumption of SVS was reduced in the UR, but not the 7D and 3D rats. These data demonstrate that intermittent access to SVS dampens the corticosterone response to restraint stress and that stressful events do not induce bingeing in non-bingeing animals with access to a high sucrose/high fat food.