Nutrition Research Center Research Articles

Introduction to the 8th Starch Digestion Consortium Workshop

Congenital sucrase-isomaltase deficiency (CSID) is a rare autosomal intestinal disease caused by mutations of the sucrase-isomaltase gene. Patients with CSID have different phenotypes and enzymatic activities associated with sucrase-isomaltase ranging from mild reduction of sucrase activity to complete absence. Low sucrase activity leads to maldigestion of sucrose, resulting in dyspepsia-like symptoms such as chronic diarrhea, abdominal pain, and bloating. The severity of the symptom is related to the amount of sucrase activity and quantity of sucrose ingested. Reduced maltase activity is expected to occur in patients with CSID because both subunits of the SI complex contribute to the total mucosal maltose activity. Indeed, low maltase activity can also lead to maldigestion of starches contributing to the symptoms of dyspepsia. When children are assessed for this gene mutation, duodenal mucosal histology is invariably normal. Because there are no noninvasive methods for specific confirmation of sucrase-isomaltase deficiency, a novel noninvasive 13C-sucrose labeled substrate has been developed and validated as a sucrase activity breath test for screening and confirmation of CSID. It has been shown that primary sucrase deficiency can be confirmed using this new 13C breath test, as well as the effectiveness of sucrase replacement therapy. On December 21 and 22, 2011, the 8th Workshop of the Starch Digestion Consortium (SDC) was held at the Children's Nutrition Research Center at the Baylor College of Medicine and Texas Children's Hospital. The theme of the workshop was “50 Years of Progress Since Congenital Sucrase-Isomaltase Deficiency (CSID) Recognition.” This was a multidisciplinary workshop that blended clinical medicine with nutritional and food science. The purpose of this workshop was to review progress toward clinical diagnosis and management of sucrase-isomaltase enzyme deficiency during the past 50 years. The nutritional and food technological objectives of the conference were 2-fold: first, to define the role of sucrase-isomaltase enzyme complex in human starch digestion to glucose (α-glucogenesis), and second, by studying sucrase-isomaltase–deficient patients with CSID, envision approaches to botanical and technological alterations in food that will benefit all populations. More than 50 authors and attendees participated in this workshop from 12 different countries. Eighteen original communications were presented. Special thanks go to QOL Medical, the supplier of Sucraid oral enzyme supplement, for sponsoring this event. This supplement to the Journal of Pediatric Gastroenterology and Nutrition reports the proceedings of this workshop. E. Roseland Klein served as the technical editor of the workshop publication. Beth Mays was responsible for all travel arrangements and the workshop organization. Adam Gillum was responsible for graphic and audio arrangements. The group of participants standing among the lobby statuary at the SDC/CSID workshop held at the Children's Nutrition Research Center, December 21–22, 2011 is shown in Figure 1. Statues are identified by italics; Borden is by Joseph Paderewski (1914–2000) and the others are copies of the work of Elizabet Ney (1833–1907).FIGURE 1: From left to right: back row, William Bryant, Justus Leibig, Mohammad Chegeni, Peter Zimmer, David Rose, Mark Gilger, Antone Opekun, Gale Borden, Christina Lecea; third row, Bruno Chumpitazi, Ronald Scott, William Treem, Sursum, Derick Cooper, Zihua Ao, Byung-Hoo Lee; second row, Amy Lin, Beth Mays, William Dupere, Susan Baker, Buford Nichols, Teresa Davis, Bruce Hamaker, Roberto Quezada-Calvillo, Steve Avery; front row, Kyra Jones, Marcia Chaudet, Hassan Naim, Mary Money-Waldman, Veda Nichols, Fatimata Cisse, Meric Simsek, Like Yan, Ann McMeans, Mary Slawson.

Vitamin D deficiency: A potential risk factor for Clostridium difficile infection

Vitamin D deficiency: A potential risk factor for Clostridium difficile infection Dima Youssef,1 William B Grant,2 Alan N Peiris3,41Department of Internal Medicine, Division of Infectious Diseases, 2Sunlight, Nutrition and Health Research Center, San Francisco, CA USA; 3Department of Medicine, Mountain Home VAMC, 4Department of Medicine, East Tennessee State University, Johnson City, Tennessee, USA In the July 3, 2012 issue of the journal of Risk Management and Healthcare Policy, Martinez et al present a nice review on Clostridium difficile (C. difficile) infections.1 The different manifestations of this challenging disease along with the high cost and burden on the health care system were discussed. While the authors did an admirable job in discussing traditional risk factors, they do not mention vitamin D deficiency.View original paper by Martinez and colleagues.

A closer look at diabetes remission after gastric bypass surgery: a case study

A closer look at diabetes remission after gastric bypass surgery: a case study Katrina Brakoniecki, B.A., Christine Ren-Fielding, M.D., Blandine Laferrere, M.D.* New York Obesity Nutrition Research Center, Department of Medicine, St. Luke’s-Roosevelt Hospital Center, New York, New York New York University Bariatric Associates, New York University Langone Medical Center, New York, New York Columbia University College of Physicians and Surgeons, New York, New York Received May 1, 2012; accepted July 15, 2012

Journal of Diabetes NEWS

<i>Journal of Diabetes</i> NEWS

Editorial introductions

Editorial introductions

EGCG protects against 6‐OHDA induced neurotoxicity in a cell culture model

Disruption of iron metabolism may involve in the progression of Parkinson's disease. Our objective was to test whether the protective effect of (−)‐epigallocatechin‐3‐gallate (EGCG) against 6‐hydroxydopamine (6‐OHDA) induced neurotoxicity was by regulating iron homeostasis in N27 cells. EGCG pretreatment significantly protected against 6‐OHDA‐induced neurotoxicity (MTT, SYTOX Green and Caspase‐3 activity assays). EGCG with 6OHDA treatment significantly increased (p&lt;0.0001) TH+ cell count (3.1‐fold) and neurite length (12.5‐fold) compared with 6‐OHDA alone in primary mesencephalic neurons. 6‐OHDA treatment significantly (p&lt;0.05) increased divalent metal transporter‐1 (DMT1), hepcidin, transferrin receptor‐2 (TfR2), H‐ferritin and decreased ferroportin‐1 (Fpn1), TfR1 mRNA expressions. The protein expressions of DMT1, hepcidin and Fpn1 matched with the gene expression data. However, EGCG significantly reversed the effect of 6‐OHDA on above genes and proteins expression. The increased ~2‐fold (p&lt;0.001) 55Fe cell uptake with 6‐OHDA and normalization with EGCG pretreatment confirmed iron burden associated with neurotoxicity and protection by EGCG. In conclusion, EGCG protected against 6‐OHDA induced neurotoxicity by regulating genes and proteins involved in brain iron homeostasis. However, further studies are warranted to determine the mechanism of that regulation.Grant Funding Source : Nutrition Wellness and Research Center

A Worksite‐based Weight Loss Intervention for Obesity Prevention

Worksites are increasingly being used as locations for implementing healthy diet and weight loss interventions. Hence, there is an urgent need to identify programs that are both successful and sustainable. We conducted a 6‐month pilot randomized controlled trial in overweight and obese employees at 4 worksites (2 intervention; 2 delayed intervention sites) to examine the effects of a worksite‐based intervention on weight loss and changes in cardiovascular risk factors. The intervention combined recommendations to consume a high fiber, low glycemic load diet with education on nutrition and behavior change. Fasting body weight, cholesterol, glucose, and blood pressure were measured at baseline and 6 months in 118 subjects. Results were analyzed using an ANCOVA model with baseline values as covariates. Participants at the intervention sites (n=82) lost significantly more weight (−8.0±6.7 vs. +0.6±2.8 kg, p&lt;0.0001) and had greater decreases in fasting total cholesterol (−13.2±25.0 vs. −2.4±24.2 mg/dl, p=0.0423), fasting glucose (−6.4±13.2 vs. +5.7±18.0 mg/dl, p=0.0006), systolic blood pressure (−8.6±12.6 vs. +5.5±10.8 mmHg, p&lt;0.0001), and diastolic blood pressure (− 8.2±10.9 vs. −0.5±6.7 mmHg, p=0.0007) as compared to participants at control sites (n=33). This worksite intervention resulted in significant weight loss and improvements in cardiovascular risk factors relative to no intervention.Grant Funding Source: USDA Human Nutrition Research Center

Differences in vitamin D status likely explain racial disparities in breast cancer mortality rates in the southeast

The recent article in Cancer by Adams and colleagues1 found that after diagnosis of breast cancer, African American women had significantly higher breast cancer–specific and all-cause mortality rates than did European American women, and this effect persisted after consideration of commonly accepted risk factors. One factor not considered was vitamin D status. Solar ultraviolet B (UVB) irradiance is the most important source of vitamin D for most North Americans. Solar UVB dose has been found to be inversely correlated with breast cancer mortality rates in ecological studies for both African American and European American women.2 Vitamin D has also been found to be associated with survival rates after diagnosis of breast cancer. In a study in Canada with an 11.6-year follow-up period after breast cancer diagnosis, women with deficient vitamin D levels had an increased risk of distant recurrence and death compared with those who had sufficient levels.3 In detail, women with serum 25-hydroxyvitamin D (25(OH)D) levels <20 ng/mL, compared with those who had levels >30 ng/mL, had a multivariate adjusted hazard ratio of 1.71 (95% confidence interval, 1.02-2.86) for distant recurrence, and of 1.60 (95% confidence interval, 0.96-2.64) for death.3 There is also evidence from observational studies that serum 25(OH)D level affects breast cancer incidence rates.4 The relative risk versus 25(OH)D level outlined in that study4 might be used to estimate the breast cancer disparity in the United States. It was found that in the 2001 to 2004 period, mean serum 25(OH)D levels was 15 ng/mL in African American women and 26 ng/mL in European American women.5 These levels indicate a 46% higher breast cancer incidence rate for African Americans based on the relationship in the results of Grant.4 Because it is likely that vitamin D competes with more risk-modifying factors in cancer incidence than in cancer mortality rates (vitamin D reduces tumor angiogenesis and metastasis), the disparity for mortality rates might be higher. Therefore, future studies on racial disparities in breast cancer mortality should include serum 25(OH)D levels at the time of diagnosis, as well as, if necessary, vitamin D supplementation to reach and maintain serum 25(OH)D levels between 30 and 40 ng/mL. Dr Grant receives funding from the UV Foundation (McLean, Virginia), Bio-Tech Pharmacal (Fayetteville, Arkansas), the Vitamin D Council (San Luis Obispo, California), and the Vitamin D Society (Canada). The other authors make no disclosures. William B. Grant PhD*, Luca Mascitelli MD , Mark R. Goldstein MD , * Sunlight, Nutrition, and Health Research Center (SUNARC), San Francisco, California, Comando Brigata Alpina “Julia”, Medical Service, Udine, Italy, 1845 Veterans Park Drive, Suite 110, Naples, Florida.

Sarcopenia: biomarkers and imaging (International Conference on Sarcopenia research).

1. Gerontopole Toulouse, Department of Geriatric Medicine, Toulouse University Hospital, Toulouse France, INSERM 1027; 2. Vice President, Clinical Research & Operations, Neuroscience & Neuromuscular Disorders, Cytokinetics, Inc. 280 East Grand Avenue, South San Francisco, CA 94080, USA; 3. Neurotune AG, Wagistr. 27A, 8952 Schlieren, Switzerland; 4. Senior Scientist and Director, Nutrition, Exercise Physiology, and Sarcopenia Laboratory, Jean Mayer USDA Human Nutrition Research Center on Aging, Tufts University, Boston, MA 02111 USA; 5. Department of Medicine, University of Pittsburgh, USA; 6. Human Medicine Special Areas, Scientific Advice Section, European Medicines Agency (EMA), 7 Westferry Circus, Canary Wharf, London E14 4HB UK; 7. Novartis Institutes for Biomedical Research, Fabrikstrasse 10-2.40.4, CH-4056 Basel, Switzerland; 8. Division of Geriatric Medicine, Saint Louis University School of Medicine and GRECC, VA Medical Center, St. Louis, Missouri USA; 9. Department of Aging and Geriatric Research and Institute on Aging, University of Florida, 1329 SW 16th Street, Room 5161, Gainesville, FL 32608, PO Box 100107, zip 32610-0107, USA; 10.Translational Medicine, Cambridge, MA, USA; 11. Associate Professor of Neurology, Harvard Medical School, Boston, Massachusetts, USA

Should Protein Be Included in CHO-Based Sports Supplements?

Should Protein Be Included in CHO-Based Sports Supplements?

An unusual complication of a takotsubo cardiomyopathy: A not so benign disease?

non-diabetic obese women. Low education and old age rather than anti-diabetic medications were more likely to be barriers for weight loss in this study population. We would like to thank our patients for their help in collecting these data. This work was financially supported by Nutrition Research Center, Ahvaz Jundishapur University of Medical Sciences. The authors of this manuscript have certified that they comply with the Principles of Ethical Publishing in the International Journal of Cardiology [9]. References

Whole body counter calibration using Monte Carlo modeling with an array of phantom sizes based on national anthropometric reference data

During construction of the whole body counter (WBC) at the Children's Nutrition Research Center (CNRC), efficiency calibration was needed to translate acquired counts of 40K to actual grams of potassium for measurement of total body potassium (TBK) in a diverse subject population. The MCNP Monte Carlo n-particle simulation program was used to describe the WBC (54 detectors plus shielding), test individual detector counting response, and create a series of virtual anthropomorphic phantoms based on national reference anthropometric data. Each phantom included an outer layer of adipose tissue and an inner core of lean tissue. Phantoms were designed for both genders representing ages 3.5 to 18.5 years with body sizes from the 5th to the 95th percentile based on body weight. In addition, a spherical surface source surrounding the WBC was modeled in order to measure the effects of subject mass on room background interference. Individual detector measurements showed good agreement with the MCNP model. The background source model came close to agreement with empirical measurements, but showed a trend deviating from unity with increasing subject size. Results from the MCNP simulation of the CNRC WBC agreed well with empirical measurements using BOMAB phantoms. Individual detector efficiency corrections were used to improve the accuracy of the model. Nonlinear multiple regression efficiency calibration equations were derived for each gender. Room background correction is critical in improving the accuracy of the WBC calibration.

Low dose dietary resveratrol interacts with adiponectin to attenuate obesity‐associated colorectal tumorigenesis

Obesity is associated with a decrease in the anti-inflammatory hormone, adiponectin (Adn), and a subsequent increase in pro-inflammatory cytokine release into the circulation. These changes contribute to initiation and propagation of colon tumorigenesis. Resveratrol has been effective at attenuation of colon cancer and has been shown to increase Adn production in adipocytes. Thus, we hypothesized that resveratrol interacts with Adn in obesity to inhibit colorectal tumorigenesis. To investigate this we induced tumorigenesis in Adn knockout (KO) and wild type (Wt) C57BL/6 mice through azoxymethane injection (10 mg/kg body weight) followed by 1% dextran sodium sulfate in drinking water for 5 days. Concurrently, mice were fed one of two ad libitum obesigenic diets for 14 weeks: high fat lard (HFL) and HFL with 20mg/kg diet resveratrol (HFL+R). Wt mice gained more weight, had higher percent fat mass, and lower lean mass than KO, and HFL+R diet tended to attenuate this response in male Wt mice. There was a strong tendency for an interaction between genotype and diet whereby HFL+R diet increased lesion development in KO male mice, and HFL diet decreased lesion formation in WT male mice. HFL+R also tended to decrease serum insulin and interleukin 6 in Wt mice. Thus, HFL+R diet improved overall heath of obese Wt male but not KO male mice. Supported by grant 2008-34115-19372 to the Nutrition and Wellness Research Center from USDA. Grant Funding Source: Supported by grant 2008-34115-19372 to the Nutrition and Wellness Research Center from USDA

A potential control point of glucose delivery from starchy foods: intestinal mucosal α‐glucosidase digestion

To control the glucose delivery from starchy foods, much attention has been given to α‐amylase (AMY), as opposed to the contribution from mucosal α‐glucosidases. The aim of this research was to investigate the digestion capability of mucosal α‐glucosidases on various starch structures to explore their possible expanded roles in digestion. Substrates were incubated with recombinant N‐ (Nt) and C‐terminals (Ct) of maltase‐glucoamylase (MGAM) and sucrase‐isomaltase (SI) for different digestion periods, and the glucogenesis and residue structures were examined. At raw starch granule level, mucosal α‐glucosidases showed the capability to produce glucose from uncooked starch granules at a low digestion completion. At the cooked starch level, CtMGAM showed high digestion completion near 80% without AMY participation; other three subunits reached 20–30% digestion. At the α‐limit dextrin (LDx) level, the four subunits showed different roles where NtMGAM only digested short linear oligomers but the other three subunits individually digested large branched molecules with different completion percentage. Collectively, these findings suggest mucosal α‐glucosidases, particularly CtMGAM, may be potential control points for glucose delivery in the human body. This work was supported by internal funding from the Whistler Center and Children's Nutrition Research Center of the ARS/USDA.

RESPONSE

Dear Editor-in-Chief: We thank Dr. Kwon for his letter regarding our paper (1) and welcome the opportunity to respond. Dr. Kwon's major concern is whether our Asian sample was representative of the US population. He states that "…Asians represent 45% of the study participants…" and "…the mean height and BMI of Asians were 0.5 cm and 0.6 kg·m−2higher for men, and 0.2 cm lower and 1.9 kg·m−2higher for women…." These statements are inaccurate. Asians represented 13% (181/1394) of the TIGER sample but were excluded from the analyses used to develop the prediction equations (p. 1960). We reported no descriptive statistics for Asians and do not know the source of the data to which Dr. Kwon refers. He further states that "their study data indicate that given BMI level, Asians had a lower BF% than non-Hispanic whites," which is also inaccurate. Our BMI regression models included both skinfold thicknesses (∑3S) and BMI (Table 3). Thus, the correct interpretation is that, for a given BMI and ∑3S, Asian men had equivalent BF% and Asian women had a slightly higher BF% than non-Hispanic whites-opposite of Dr. Kwon's statement. With respect to representativeness, we used a large sample with subjects from the three major ethnic groups in the United States. These subjects' stature and overweight/obesity prevalence were within sampling error of US population values (p. 1964). Skinfold thicknesses, BMI, and DXA percent body fat were widely distributed (Table 1). Dr. Kwon's second concern is "whether race/ethnicity-specific equations are necessary." He presents several points, which were all addressed in our article. The differences in accuracy between equations were not "minimal." Using the non-Hispanic whites' BMI model for Hispanic women would result in a nearly 2% underestimation of DXA percent body fat (Tables 2 and 3), a substantial bias. The men's non-Hispanic white and Hispanic equations did not differ appreciably-which is why we presented a single equation for both groups (Table 3). We demonstrated that "the equations for Hispanic women can be accurately applied to Asian women" on page 1963 and in Table 4. The inclusion of race/ethnicity did "provide a better fit than the reduced model," seen in the P values of the ethnicity regression coefficients (Table 2), which are exactly equivalent to comparing models including and excluding these coefficients. The ethnicity-specific equations did "increase the accuracy of estimated BF%" if one considers total error (bias + random error). We described these bias components (p. 1962-3): "race/ethnic group bias is well documented forseveral BMI prediction models…" with nine references. Dr. Kwon's questions whether the "estimates of ∑3S, ∑3S2, and BMI may differ by race/ethnicity." No: the interactions of each measure with ethnicity failed to attain statistical significance. Most body composition regression equations have been developed in non-Hispanic white subjects. Our large sample was ethnically diverse. Our concurrent validity study has standard errors among the lowest reported in the literature and reports ethnicity-specific error estimates. As we stated (p. 1963), these equations should be cross-validated with other populations, including Asians, Asian-Indians, and subjects older than 35 years. Daniel P. O'Connor, PhD Andrew S. Jackson, PED Brian K. McFarlin, PhD Department of Health and Human Performance University of Houston Houston, TX Molly S. Bray, PhD Mary H. Sailors, PhD Department of Epidemiology University of Alabama-Birmingham Birmingham, AL Kenneth J. Ellis, PhD USDA/ARS Children's Nutrition Research Center Baylor College of Medicine

Evidence-Based Nutrition-Managing Expectations

Alice H. Lichtenstein, DSc, Cardiovascular Nutrition Laboratory, Jean Mayer USDA Human Nutrition Research Center at Tufts University, Boston, Massachusetts. Joseph Lau, MD, Tufts Evidence-Based Practice Center, Institute for Clinical Research and Health Policy Studies, Tufts Medical Center, Boston, Massachusetts. Correspondence: Alice H. Lichtenstein, DSc, Tufts University, 711 Washington St, Boston, MA 02111 ([email protected]).

The roles of ultraviolet-B irradiance, vitamin D, apolipoprotein E ε4, and diet in the risk of prostate cancer

There have been a number of papers investigating the riskmodifying factors for prostate cancer, with diet, ultraviolet-B (UVB), and genetics among the leading factors considered, but there is still no agreement on the relative contribution of these factors. For example, the paper by Barnett et al. [1] found no link in their recent study between prediagnostic serum 25-hydroxyvitamin D [25(OH)D] and prostate cancer incidence in older men during a mean 5.3-year followup period [1]. This finding agrees with those of other recent reviews [2–4]. However, studies looking at prostate cancer incidence with respect to personal UVB irradiance ([5] and Refs. 31–33 in [1]) offer some of the more convincing evidence for a role of UVB and vitamin D in reducing the risk of prostate cancer. These studies were based on earlylife and/or long-term UVB irradiance, and prostate cancer is a type of cancer that progresses very slowly. There is also good evidence that vitamin D improves survival for those diagnosed with prostate cancer (Refs. 34 and 35 in [1]). Thus, vitamin D appears to be important in reducing the risk of prostate cancer over many years, so measuring 25(OH)D levels shortly before diagnosis of prostate cancer may not provide an accurate indication of the overall effect of vitamin D on prostate cancer risk. Although ecological studies have reported inverse correlations between solar UVB and prostate cancer incidence and/or mortality rates (Refs. 2, 28–30 in [1]), UVB may not be the only factor affecting the geographic variations. An inspection of the prostate cancer mortality rate maps in the Atlas of Cancer Mortality Rates in the United States, 1950– 1994 [6] indicates that the mortality rates are dissimilar from those of well-known vitamin D–sensitive cancers such as breast and colorectal cancer [4]. The highest rates for prostate cancer are in the northwest and the lowest are in the southeast, whereas the highest rates for breast and colorectal cancer are in the northeast and the lowest are in the southwest. Analysis of the map of greatest ancestry by county in the United States [7] found high correlations for many of the high-resolution features in prostate cancer and ancestry maps. This finding suggested that ethnic background played an important role in prostate cancer risk, which could be due to a combination of dietary and genetic factors. This finding formed the basis for a multicountry ecological study in which the apolipoprotein E e4 (ApoE4) allele and per capita gross domestic product correlated directly with prostate cancer incidence and mortality rates, and fraction of energy derived from cereals/grains correlated inversely [8]. Although this result is currently a hypothesis, it also explains several findings of prostate cancer epidemiology. It explains why black Americans, with nearly twice the ApoE4 allele prevalence of white Americans, have about twice the rate of prostate cancer [6]. It supports the finding that cholesterol is often a risk factor for prostate cancer but not for any other cancer [9]. It explains why those who develop type 2 diabetes mellitus have a reduced risk for prostate cancer [10]: the ApoE2 allele is an important risk factor for type 2 diabetes mellitus [11], and those who have ApoE2 have a reduced prevalence of ApoE4 [12]. Trying to evaluate the ApoE4 hypothesis, perhaps by looking at frequencies of various ApoE alleles of those diagnosed with prostate cancer, seems worthwhile. The literature contains one paper [13] that supports this W. B. Grant (&) Sunlight, Nutrition, and Health Research Center (SUNARC), P.O. Box 641603, San Francisco, CA 94164-1603, USA e-mail: wbgrant@infionline.net URL: www.sunarc.org

The use of a commercial vegetable juice as a practical means to increase vegetable intake: a randomized controlled trial

BackgroundRecommendations for daily dietary vegetable intake were increased in the 2005 USDA Dietary Guidelines as consumption of a diet rich in vegetables has been associated with lower risk of certain chronic health disorders including cardiovascular disease. However, vegetable consumption in the United States has declined over the past decade; consequently, the gap between dietary recommendations and vegetable intake is widening. The primary aim of this study is to determine if drinking vegetable juice is a practical way to help meet daily dietary recommendations for vegetable intake consistent with the 2005 Dietary Guidelines and the Dietary Approaches to Stop Hypertension (DASH) diet. The secondary aim is to assess the effect of a vegetable juice on measures of cardiovascular health.MethodsWe conducted a 12-week, randomized, controlled, parallel-arm study consisting of 3 groups of free-living, healthy volunteers who participated in study visits at the Ragle Human Nutrition Research Center at the University of California, Davis. All subjects received education on the DASH diet and 0, 8 or 16 fluid ounces of vegetable juice daily. Assessments were completed of daily vegetable servings before and after incorporation of vegetable juice and cardiovascular health parameters including blood pressure.ResultsWithout the juice, vegetable intake in all groups was lower than the 2005 Dietary Guidelines and DASH diet recommendations. The consumption of the vegetable juice helped participants reach recommended intake. In general, parameters associated with cardiovascular health did not change over time. However, in the vegetable juice intervention groups, subjects who were pre-hypertensive at the start of the study showed a significant decrease in blood pressure during the 12-week intervention period.ConclusionIncluding 1-2 cups of vegetable juice daily was an effective and acceptable way for healthy adults to close the dietary vegetable gap. Increase in daily vegetable intake was associated with a reduction in blood pressure in subjects who were pre-hypertensive at the start of the trial.Trial RegistrationClinicaltrials.gov NCT01161706

Power spectrum analyses of nuclear decay rates

We provide the results from a spectral analysis of nuclear decay data displaying annually varying periodic fluctuations. The analyzed data were obtained from three distinct data sets: 32Si and 36Cl decays reported by an experiment performed at the Brookhaven National Laboratory (BNL), 56Mn decay reported by the Children’s Nutrition Research Center (CNRC), but also performed at BNL, and 226Ra decay reported by an experiment performed at the Physikalisch–Technische Bundesanstalt (PTB) in Germany. All three data sets exhibit the same primary frequency mode consisting of an annual period. Additional spectral comparisons of the data to local ambient temperature, atmospheric pressure, relative humidity, Earth–Sun distance, and their reciprocals were performed. No common phases were found between the factors investigated and those exhibited by the nuclear decay data. This suggests that either a combination of factors was responsible, or that, if it was a single factor, its effects on the decay rate experiments are not a direct synchronous modulation. We conclude that the annual periodicity in these data sets is a real effect, but that further study involving additional carefully controlled experiments will be needed to establish its origin.

Effects Of Adding A Technology-based System To An In-Person Behavioral Weight Loss Program

With the intention of improving weight outcomes, more behavioral weight loss interventions have added the use of technology. The commercially available GoWear Fit® System (BodyMedia Inc.) includes a multi-sensor armband and display to measure and provide real-time feedback on energy expenditure, and a website to monitor energy intake and daily energy balance. PURPOSE: To examine the influence of adding the GoWear Fit® System to an in-person behavioral program on weight loss in overweight and obese adults. METHODS: Thirty-four overweight and obese (BMI: 33.8 ± 3.6 kg·m-2) adults (age: 43.6 ± 9.2 kg·m-2) participated in a behavioral weight loss intervention and were randomized to one of two groups: standard behavioral weight loss (SBWL) or standard behavioral weight loss plus technology (SBWL+GoWearFit). Energy intake was reduced to 1200-1800 kcal/day based on baseline weight. Exercise was progressed from 100 to 150 min/week. Body weight was measured at 0 and 6 weeks. RESULTS: At 6 weeks, percent weight loss was -2.9±2.2% in SBWL+GoWearFit and -1.5±2.0% in SBWL (p =.07). In SBWL+GoWearFit, the multisensory armband was worn for 16.9±4.7 hours per day. SBWL+GoWearFit logged meals online significantly more days per week (6.5±1.3 days/week) than SBWL tracked meals in paper diaries (5.1±2.8 days/ week) (p <.001). SBWL+GoWearFit also reported more days per week of moderate intensity physical activity of at least 10 minutes per bout (5.1±2.1 days/week) than SBWL (3.2±2.3 days/week) (p <.001). CONCLUSION: The trend for percent weight loss to improve over the initial 6 weeks of a behavioral weight loss program with the addition of the GoWear Fit® System is a promising finding. Moreover, it appears that individuals are willing to wear the multi-sensor armband and use the website provided with the GoWear Fit® System, and this appears to have promising effects on exercise participation and self-monitoring of eating behaviors when compared to the SBWL group during this 6 week period. Long-term evaluation of the GoWear Fit® System is necessary to determine feasibility and effectiveness of this system to improve weight loss in overweight and obese adults. Supported by the University of Pittsburgh Obesity and Nutrition Research Center (NIH P30 DK46204)