A 12-week lutein supplementation improves visual function in Chinese people with long-term computer display light exposure

March 25th, 2009

by Le Ma, Xiao-Ming Lin, et al.

We aimed to examine the effect of different doses of lutein supplementation on visual function in subjects with long-term computer display light exposure.

Thirty-seven healthy subjects with long-term computer display light exposure ranging in age from 22 to 30 years were randomly assigned to one of three groups: Group L6 (6 mg lutein/day, n 12); Group L12 (12 mg lutein/day, n 13); and Group Placebo (maltodextrin placebo, n 12).

Levels of serum lutein and visual performance indices such as visual acuity, contrast sensitivity and glare sensitivity were measured at weeks 0 and 12. [Contrast sensitivity is ability to distinguish an object from its background. Glare sensitivity is ability to see objects in the presence of bright light.]

After 12-week lutein supplementation, serum lutein concentrations of Groups L6 and L12 increased from 0-356 (SD 0-117) to 0-607 (SD 0-176) mol/l, and from 0-328 (SD 0-120) to 0-733 (SD 0-354) mol/l, respectively. No statistical changes from baseline were observed in uncorrected visual acuity and best-spectacle corrected visual acuity, whereas:

• There was a trend toward increase in visual acuity in Group L12.

• Contrast sensitivity in Groups L6 and L12 increased with supplementation, and statistical significance was reached at most visual angles of Group L12.

• No significant change was observed in glare sensitivity over time.

Visual function in healthy subjects who received the lutein supplement improved, especially in contrast sensitivity, suggesting that a higher intake of lutein may have beneficial effects on the visual performance.

British Journal of Nutrition, Feb 19, 2009.

Astaxanthin: a novel potential treatment for oxidative stress and inflammation in cardiovascular disease.

March 25th, 2009

John A. Burns School of Medicine, University of Hawaii, Honolulu, Hawaii, USA. fpashkow@cardaxpharma.com

Oxidative stress and inflammation are implicated in several different manifestations of cardiovascular disease (CVD). They are generated, in part, from the overproduction of reactive oxygen species (ROS) and reactive nitrogen species (RNS) that activate transcriptional messengers, such as nuclear factor-kappaB, tangibly contributing to endothelial dysfunction, the initiation and progression of atherosclerosis, irreversible damage after ischemic reperfusion, and even arrhythmia, such as atrial fibrillation. Despite this connection between oxidative stress and CVD, there are currently no recognized therapeutic interventions to address this important unmet need. Antioxidants that provide a broad, “upstream” approach via ROS/RNS quenching or free radical chain breaking seem an appropriate therapeutic option based on epidemiologic, dietary, and in vivo animal model data. However, human clinical trials with several different well-known agents, such as vitamin E and beta-carotene, have been disappointing. Does this mean antioxidants as a class are ineffective, or rather that the “right” compound(s) have yet to be found, their mechanisms of action understood, and their appropriate targeting and dosages determined? A large class of potent naturally-occurring antioxidants exploited by nature-the oxygenated carotenoids (xanthophylls)-have demonstrated utility in their natural form but have eluded development as successful targeted therapeutic agents up to the present time.

This article characterizes the mechanism by which this novel group of antioxidants function and reviews their preclinical development. Results from multiple species support the antioxidant/anti-inflammatory properties of the prototype compound, astaxanthin, establishing it as an appropriate candidate for development as a therapeutic agent for cardiovascular oxidative stress and inflammation.

Am J Cardiol. 2008 May 22;101(10A):58D-68D.Click here to read

Relationship between intake of green tea and periodontal disease.

March 14th, 2009

Background: Green tea is a very popular beverage, and in vitro studies have shown that green tea polyphenols inhibit the growth and cellular adherence of periodontal pathogens and their production of virulence factors. We investigated the epidemiologic relationship between the intake of green tea and periodontal disease.

Methods: We analyzed 940 Japanese men aged 49 to 59 years as part of a comprehensive health examination. Probing depth (PD), clinical attachment loss (AL), and bleeding on probing (BOP) were used as the periodontal parameters. We examined the relationship between the intake of green tea and periodontal parameters. The intake of green tea was defined as the number of cups per day in a self-administered questionnaire.

Results: The intake of green tea was inversely correlated with the mean PD, mean clinical AL, and BOP. In multivariate linear regression models, every one cup/day increment in green tea intake was associated with a 0.023-mm decrease in the mean PD (P <0.05), a 0.028-mm decrease in the mean clinical AL (P <0.05), and a 0.63% decrease in BOP (P <0.05), after adjusting for other confounding variables.

Conclusion: There was a modest inverse association between the intake of green tea and periodontal disease.

J Periodontol. 2009 Mar;80(3):372-7.

Vitamin C intake and the risk of gout in men: a prospective study.

March 14th, 2009

Choi HK, Gao X, Curhan G.

Division of Rheumatology, Department of Medicine, Arthritis Research Centre of Canada, Vancouver General Hospital, University of British Columbia, Vancouver, Canada. hchoius@bu.edu

BACKGROUND: Several metabolic studies and a recent double-blind, placebo-controlled, randomized trial have shown that higher vitamin C intake significantly reduces serum uric acid levels. Yet the relation with risk of gout is unknown.

METHODS: We prospectively examined, from 1986 through 2006, the relation between vitamin C intake and risk of incident gout in 46 994 male participants with no history of gout at baseline. We used a supplementary questionnaire to ascertain the American College of Rheumatology criteria for gout. Vitamin C intake was assessed every 4 years through validated questionnaires.

RESULTS: During the 20 years of follow-up, we documented 1317 confirmed incident cases of gout. Compared with men with vitamin C intake less than 250 mg/d, the multivariate relative risk (RR) of gout was 0.83 (95% confidence interval [CI], 0.71-0.97) for total vitamin C intake of 500 to 999 mg/d, 0.66 (0.52-0.86) for 1000 to 1499 mg/d, and 0.55 (0.38-0.80) for 1500 mg/d or greater (P < .001 for trend). The multivariate RR per 500-mg increase in total daily vitamin C intake was 0.83 (95% CI, 0.77-0.90). Compared with men who did not use supplemental vitamin C, the multivariate RR of gout was 0.66 (95% CI, 0.49-0.88) for supplemental vitamin C intake of 1000 to 1499 mg/d and 0.55 (0.36-0.86) for 1500 mg/d or greater (P < .001 for trend).

CONCLUSIONS: Higher vitamin C intake is independently associated with a lower risk of gout. Supplemental vitamin C intake may be beneficial in the prevention of gout.

Arch Intern Med. 2009 Mar 9;169(5):502-7.Click here to read

Folic Acid and Risk of Prostate Cancer: Results From a Randomized Clinical Trial.

March 14th, 2009

Figueiredo JC, Grau MV, Haile RW, Sandler RS, Summers RW, Bresalier RS, Burke CA, McKeown-Eyssen GE, Baron JA.

Affiliations of authors: Department of Preventive Medicine, Keck School of Medicine, University of Southern California, Los Angeles, CA (JCF, RWH); Departments of Medicine and Community and Family Medicine, Dartmouth Medical School, Hanover, NH (MVG, JAB); Division of Gastroenterology and Hepatology, Department of Medicine, University of North Carolina, Chapel Hill, NC (RSS); Division of Gastroenterology and Hepatology, Department of Internal Medicine, University of Iowa, Carver College of Medicine, Iowa City, IA (RWS); Department of Gastrointestinal Medicine and Nutrition, University of Texas MD Anderson Cancer Center, Houston, TX (RSB); Department of Gastroenterology and Hepatology, Cleveland Clinic Foundation, Cleveland, OH (CAB); Dalla Lana School of Public Health and Department of Nutritional Sciences, University of Toronto, Toronto, Canada (GEM-E).

Data regarding the association between folate status and risk of prostate cancer are sparse and conflicting. We studied prostate cancer occurrence in the Aspirin/Folate Polyp Prevention Study, a placebo-controlled randomized trial of aspirin and folic acid supplementation for the chemoprevention of colorectal adenomas conducted between July 6, 1994, and December 31, 2006. Participants were followed for up to 10.8 (median = 7.0, interquartile range = 6.0-7.8) years and asked periodically to report all illnesses and hospitalizations. Aspirin alone had no statistically significant effect on prostate cancer incidence, but there were marked differences according to folic acid treatment. Among the 643 men who were randomly assigned to placebo or supplementation with folic acid, the estimated probability of being diagnosed with prostate cancer over a 10-year period was 9.7% (95% confidence interval [CI] = 6.5% to 14.5%) in the folic acid group and 3.3% (95% CI = 1.7% to 6.4%) in the placebo group (age-adjusted hazard ratio = 2.63, 95% CI = 1.23 to 5.65, Wald test P = .01). In contrast, baseline dietary folate intake and plasma folate in nonmultivitamin users were inversely associated with risk of prostate cancer, although these associations did not attain statistical significance in adjusted analyses. These findings highlight the potential complex role of folate in prostate cancer and the possibly different effects of folic acid-containing supplements vs natural sources of folate.

J Natl Cancer Inst. 2009 Mar 10. [Epub ahead of print]Click here to read

Exercise for the management of cancer-related fatigue in adults.

March 14th, 2009

Cramp F, Daniel J.

University of the West of England, School of Allied Health Professions, Glenside Campus, Blackberry Hill, Bristol, UK, BS16 1DD. fiona.cramp@uwe.ac.uk

BACKGROUND: Cancer-related fatigue is now recognised as an important symptom associated with cancer and its treatment. A number of studies have investigated the effects of physical activity in reducing cancer-related fatigue with no definitive conclusions regarding its effectiveness.

OBJECTIVES: To evaluate the effect of exercise on cancer-related fatigue both during and after cancer treatment.

SEARCH STRATEGY: The Cochrane Controlled Trials Register (CENTRAL/CCTR), MEDLINE (1966 to July 2007), EMBASE (1980 to July 2007), CINAHL (1982 to July 2007), British Nursing Index (January 1984 to July 2007), AMED (1985 to July 2007), SIGLE (1980 to July 2007), and Dissertation Abstracts International (1861 to July 2007) were all searched using key words. Reference lists off all studies identified for inclusion and relevant reviews were also searched. In addition, relevant journals were hand searched and experts in the field of cancer-related fatigue were contacted.

SELECTION CRITERIA: Randomised controlled trials (RCTs) that investigated the effect of exercise on cancer-related fatigue in adults were included.

DATA COLLECTION AND ANALYSIS: Two review authors independently assessed the methodological quality of studies and extracted data based upon predefined criteria. Where data were available meta-analyses were performed for fatigue using a random-effects model.

MAIN RESULTS: Twenty-eight studies were identified for inclusion (n = 2083 participants), with the majority carried out on participants with breast cancer (n = 16 studies; n = 1172 participants). A meta-analysis of all fatigue data, incorporating 22 comparisons provided data for 920 participants who received an exercise intervention and 742 control participants. At the end of the intervention period exercise was statistically more effective than the control intervention (SMD -0.23, 95% Confidence Interval (CIs) -0.33 to -0.13).

AUTHORS’ CONCLUSIONS: Exercise can be regarded as beneficial for individuals with cancer-related fatigue during and post cancer therapy. Further research is required to determine the optimal type, intensity and timing of an exercise intervention.

Cochrane Database Syst Rev. 2008 Apr 16;(2):CD006145.Click here to read
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Aust J Physiother. 2008;54(3):216.

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March 12th, 2009

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