Uric acid, an antioxidant found in high concentrations in serum and in the brain, has been hypothesized to protect against oxidative damage and cell death in Parkinson's disease. The authors tested this hypothesis among men participating in a 30-year prospective study known as the Honolulu Heart Program. Serum uric acid was measured in 7,968 men at the baseline examination held from 1965 to 1968. Of these men, 92 subsequently developed idiopathic Parkinson's disease (IPD). In analyses adjusted for age and smoking, men with uric acid concentrations above the median at enrollment had a 40% reduction in IPD incidence (rate ratio (RR) = 0.6; 95% confidence interval (CI) 0.4-1.0). Reduced IPD incidence rates persisted in analyses restricted to nonsmokers (RR = 0.5; 95% CI 0.3-1.0) and cases younger than age 75 years (RR = 0.5; 95% CI 0.3-0.9). Incidence rates were not notably affected when analyses were restricted to cases that occurred more than 5 years after uric acid measurement (RR = 0.6; 95% CI 0.4-1.0). Inclusion of known or computed correlates of uric acid in regression models did not substantially change risk of IPD. This study provides prospective evidence of an association between uric acid and reduced occurrence of IPD and indicates that further investigations of this association are warranted.

Lipodystrophy with peripheral fat wasting following treatment with NRTI-containing HAART is associated with a decrease in subcutaneous adipose tissue mtDNA content.

A nested case-control study of 84 incident cases of patients with idiopathic Parkinson's disease (PD) detected by June 30, 1994 and 336 age-matched control subjects, compared previously-documented intake of total dietary vitamin E and of selected vitamin E-containing foods. All study subjects had been followed for 27 to 30 years after diet recording in the 8,006-man Honolulu Heart Study cohort. We determined PD outcomes by periodic cohort re-examination and neurologic testing, private physician reports, examination of O'ahu neurologists' office records, and continual death certificate and hospital discharge diagnosis surveillance. Data on vitamin E intake, obtained from three dietary data sets at the time of cohort enrollment (1965 to 1968), included a food-frequency questionnaire and a 24-hour photograph-assisted dietary recall administered by trained dietitians. Although absence of PD was significantly associated with prior consumption of legumes (adjusted OR = 0.27, 95% CI 0.09 to 0.78), a dietary variable preselected for high vitamin E content, neither food categories nor quartiles nor continuous variables of vitamin E consumption were significantly associated with PD occurrence. Though consistent with prior reports of PD protection afforded by legumes, and with speculation on the possible benefits of dietary or supplemental vitamin E in preventing PD, these preliminary data do not conclusively document a beneficial effect of dietary vitamin E on PD occurrence.

Prevalence of obesity and type-2-diabetes requires dietary manipulation. It was hypothesized that wheat-legumecomposite breads will reduce the spike of blood glucose and increase satiety. Four pan bread samples were prepared: White bread (WB) as standard, Whole-wheat bread (WWB), WWB supplemented with chickpea flour at 25 % (25%ChB) and 35 % (35%ChB) levels. These breads were tested in healthy female subjects for acceptability and for effect on appetite, blood glucose, and physical discomfort in digestion. The breads were rated >5.6 on a 9-point hedonic scale with WB significantly higher than all other breads. No difference in area under the curve (AUC) for appetite was found, but blood glucose AUC was reduced as follows: 35%ChB < WB and WWB, WB >25%ChB = WWB or 35%ChB. We conclude that addition of chickpea flour at 35 % to whole wheat produces a bread that is acceptable to eat, causing no physical discomfort and lowers the glycemic response.

No abstract

Objective-The association of type 2 diabetes (T2DM) with the overall dietary pattern and its relation with ethnicity were examined.Methods-A cross-sectional study with 1257 participants with four ethnicities (Caucasian, Filipino, Native Hawaiian and Japanese) in the North Kohala region of Hawaii was conducted. Participants aged 18-95 years were surveyed for their ethnic and demographic backgrounds, dietary intakes and biochemical indexes of glucose intolerance between 1997 and 2000.Results-Three dietary patterns from the food frequency questionnaire were identified by factor analysis. Factor 1 was characterized by a healthy diet with a frequent intake of vegetables and fruits, and factor 2 was dominated by animal foods and local ethnic dishes. Factor 3 was characterized by a Western diet, which was dominated by French fries, fast-food hamburgers, pizza, and chips. Multivariate logistic regression model for the T2DM prevalence included ethnicity and 3 dietary factors after adjustment for age, sex, BMI, income, physical activity, smoking status and energy intake. Ethnicity was significantly associated with T2DM showing odds ratios (OR's) for Native Hawaiians and Filipinos compared to Caucasians are 1.83 (95% CI 1.12-3.00) and 1.92 (95% CI 1.12-3.29), respectively. Among the three dietary factors, factor 2 HSK prepared the draft of the manuscript; HSK and CW contributed to the conception and design of the study; AG and CW contributed to the generation, collection and assembly of data; SYP, AG and PSH contributed to analysis and interpretation of data; All coauthors contributed to the revision of the manuscript and approved the final version of the manuscript.Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. HHS Public Access Author ManuscriptAuthor Manuscript Author ManuscriptAuthor Manuscript was positively associated with T2DM (OR=1.30, 95% CI of 1.03-1.68), but the significance disappeared after adjustment for energy intake.Conclusions-The findings show that ethnicity is a stronger risk factor for T2DM than dietary patterns when energy intake is adjusted for. Reducing energy intake to prevent T2DM deserves more attention during health promotion for the multiethnic population of Hawaii.

The etiology of the racial disparity in bone mass and fracture rate is unknown. Since the PTH-vitamin D endocrine system is a major regulator of calcium metabolism and bone turnover, this cross-sectional study examined the relationship of radial and lumbar bone density to vitamin D metabolite and PTH concentrations and to calcium intake and excretion in 67 white and 70 black highly comparable, healthy, premenopausal women. Bone density at both radial and lumbar sites was higher in blacks than in whites. Serum 25-hydroxyvitamin D was slightly but not statistically significantly (P = 0.08), lower in blacks than in whites, but there were no racial differences in 1,25-dihydroxyvitamin D, PTH, or renal tubular maximum for reabsorption of phosphate. The mean 25-hydroxyvitamin D concentration in blacks was well within the normal range and was not associated with evidence of secondary hyperparathyroidism. There were no correlations of bone density to vitamin D or PTH concentrations. Although there were no racial differences in dietary intake of calcium and vitamin D or in sodium excretion, 24-h urinary calcium excretion was significantly lower in blacks than in whites, and calcium excretion was inversely associated with radial bone density. In contrast to previous reports, in healthy, normal weight, premenopausal black women there is no evidence of vitamin D deficiency or secondary hyperparathyroidism, suggesting that factors other than the vitamin D-PTH axis are responsible for racial differences in bone mass.

Background-Remnant-like particles have been proposed as a new risk factor for coronary heart disease (CHD). This is the first long-term prospective investigation of the relationship between remnant-like particles and a cardiovascular disease outcome in healthy men. Methods and Results-A cohort of 1156 Japanese-American men aged 60 to 82 from the Honolulu Heart Program was followed for 17 years. During that period 164 incident cases of CHD were identified. In multivariate Cox regression analyses, baseline remnant-like particle cholesterol (RLP-C) and triglyceride (RLP-TG) levels were significantly related to CHD incidence independently of nonlipid cardiovascular risk factors and of total cholesterol or high-density and low-density lipoprotein cholesterol levels. Total triglyceride levels were an independent predictor of CHD incidence. However, in models including RLP and triglyceride level simultaneously, neither variable was significant when adjusted for the other. This finding can be attributed to the strong correlation between RLP-C and RLP-TG levels and total triglycerides. When individuals with normal triglyceride levels (nϭ894) were separated from those with elevated triglycerides (nϭ260), the association between RLPs and CHD relative risk was only significant for the group with elevated triglyceride levels. Conclusions-RLP levels predicted CHD incidence independently of nonlipid risk factors and of total cholesterol or high-density and low-density lipoprotein cholesterol levels. However, RLP levels did not provide additional information about CHD incidence over and above total triglyceride levels.