Hemoglobin A1c reproducibility.
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Biomedical subjects
Publications and source records attributed to G G Rhoads.
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A survey of systemic lupus erythematosus (SLE) patients was conducted in civilian general hospitals on Oahu, Hawaii for the years 1970-75. One hundred sixty-eight cases were ascertained, of which 107 were considered "definite." Age-adjusted prevalence rates per 100,000 were estimated for definite cases at the end of 1975 as follows: white 5.8, Chinese 24.1, Filipino 19.9, part-Hawaiian 20.4, and Japanese 18.2. There was a heavy preponderance of females in each ethnic group, averaging 90% of the definite cases overall. Review of vital statistics for the United States and Hawaii during this period showed age-adjusted SLE mortality rates per million as follows: U.S. white 3.04, U.S. non-white 8.82, Hawaii white 1.89, Hawaii non-white 14.46. The cause of the very high SLE prevalence and mortality in the Oriental and Polynesian people of Hawaii is not clear.
Obesity, alcohol consumption, and hematocrit provide an index of plasma uric acid, which in path analysis has a cultural heritability of 0.11 in children and 0.23 in parents, a small maternal effect, and a genetic heritability of 0.25 in both generations. Preliminary evidence for a major locus is destroyed by the omission of one exceptional child. There is no evidence against the polygenic hypothesis for hyperuricemia in the Japanese-American population studied.
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Possible effects of cultural variables on the risk of coronary heart disease (CHD) were examined in 7705 men of Japanese ancestry living in Hawaii. The six-year incidence of CHD was related to birthplace (Japan or elsewhere), number of years spent in Japan, ability to read and write Japanese, ability to speak Japanese, and to an index of preference for a traditional Japanese diet. Statistically significant inverse relationships were found between CHD incidence and all of these variables which reflect the degree of exposure to Japanese culture during childhood. In multivariate analyses where the major CHD risk factors were taken into account, years spent in Japan and ability to read and write Japanese remained significant. Hence, exposure to Japanese culture during childhood appears to protect against CHD in adulthood. This may explain, in part, the gradient of CHD frequency among Japanese in Japan, Japanese-Americans, and Caucasians that could not be entirely attributed to the established risk factors.
A general linear model is presented here for biological and cultural inheritance involving ten parameters to be estimated from 16 correlations in nuclear families, providing ample degrees of freedom to test goodness of fit. Applied to six lipoprotein traits the model fits acceptably to all, although there is evidence of transient maternal effects for cholesterol and lipemia. Genetic heritability in children ranges from 0.175 for triglyceride to 0.562 for total cholesterol. Cultural heritability in children ranges from 0.012 for VLDL to 0.149 for HDL-cholesterol.
Japanese men long resident in Honolulu, Hawaii have significantly more ischemic heart disease but significantly fewer small cardiac scars than men in Hiroshima, Japan. These scars occur in three forms:(1)small scars in the mural myocardium which account for the difference in frequency of small lesions in the two cities and are of uncertain etiology; (2)areas of diffuse fibrosis in the papillary muscles. These are equally frequent in the two cities and are associated with advancing age and sclerosis of papillary muscle arteries; and(3)focal scars in the papillary muscles. These are more frequent in Honolulu than Hiroshima. They are healed infarcts due to ischemic heart disease and are associated with a severe degree of extramural coronary artery atherosclerosis. Small mural myocardial scars, when present, are usually found in multiple sites. Their increased frequency in Hiroshima is not explained by differences in age or heart weight. They are more common in the presence of sclerosis of intramural small arteries, but this association also fails to explain the intercity difference. It is supected that the excess of these small cardiac scars in Hiroshima males reflects past privation. There is no evidence that is is related to A-bomb radiation exposure.
The relationship of dietary intakes to subsequent development of coronary heart disease (CHD) during a 6-year follow-up period was investigated in 7705 men of Japanese ancestry, ages 45 to 68 and living in Hawaii. Data on the intakes of calories and nutrients were obtained by 24-hr diet recall interviews at the base-line examination. An index for ingestion of traditional Japanese diet (Japanese diet score) was also calculated for each man. The men who subsequently developed myocardial infarction or died of CHD generally ate less than those who remained free of CHD, with statistically significant differences for total calories, total carbohydrate, complex carbohydrate or starch, simple carbohydrate other than sucrose, vegetable protein, alcohol, and Japanese diet score. However, when other major risk factors for CHD were taken into account, the negative association with CHD remained statistically significant only for alcohol and, to a lesser extent, total carbohydrate intakes. The lower total caloric intakes in CHD cases, largely due to decreased alcohol and carbohydrate intakes, could not be accounted for by either under-reporting of food consumption among obese men or diminished physical activity in CHD cases.
A "sinking" pre-beta lipoprotein was sought in a probability sample of 1854, 50--72-year-old men of Japanese ancestry in Honolulu by ultracentrifugation of plasma and electrophoresis of the bottom fraction (density greater than 1.006) in agarose. A definite electrophoretic band was found in 5.6% of the men and a trace band was found in 4.6% of them. The frequency of such a band increased with age and decreased with adiposity. The relative risk for coronary heart disease, based on prevalence cases was found to be 1.7 in men with a definite band, and 1.4 in those with a trace band, when compared to men without. This association could not be explained by the higher low density lipoprotein levels in men with trace or definite bands. These data are consistent with previous reports suggesting that the Lp antigen (for which a sinking pre-beta lipoprotein is probably an insensitive marker) is associated with coronary disease.
The Lp gene frequency is estimated to be 0.083 in Japanese, but with our method of assay the evidence favoring a major locus is marginal. The sinking pre-beta band is significantly associated with elevated cholesterol and depressed triglyceride. The biological significance of these observations is discussed.
During the years 1965 to 1974, 481 men who had participated in a standardized examination at the Honolulu Heart Study died. Autopsies were conducted in 226 of the men, and in 137 the extent of coronary and/or aortic atherosclerosis was estimated by the American Heart Association panel method. This method was found to be simple and highly reproducible. In multivariate analysis, statistically independent associations were found between aortic atherosclerosis and age at death, cigarettes per day, serum cholesterol, and systolic blood pressure; between coronary atherosclerosis and relative weight, cigarettes per day, and serum cholesterol; and between heart weight and height, relative weight, and systolic blood pressure. Alcohol consumption was lower and hematocrit was higher in men with infarcts than in other decedents, but no statistically significant relation between these variables and coronary or aortic atherosclerosis could be demonstrated.
In more than 500 families of Japanese ancestry, selected in part through fathers with hyperlipemia or coronary heart disease, a major locus for hyper-beta-cholesterolemia (hyperlipoproteinemia type IIa) is highly significant (chi22 = 24.02), with an allele frequency .002 in the general population. This gene is revealed with about the same power by fasting levels of LDL (low density lipoprotein) cholesterol and total cholesterol. However, VLDL (very low density lipoprotein) cholesterol, HDL (high density lipoprotein) cholesterol, and triglyceride give no convincing evidence for a major locus in this population, nor was a gene for combined hyperlipoproteinemia detected.
We examined the relation of coffee and alcohol consumption to the risk of coronary heart disease during a six-year period in a cohort of 7705 Japanese men living in Hawaii. The analysis was based on 294 new cases of coronary heart disease. There was a positive association between coffee intake and risk, but it became statistically insignificant when cigarette smoking was taken into account. There was a strong negative association between moderate alcohol consumption (up to 60 ml per day), mainly from beer, and the risk of nonfatal myocardial infarction and death from coronary heart disease. This association remained significant in multivariate analysis, taking into account smoking and other risk factors. The correlation of alcohol consumption with the level of alpha cholesterol (positive) and beta cholesterol (negative) may partly account for the observed negative association between alcohol and coronary heart disease.
The incidence of myocardial infarction and death from coronary heart disease was studied in defined samples of 45 to 68 year old Japanese men in Japan, Hawaii and California. The incidence rate was lowest in Japan where it was half that observed in Hawaii (P less than 0.01). The youngest men in the sample in Japan were at particularly low risk. The incidence among Japanese men in California was nearly 50 percent greater than that of Japanese in Hawaii (P less than 0.05). A striking increase in the incidence of myocardial infarction appears to have occurred in the Japanese who migrated to the United States; this increase is more pronounced in California than in Hawaii.
Various risk factors were evaluated to explain a significantly greater incidence of coronary heart disease in men of Japanese ancestry resident in Hawaii compared with men resident in Japan. The independent predictors of incidence of coronary heart disease in both Japan and Hawaii were systolic blood pressure, serum cholesterol, relative weight and age. These factors appeared to influence incidence similarly in both areas because in each case the correlation coefficients for Japan and Hawaii did not differ significantly. The hypothesis that the greater incidence in Hawaii could be attributed to differences in levels of these risk factors was tested with the Walker-Duncan method. The four variable multiple logistic function describing the probability of coronary heart disease in Japan was applied to the cohort characteristics observed in Hawaii. The estimated incidence thus obtained was not significantly different from that actually observed in the men resident in Hawaii. Therefore the increased coronary risk profile in Hawaii compared with Japan can account for the greater incidence of coronary heart disease in the former. Current cigarette smoking was significantly related to the risk of coronary heart disease in Hawaii but not in Japan. This difference requires further investigation.
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A total of 161 patients with chronic obstructive pulmonary disease (COPD) plus 100 control subjects (identified during a study of heart disease in 6,860 Japanese-American men aged 52 to 75 years who were residing in Hawaii) were analyzed for phenotype in search of the antitrypsin gene Z, which has been shown to be associated with pulmonary emphysema in other racial groups. No carriers of the Z gene were found, and the question of whether the rarity or absence of this gene relates to a low frequency of COPD among Japanese-Americans is reviewed.
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