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Joseph T. Anderson

Other affiliations: Hastings Entertainment
Bio: Joseph T. Anderson is an academic researcher from University of Minnesota. The author has contributed to research in topics: Blood serum & Cholesterol. The author has an hindex of 39, co-authored 58 publications receiving 8908 citations. Previous affiliations of Joseph T. Anderson include Hastings Entertainment.


Papers
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Journal ArticleDOI
TL;DR: It is shown that in a system consisting of two additive components which are mixed but the densities of which are known, the determination of the density of the system allows one to calculate the proportional masses of the two components.
Abstract: One can trace to Archimedes the idea that in a system consisting of two additive components which are mixed but the densities of which are known ( d l , d 2 ) , the determination of the density of the system ( D ) allows one to calculate the proportional masses of the two components. Let’s denote these components as W1 and W2.S Then, in a system with total weight W = W1 + Wz, the general equation for calculating component W1 expressed as a fraction (w1) of the total body weight is:

2,221 citations

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TL;DR: Least-squares analysis indicates that stearic acid, as well as saturated fatty acids containing fewer than 12 carbon atoms, have little or no effect on serum cholesterol in man and resolves heretofore puzzling discrepancies in the literature.
Abstract: For many dietary changes satisfactory prediction of the average change in the serum cholesterol level of man in mg./100 ml., is given by Δ Chol. = 1.35(2ΔS − ΔP) + 1.5ΔZ where S and P are percentages of total calories provided by glycerides of saturated and polyunsaturated fatty acids in the diet and Z2 = mg. of dietary cholesterol/1000 Cal. This formula fails, however, when the dietary change involves large amounts of cocoa butter and discrepancies also appear with beef tallow or hydrogenated coconut oil diets. Controlled dietary experiments at the University of Minnesota and at 2 other centers, provide 63 sets of comparisons of serum cholesterol averages for groups of men on each of 2 chemically characterized diets. Least-squares analysis indicates that stearic acid, as well as saturated fatty acids containing fewer than 12 carbon atoms, have little or no effect on serum cholesterol in man. The equation, Δ Chol. = 1.2(2ΔS′ − ΔP) + 1.5ΔZ, yields good correlation (r = 0.93) with the observed values in these 63 sets of data. This formulation also resolves heretofore puzzling discrepancies in the literature.

972 citations

Journal ArticleDOI
TL;DR: The series of metabolic ward experiments, with 22 physically healthy men in each, covered dietary cholesterol intakes from 50 to 1450 mg.
Abstract: Data from 227 men in 10 sets of controlled dietary experiments in 5 institutions gave the least-squares solution: [see text] with S.E. of slope --±0.44, where X is the serum cholesterol level of an individual, X is the average for all men on the same diet, and Δ is the response to a given dietary change. Equations, a chart and a table are provided for the prediction of the serum cholesterol response when change is made from one diet to another when cholesterol and fatty acid compositions of the diets are known. Comparison of predicted with observed average values in recently published data on samples of free-living people changing diets on prescription designed to lower serum cholesterol gave, predicted versus observed Δ: −30.0 vs. −28.5 and −27.2 vs. -30.1 mg./l00 ml. in men and women in caloric balance. In a sample of men who were also losing weight on a low-fat, low-cholesterol diet a change of −33.5 was predicted versus −39.8 observed.

609 citations

Journal ArticleDOI
TL;DR: In men in calorie equilibrium, changes in dietary fat produce responses in the serum cholesterol level that, on the average, are predictable from the percentages of total calories provided by saturated and polyunsaturated fatty acid glycerides in the diets concerned.
Abstract: In men in calorie equilibrium, changes in dietary fat produce responses in the serum cholesterol level that, on the average, are predictable from the percentages of total calories provided by saturated (S) and polyunsaturated (P) fatty acid glycerides in the diets concerned. S and P have opposing actions and, in general, Δ Cholesterol (mg./100 ml.) = 2.7ΔS − 1.3ΔP, where Δ refers to the difference between 2 diets. Increasing the number of double bonds beyond 2 in polyunsaturated fatty acids does not result in proportionate increases in serum cholesterol-lowering effect. The mono-enes oleic and erucic acid have little or no effect on the serum cholesterol level when they are exchanged in the diet for equal calories of simple carbohydrate. Changes of fats in the diet produce serum cholesterol responses that are also correlated with the iodine values, or the square-roots of those values, of the fats concerned when the iodine value happens to be highly correlated with 2.7S - 1.3P. When changes in diet fats involve substantial differences in amounts of mono-enes, or of fatty acids containing more than 2 double bonds, the serum cholesterol response has a low or negligible correlation with the iodine value, or its square-root, of the fats.

373 citations


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Journal ArticleDOI
TL;DR: Skinfold thicknesses at four sites – biceps, triceps, subscapular and supra-iliac – and total body density were measured on 209 males and 272 females aged from 16 to 72 years, finding it necessary to use the logarithm of skinfold measurements in order to achieve a linear relationship with body density.
Abstract: The fat content of the human body has physiological and medical importance. It may influence morbidity and mortality, it may aIter the effectiveness of drugs and anaesthetics, and it may affect the ability to withstand exposure to cold and starvation. Thus the measurement of the total body fat provides useful information. In many people, but by no means everyone, a moderately satisfactory estimate of the body fat content can be obtained from the height and weight. However, for more precise evaluation several methods are available which give a reasonably accurate measure of body fat both in normal subjects and in individuals with unusual body builds. Most of these methods are based on the assumption that the body can be considered to consist of two compartments of relatively constant composition but which are distinctly different; these compartments are: (I) the body fat, which includes the entire content of chemical fat or lipids in the body, and (2) the fat-free mass (FFM), which includes all the rest of the body apart from fat. The body fat compartment is anhydrous, contains no potassium and has a fairly constant density of about 0.90 x 103 kg/m3. The fat-free compartment on the other hand probably has a fairly constant density of about 1.10 x 103 kg/m3, a potassium content of about 68 mequiv./kg in males (about 10% less in females) and a water content of about 720 g/kg. Thus measurement of body density or of total body K or of total body water allows a calculation of the relative proportion of these two compartments in the body and therefore also of the total fat content. The accuracy of these measures, however, is limited by the variability of the composition and density of the fat-free compartment in different individuals. In particular, individuals with a relatively high or

6,287 citations

Journal ArticleDOI
TL;DR: Bayesian model averaging (BMA) provides a coherent mechanism for ac- counting for this model uncertainty and provides improved out-of- sample predictive performance.
Abstract: Standard statistical practice ignores model uncertainty. Data analysts typically select a model from some class of models and then proceed as if the selected model had generated the data. This approach ignores the uncertainty in model selection, leading to over-confident inferences and decisions that are more risky than one thinks they are. Bayesian model averaging (BMA)provides a coherent mechanism for accounting for this model uncertainty. Several methods for implementing BMA have recently emerged. We discuss these methods and present a number of examples.In these examples, BMA provides improved out-of-sample predictive performance. We also provide a catalogue of currently available BMA software.

3,942 citations

Journal ArticleDOI
TL;DR: Results demonstrate the importance of including different types of health measures in health psychology research, and indicate that self-report health measures reflect a pervasive mood disposition of negative affectivity (NA), which will act as a general nuisance factor in health research.
Abstract: Most current models in health psychology assume that stress adversely affects physical health. We re-examined this assumption by reviewing extensive data from the literature and from six samples of our own, in which we collected measures of personality, health and fitness, stress, and current emotional functioning. Results indicate that self-report health measures reflect a pervasive mood disposition of negative affectivity (NA); self-report stress scales also contain a substantial NA component. However, although NA is correlated with health compliant scales, it is not strongly or consistently related to actual, long-term health status, and thus will act as a general nuisance factor in health research. Because self-report measures of stress and health both contain a significant NA component, correlations between such measures likely overestimate the true association between stress and health. Results demonstrate the importance of including different types of health measures in health psychology research.

3,097 citations

Journal ArticleDOI
TL;DR: The regression equations were shown to be valid for adult men varying in age and fatness, in combination with age, waist and forearm circumference.
Abstract: 1. Skinfold thickness, body circumferences and body density were measured in samples of 308 and ninety-five adult men ranging in age from 18 to 61 years. 2. Using the sample of 308 men, multiple regression equations were calculated to estimate body density using either the quadratic or log form of the sum of skinfolds, in combination with age, waist and forearm circumference. 3. The multiple correlations for the equations exceeded 0.90 with standard errors of approximately +/- 0.0073 g/ml. 4. The regression equations were cross validated on the second sample of ninety-five men. The correlations between predicted and laboratory-determined body density exceeded 0.90 with standard errors of approximately 0.0077 g/ml. 5. The regression equations were shown to be valid for adult men varying in age and fatness.

3,083 citations

Journal ArticleDOI
TL;DR: Suggestions to improve the assessment of behavioral interventions include more complete delineation of the physiological mechanisms by which such interventions might work; increased use of new, more convenient "alternative" end points for behavioral intervention trials; development of specifically targeted behavioral interventions (based on profiling of patient factors); and evaluation of previously developed models of predicting behavioral change.
Abstract: Recent studies provide clear and convincing evidence that psychosocial factors contribute significantly to the pathogenesis and expression of coronary artery disease (CAD). This evidence is composed largely of data relating CAD risk to 5 specific psychosocial domains: (1) depression, (2) anxiety, (3) personality factors and character traits, (4) social isolation, and (5) chronic life stress. Pathophysiological mechanisms underlying the relationship between these entities and CAD can be divided into behavioral mechanisms, whereby psychosocial conditions contribute to a higher frequency of adverse health behaviors, such as poor diet and smoking, and direct pathophysiological mechanisms, such as neuroendocrine and platelet activation. An extensive body of evidence from animal models (especially the cynomolgus monkey, Macaca fascicularis) reveals that chronic psychosocial stress can lead, probably via a mechanism involving excessive sympathetic nervous system activation, to exacerbation of coronary artery atherosclerosis as well as to transient endothelial dysfunction and even necrosis. Evidence from monkeys also indicates that psychosocial stress reliably induces ovarian dysfunction, hypercortisolemia, and excessive adrenergic activation in premenopausal females, leading to accelerated atherosclerosis. Also reviewed are data relating CAD to acute stress and individual differences in sympathetic nervous system responsivity. New technologies and research from animal models demonstrate that acute stress triggers myocardial ischemia, promotes arrhythmogenesis, stimulates platelet function, and increases blood viscosity through hemoconcentration. In the presence of underlying atherosclerosis (eg, in CAD patients), acute stress also causes coronary vasoconstriction. Recent data indicate that the foregoing effects result, at least in part, from the endothelial dysfunction and injury induced by acute stress. Hyperresponsivity of the sympathetic nervous system, manifested by exaggerated heart rate and blood pressure responses to psychological stimuli, is an intrinsic characteristic among some individuals. Current data link sympathetic nervous system hyperresponsivity to accelerated development of carotid atherosclerosis in human subjects and to exacerbated coronary and carotid atherosclerosis in monkeys. Thus far, intervention trials designed to reduce psychosocial stress have been limited in size and number. Specific suggestions to improve the assessment of behavioral interventions include more complete delineation of the physiological mechanisms by which such interventions might work; increased use of new, more convenient "alternative" end points for behavioral intervention trials; development of specifically targeted behavioral interventions (based on profiling of patient factors); and evaluation of previously developed models of predicting behavioral change. The importance of maximizing the efficacy of behavioral interventions is underscored by the recognition that psychosocial stresses tend to cluster together. When they do so, the resultant risk for cardiac events is often substantially elevated, equaling that associated with previously established risk factors for CAD, such as hypertension and hypercholesterolemia.

2,774 citations