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

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Body fat assessed from total body density and its estimation from skinfold thickness: measurements on 481 men and women aged from 16 to 72 years

Diabetes mellitus is commonly associated with systolic/diastolic hypertension, and a wealth of epidemiological data suggest that this association is independent of age and obesity. Much evidence indicates that the link between diabetes and essential hypertension is hyperinsulinemia. Thus, when hypertensive patients, whether obese or of normal body weight, are compared with age- and weight-matched normotensive control subjects, a heightened plasma insulin response to a glucose challenge is consistently found. A state of cellular resistance to insulin action subtends the observed hyperinsulinism. With the insulin/glucose-clamp technique, in combination with tracer glucose infusion and indirect calorimetry, it has been demonstrated that the insulin resistance of essential hypertension is located in peripheral tissues (muscle), is limited to nonoxidative pathways of glucose disposal (glycogen synthesis), and correlates directly with the severity of hypertension. The reasons for the association of insulin resistance and essential hypertension can be sought in at least four general types of mechanisms: Na+ retention, sympathetic nervous system overactivity, disturbed membrane ion transport, and proliferation of vascular smooth muscle cells. Physiological maneuvers, such as calorie restriction (in the overweight patient) and regular physical exercise, can improve tissue sensitivity to insulin; evidence indicates that these maneuvers can also lower blood pressure in both normotensive and hypertensive individuals. Insulin resistance and hyperinsulinemia are also associated with an atherogenic plasma lipid profile. Elevated plasma insulin concentrations enhance very-low-density lipoprotein (VLDL) synthesis, leading to hypertriglyceridemia. Progressive elimination of lipid and apolipoproteins from the VLDL particle leads to an increased formation of intermediate-density and low-density lipoproteins, both of which are atherogenic. Last, insulin, independent of its effects on blood pressure and plasma lipids, is known to be atherogenic. The hormone enhances cholesterol transport into arteriolar smooth muscle cells and increases endogenous lipid synthesis by these cells. Insulin also stimulates the proliferation of arteriolar smooth muscle cells, augments collagen synthesis in the vascular wall, increases the formation of and decreases the regression of lipid plaques, and stimulates the production of various growth factors. In summary, insulin resistance appears to be a syndrome that is associated with a clustering of metabolic disorders, including non-insulin-dependent diabetes mellitus, obesity, hypertension, lipid abnormalities, and atherosclerotic cardiovascular disease.

Insulin Resistance: A Multifaceted Syndrome Responsible for NIDDM, Obesity, Hypertension, Dyslipidemia, and Atherosclerotic Cardiovascular Disease

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.

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Bayesian Model Averaging: A Tutorial

The importance of the ratio of omega-6/omega-3 essential fatty acids.

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.

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Generalized equations for predicting body density of men

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:

Densitometric analysis of body composition: revision of some quantitative assumptions*

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.

Serum cholesterol response to changes in the diet: IV. Particular saturated fatty acids in the diet.

Prediction of serum-cholesterol responses of man to changes in fats in the diet

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.

Serum cholesterol response to changes in the diet: III. Differences among individuals.

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.

Francisco Grande

Papers

Densitometric analysis of body composition: revision of some quantitative assumptions*

Serum cholesterol response to changes in the diet: IV. Particular saturated fatty acids in the diet.

Prediction of serum-cholesterol responses of man to changes in fats in the diet

Serum cholesterol response to changes in the diet: III. Differences among individuals.

Serum cholesterol response to changes in the diet: I. Iodine value of dietary fat versus 2S-P.